CONTENT

IDENTITY .......................................................................................................................3
PHYSICAL EXAMINATION (January 5th 2016).............................................................6
General Status...................................................................................................................6
Antropometry Status ........................................................................................................ 6
Head to Toe Examination ................................................................................................. 8
Neurological Examination................................................................................................. 9
Meningeal Sign ....................................................................................................... 9
Motoric Examination .............................................................................................. 9
Autonom Examination............................................................................................. 10
Laboratory Investigation ......................................................................................... 10
FOLLOW UP ................................................................................................................... 12
LITERATURE REVIEW..................................................................................................15
DEFINITION .......................................................................................................... 15
ETIOLOGY.............................................................................................................15
PATOPHYSIOLOGY..............................................................................................17
CLINICAL MANIFESTATION.............................................................................. 20
DIAGNOSIS ........................................................................................................... 21
TREATMENT.......................................................................................................... 22
PROGNOSIS .......................................................................................................... 26
REFERENCES.................................................................................................................. 27

IDENTITY
Patient
Name
Birth Date
Age
Gender
Address
Nationality
Religion
Date of admission
Date of examination

: Citra Alhumaira
: July 27th 2009
: 7 years old
: Female
: Jalan Kerja Bakti RT 01/04 Makassar
: Indonesia
: Islam
: January 5th 2016
: January 7th 2016

ANAMNESIS
The anamnesis was taken on January 5th 2016, by alloanamnesis (from patients mother).
Chief complain
Additional complains

: Hard to breath since 3 hours before admission to the hospital.

: Cough, shortness of breath.
1

History Of Present Ilness

A 7 years old child came to Raden Said Sukanto Police Center Hospital emergency room
suffering from hard to breath since 3 hours before admission the hospital, right after cold
water consumption and playing with friends. Patients mother also complaining cough
continuously. Mother said that her child got this disease when she was 1 years old.
History Of Past Illness
Pharyngitis/Tonsilitis

Asthma

Pneumonia

Morbilli

Pertussis

Varicella

Diphteria

Malaria

Polio

Enteritis

Bacillary Dysentry

Amoeba Dysentry

Diarrhea

Thypoid

Worms

Surgery

Brain Concussion

Fracture

Drug Reaction

Birth History
Mothers Pregnancy History

The mother routinely checked her pregnancy to the doctor in the hospital. She denied any
problem noted during her pregnancy. She took vitamins routinely given.
Childs Birth History
Labor

: Hospital

Birth attendants

: Doctor

Mode of delivery

: pervaginam

Gestation

: 38 weeks

Infant state

: healthy

Birth weight

: 3200 grams

Body length

: 49 cm

According to the mother, the baby started to cry and the baby's skin is red, no
congenital defects were reported
Development History
First dentition: 6 months
Psychomotor development

Head Up

: 1 month old

Smile

: 1 month old

Laughing

: 1- 2 month old

Slant

: 2,5 months old

Speech Initation

: 5 months old

Prone Position

Food Self

Sitting

: 5 months old
: 5 6 months old
: 6 months old

Mental Status : Normal

Conclusion

: Growth and development status is still in the normal limits and was

appropriate according to the patients age

Immunization History

Immunization

Frequency

Time

BCG

1 time

1 month old

Hepatitis B

3 times

0, 1, 6 months old

DPT

5 times

2, 4, 6 months old. 2, 5 years old

Polio

6 times

0, 2, 4, 6 months old. 2, 5 years old

PCV

4 times

2, 4, 6 12 months old

Hib

4 times

2, 4, 6, 15 months old

Family History

This is their second children.

There are not any significant illnesses or chronic illnesses in the family declared.
Father have some kind of allergic to food.

History of Disease in Other Family Members / Around the House

There is no one living around their home known for having the same condition as the patient.
PHYSICAL EXAMINATION (January 7th 2016)
General Status
-

General condition
Awareness
Pulse
Breathing rate
Temperature

: mild ill
: Kompos Mentis
: 120 x/min, regular, full, strong.
: 45x/min
: 36,4oC (per axilla)

Antropometry Status
- Weight
- Height

: 15 kilogram
: 110 cm

Nutritional Status based NCHS (National Center for Health Statistics) year 2000:
WFA (Weight for Age): 15/18 x 100 % = 83 % ( good nutrition)
HFA (Height for Age): 110/115 x 100 % = 95 % (good nutrition)
WFH (Weight for Height): 15/17 x 100 % = 88 % (normal)
Conclusion: The patient has good nutritional status.

Head to Toe Examination

Head
Normocephaly, hair (black, normal distributon, not easily removed ) sign of trauma (-),
sunken fontanelle (+).
Eyes
Icteric sclera -/-, pale conjunctiva -/-, hyperaemia conjunctiva -/- , lacrimation -/-,
sunken eyes -/-, pupils 3mm/3mm isokor, Direct and indirect light response ++/++
Ears
Normal shape, no wound, no bleeding ,secretion or serumen
Nose
Normal shape, midline septum, secretion -/Mouth

i.
ii.
iii.
iv.

i.

Lips: moist
Teeth: no caries
Mucous: moist
Tongue: Not dirty
Tonsils: T1/T1, No hyperemia
Pharynx: hyperemia (+)

Neck
Lymph node enlargement (-), scrofuloderma (-)
Thorax
:
Inspection
: symmetric when breathing , retraction +, ictus cordis is visible
Palpation
: mass (-), tactile fremitus +/+
Percussion
: wheezing on both lungs
Auscultation :
1. Cor : regular S1-S2, murmur (-), gallop (-)
2. Pulmo
: vesicular +/+, Wheezing +/+ , Rhonchy +/+
Abdomen
:
Inspection
: Convex, epigastric retraction (-), there is no a widening of the veins,

no spider nevi.
ii. Palpation
: supple, liver and spleen not palpable, fluid wave (-), abdominal mass
(-)
iii. Percussion
iv. Auscultation
Vertebra

: The entire field of tympanic abdomen, shifting dullness (-)

: normal bowel sound, bruit (-)
: There does not appear scoliosis, kyphosis, and lordosis, do not look

any mass along the line of the vertebral

Ekstremities : warm, capillary refill time < 2 second, edema(-)
Skin
: Good turgor.

Neurological Examination
Meningeal Sign

Motoric Examination
Power
Hand
Feet
Tonus
Hand
Feet
Trophy
Hand
Feet
Physiologic Reflex
Upper extrimities
Biceps
Triceps

5 5 5 5/ 5 5 5 5
5 5 5 5/ 5 5 5 5
Normotonus / Normotonus
Normotonus / Normotonus
Normotrophy / Normotrophy
Normotrophy / Normotrophy
+/+
+/+

Lower extrimities
Patella
Achilles

+/+
+/+

Pathologic Reflex
Upper extrimities
Hoffman
Trommer

-/-/-

Lower extrimities
Babinsky
Chaddock
Oppenheim
Gordon
Schaeffer

-/-/-/-/-/-

Clonus
Patella
Achilles

-/-/7

Autonom Examination
Defecation
Urination
Sweating

Normal
Normal ( 4-5 times daily )
Normal

Laboratory Investigation
Hematology April 4th 2015
Hematology

Results

Normal Value

Haemoglobin

13,5 g/dL

13-16 g/dL

Leukocytes

17.600/L

5,000 10,000/L

Hematocrits
Trombocytes

40 %
356.000/ L

40 48 %
150,000 400,000/L

Erythrocytes

4,07 million/L

4 5 million/L

WORKING DIAGNOSIS
- Asthma Brochiale
- DD/ Bronchiolitis
MANAGEMENT
-

O2 1L/m
IVFD Kaen 3B.
Inj. Cefotaxime 2x600 mg IV
Inj. Dexamethasone 3 x 1 mg IV
Ambroxol 3x1 cth
Inhalation : twice a day
Ventolin (1,25 mg)
Bisolvon 10 drops
NaCl 2 cc

PROGNOSIS
8

Quo ad vitam
: dubia ad bonam
Quo ad functionam : dubia ad bonam
Quo ad sanactionam : dubia ad bonam

FOLLOW UP January 5th 2016 - january 7th 2016

January 6th 2016. Second day of hospitalization,
S

Fever (-)
Phlegm (+)
Breathless (+)
Productive cough (-)

General condition: Compos mentis.

Heart rate
= 115 x/min
Respiratory rate = 35x/min
Temperature
= 36,4C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi +/+, wheezing +/+

Asthma Bronchiale
DD/ Bronchiolitis

O2 1L/m
IVFD Kaen3B, , 750cc / 24 Hours.
Inj. Cefotaxime 2x600 mg IV
Inj. Dexamet 3x1 mg IV
Ambroxol syr 3 x 1 cth
Inhalation fourth a day
Ventolin (1,25 mg)
Bisolvon 10 drops
NaCl 1 cc

August 7th 2015. Third day of hospitalization.

S

Fever (-)
Phlegm (-)
Breathlless (-)
Productive cough (-)

General condition: Compos Mentis

Heart rate
= 120 x/min
Respiratory rate = 30x/min
Temperature
= 38.5C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : retraction (+) vesiculer +/+, rhonchi +/+, wheezing -/-

Astha Bronchiale

O2 1L/m
IVFD Kaen3B,
Inj. Cefotaxime 2x600 mg IV
Inj. Dexamet 3x1 mg IV
Paracetamol syr 3 x 1 cth
Ambroxol syr 3 x 1 cth
Inhalation twice a day
Ventolin (1,25 mg)
Bisolvon 10 drops
NaCl 1 cc
10

August 8th 2015, Fourth days of hospitalization

S

Fever (-)
Phlegm (-)
Productive cough (-)
Breathless (-)

General condition: Compos mentis.

Heart rate
= 110 x/min
Respiratory rate = 30x/min
Temperature
= 36C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/-

Asthma Bronchiale

IVFD Kaen3B.
Inj. Cefotaxime 2x350 mg IV
Inj. Dexamet 3x1 mg IV
Paracetamol syr 3 x 0,7 cc
Inhalation twice a day
Ventolin (1,25 mg)
Bisolvon 3 drops
NaCl 1 cc

LITERATURE REVIEW

DEFINITION
Asthma is a chronic inflammatory disorder associated with variable airflow
obstruction and bronchial hyperresponsiveness. It presents with recurrent episodes of wheeze,
cough, shortness of breath, and chest tightness.1

CLASIFICATION
To address diversity and guide management, several factors have been used to classify
pediatric asthma (Fig. 1).1

11

Age is an important classification factor, relevant to diagnosis and treatment. There is general
consensus that milestone ages are around 5 and 12 years, and important clinical and
epidemiological characteristics appear to change around those ages.1
There is slightly less consistency when it comes to severity and persistence, which have been
extensively used in the past to classify asthma. With respect to persistence, asthma is usually
classified as intermittent or persistent; in addition, infrequent and frequent intermittent classes
are proposed by the AAMH. With respect to severity, persistent asthma is usually classified as
mild, moderate, and severe. However, in PRACTALL and SIGN, only severe asthma is
mentioned, while in the JGCA, a most severe class is proposed. Classifications of
severity/persistence are challenging as they require differentiation between the inherent
severity of the disease, resistance to treatment, and other factors, such as adherence to
treatment. Hence, these classifications are currently recommended only for initial assessment
of the disease severity and are being replaced by the concept of control, which is more
clinically useful.1
Control is generally accepted as a dynamic classification factor, critical to guiding treatment.
Control categories are quite relevant in clinical practice. Slightly different terms are used for
the levels of asthma control, which are generally three (controlled, partly controlled, and
uncontrolled). In some cases, complete control is described, as a state with no disease
activity (Table 1).1

12

In assessing severity and control, a distinction between current impairment and future risk is
proposed by NAEPP and GINA. Although not stated in the other documents, these two
elements are clearly distinguishable and may differentially respond to treatment; therefore,
they should be considered independently.1

13

PATHOPHYSIOLOGY
Asthma symptoms most commonly occur in the setting of chronic and often systemic
inflammation, which is probably present even when there is no evidence of clinical
symptoms. Asthma is also characterized by considerable variability in activity since
symptoms and exacerbations can be triggered by a number of different factors. In addition,
repeated exacerbations may help perpetuate the disease. The relative contribution of each
trigger to disease activity may change with the age of the child.2
Asthma is particularly complex in children because several elements of the immune system
including antigen presentation, T-cell function and antibody production are immature and
thus facilitate atopic responses . Interactions between the rate of immune system maturation
and lung growth and development during the first years of life seem to be crucial in the
development of asthma . In addition, the airways of infants and children are more susceptible
to obstruction due to their smaller size and the soft ribcage offers poor support for the
underlying lung, which recoils to volumes more likely to cause airway closure . All of these
phenomena are influenced by the childs genes and by the interaction between genetic,
developmental and environmental factors.2
o Immunological abnormalities
Immunological abnormalities associated with asthma have been extensively studied in murine
models, in vitro and in adult asthma patients. Fewer studies have examined pediatric patients.
Immune responses may vary among children whose asthma is associated with different
triggers (e.g. allergen-induced vs virus-induced inflammation), but also in accordance with
the developmental changes described above. However, there is considerable overlap between
phenotypes as well as between individuals. The underlying disease in atopic (allergic) asthma
is systemic, illustrated by the involvement of the bone marrow in effector cell mobilization
and imbalances in T-cell immunity are considered central in the majority of patients.2
o T-cell immunity.
T cells play a prominent and complex role in the pathophysiology of asthma. Interleukin (IL)4 and IL-13, which are crucial in IgE class switching, and IL-5, which drives eosinophilia,
are the products of the Th2 subset of T-helper lymphocytes. A simple paradigm of imbalance
between Th1 and Th2 cytokines has long been used to describe immunological abnormalities
in asthma. However, it is becoming increasingly clear that interactions between T-cell subsets
14

and related cytokines are more complex and differ depending on a number of factors
including age and stimulus.2
Evidence from animal models suggests that dendritic cells, which present antigen to T cells,
are involved in driving the Th1/Th2 imbalance. Dendritic cell function is suboptimal in very
young children since it does not mature until later in life. An important role also appears to be
played by T-regulatory cells, which suppress immune responses by regulating inflammation
via cell-to-cell contact and the release of suppressive cytokines.2
o Atopy.
The majority of children with asthma are atopic, defined as the propensity to develop IgE
antibodies and Bacharier et al. 10 related clinical syndrome. Although the atopic phenotype is
frequently present in infancy, it becomes increasingly apparent in preschool and school-age
children and remains associated with asthma at all ages .Atopic individuals tend to have
elevated IgE antibody levels and a Th1/Th2 imbalance in response to mitogens, allergens and
viruses. The atopic environment promotes further allergen sensitization and aberrant
responses to viral infections.2
o Structurefunction interactions
In addition to inflammation, structural changes are also present in the airways of individuals
with asthmatic symptoms. These changes can persist even in the absence of symptoms for
more than 6 years and cessation of asthma therapy.2
o Airway remodeling.
Airway remodeling is a general term describing chronic, possibly irreversible changes that
occur in the airways of patients with asthma. These include smooth muscle hypertrophy,
angiogenesis and increased vascularity, chronic inflammatory cell infiltration, goblet cell
hyperplasia, collagen deposition, thickening of the basement membrane and reduced
elasticity of the airway wall. Although such abnormalities have been described in both adults
and children, they are less extensively characterized in pediatric patients. Evidence of
remodeling has been described in children with postviral wheeze, but there is evidence that
the changes do not begin until after infancy. Remodeling may be enhanced by elements of a
Th2 immune response. Early treatment (from 2 or 3 years of age) with inhaled corticosteroids
(ICS) does not appear to alter the course of these changes.2
15

o Bronchial inflammation.
Bronchial inflammation is a central characteristic of most patients who have asthma
symptoms, and involves changes at the epithelial level, recruitment of inflammatory cells,
and

production

of

multiple

mediators.

It

is

closely

associated

with

airway

hyperresponsiveness. Cellularity and other characteristics of inflammation depend upon

trigger and age and may differ between asthma phenotypes. Inflammation may persist to a
varying extent during the intervals between exacerbations.2
o Nasal inflammation.
In adult asthma, nasal inflammation is found even in the absence of symptoms and nasal
allergen challenge results in increased bronchial inflammation and vice versa. Although this
has not yet been shown in children, it appears to correlate with the clinical histories of many
children with allergic asthma. 2
o Role of epithelium.
The bronchial epithelium plays a central role in asthma by reacting to external stimuli as well
as regulating inflammatory and remodeling processes. Biopsy studies have shown that the
epithelial barrier appears to be compromised in both adults and children with asthma.2
o Inflammatory cells and their recruitment.
Eosinophils, neutrophils and T cells infiltrate the epithelium in childhood asthma and cause
inflammation. Neutrophilic inflammation is associated with both viral triggers and increased
disease severity. Eosinophilic inflammation is associated with asthma and atopy and has also
been associated with persistent symptom. Biopsy studies, bronchoalveolar lavage

and

indirect measures of inflammation, such as exhaled nitric oxide (eNO), all show that
bronchial inflammation is present in young children with respiratory symptoms and asthma.2
o Airway obstruction.
During asthma exacerbations, the airway is obstructed by a combination of edema, mucus
hypersecretion and smooth muscle contraction. This occurs at all ages and in all asthma
phenotypes and is a common endpoint induced by different triggers. 2
o Airway hyperresponsiveness and neural control.
16

Airway responsiveness to nonspecific stimuli is higher in normal infants and young children
than in older children or adults. Airway hyperresponsiveness is a hallmark of asthma. It is
also a feature of viral infection and can be present irrespective of asthma diagnosis or asthma
symptoms. It is associated with inflammation and airway remodeling and is correlated with
asthma severity. Neural regulation of the airways consists of cholinergic excitatory,
adrenergic inhibitory nerves and nonadrenergic, noncholinergic nerve pathways. Its role in
the pathogenesis of asthma has been reviewed.2

CLINICAL MANIFESTATIONS
Wheezing, a musical, high-pitched, whistling sound produced by airflow turbulence,
is one of the most common symptoms. In the mildest form, wheezing is only end expiratory.
As severity increases, the wheeze lasts throughout expiration. In a more severe asthmatic
episode, wheezing is also present during inspiration. During a most severe episode, wheezing
may be absent because of the severe limitation of airflow associated with airway narrowing
and respiratory muscle fatigue.
Asthma can occur without wheezing when obstruction involves predominantly the
small airways. Thus, wheezing is not necessary for the diagnosis of asthma. Furthermore,
wheezing can be associated with other causes of airway obstruction, such as cystic fibrosis
17

and heart failure. Patients with vocal cord dysfunction have a predominantly inspiratory
monophonic wheeze (different from the polyphonic wheeze in asthma), which is heard best
over the laryngeal area in the neck. Patients with bronchomalacia and tracheomalacia also
have a monophonic wheeze. In exercise-induced asthma, wheezing may be present after
exercise, and in nocturnal asthma, wheezing is present during the night.
Cough may be the only symptom of asthma, especially in cases of exercise-induced or
nocturnal asthma. Usually, the cough is nonproductive and nonparoxysmal. Children with
nocturnal asthma tend to cough after midnight and during the early hours of morning. Chest
tightness or a history of tightness or pain in the chest may be present with or without other
symptoms of asthma, especially in exercise-induced or nocturnal asthma.
Other nonspecific symptoms in infants or young children may be a history of
recurrent bronchitis, bronchiolitis, or pneumonia; a persistent cough with colds; and/or
recurrent croup or chest rattling. Most children with chronic or recurrent bronchitis have
asthma. Asthma is also the most common underlying diagnosis in children with recurrent
pneumonia; older children may have a history of chest tightness and/or recurrent chest
congestion

DIAGNOSIS
Diagnosing asthma in young children is difficult because children often cough and
wheeze with colds and chest infections but this is not necessarily asthma. Young children
have very small, narrow airways and on average have a 6 -8 colds per year, usually between
September and March. Some physicians are reluctant to give a diagnosis of asthma to young
infants as other conditions can be responsible for the asthma like symptoms. Children and
toddlers can wheeze when they have a viral infections. 1
Bronchiolitis is another very common cause of wheeze in children. First episodes of
cough, runny nose and fever that happen in cold/flu season- fall/winter/early spring is likely
not asthma. If your child has several more episodes of wheeze and cough, it is likely to be
asthma. The common cold triggers 90% of asthma attacks in children, compared to 40% in
adults. Since there is no diagnostic test available for children younger than 6 years of age,
making a diagnosis in this age group is more difficult than in older children. Over the age of
about 6 years it is possible for a child to have a spirometry test. This is a simple test that
18

measures a child's airflow through the large and small airways. Results reveal if the child's
airflow can be improved with medication. Reversibility of airway obstruction is a key feature
of asthma. If administering a bronchodilator reverses airway narrowing significantly, the
diagnosis is probably asthma. 1
Physical Examination
The physician will conduct a physical exam and may order some tests x ray, blood tests,
allergy skin tests and pulmonary function tests (PFTs).
History: The physician will take a detailed history of:
Family allergy/ asthma with emphasis on parents
Childs Allergy history- e.g. eczema
Childs history of illness to date e.g. frequency of colds
Childs symptoms: Severity, frequency and duration of symptoms.

19

TREATMENT
Although there is considerable variation in the way that different guidelines structure and
present the principles and components of asthma management, the key messages are
consistent, including a number of components that are a consequence of its chronic and
variable course (Fig. 3).1
Patients and their parents or caregivers should be educated to optimally manage the
disease, in collaboration with healthcare professionals. Education and the formation of a
partnership between them are crucial for the implementation and success of the treatment
plan (Evidence AB).1
Identification (Evidence A) and avoidance (Evidence BC) of specific (i.e. allergens)
and nonspecific triggers (e.g. tobacco smoke, but not exercise) and risk factors are also of
significant importance, because these may drive or augment inflammation.1
Assessment and monitoring should be performed regularly because of the variable
course of asthma and importantly to reevaluate and fine-tune treatment (Evidence AB).
Pharmacotherapy is the cornerstone of treatment. The optimal use of medication can, in most
cases, help patients control their symptoms and reduce the risk for future morbidity.1

20

Allergen-specific immunotherapy should be considered for children whose symptoms

are clearly linked to a relevant allergen (Evidence B). The management of asthma
exacerbations is a major consideration, independent of chronic treatment. There is a trend
toward considering phenotype-specific treatment choices; however, there is as yet no
consistent approach to this. Exercise-induced asthma is recognized in all guidelines, and
specific instructions are suggested for its management. In addition, the specific challenges of
treating severe and difficult asthma are highlighted throughout the documents. Age-specific
instructions are usually proposed in 2 or 3 strata. It is generally accepted that
recommendations in the youngest age-group are based on very weak evidence. Overall, the
treatment goal is disease control, including reduction in future risk of morbidity such as
exacerbations. In the past, there were suggestions that early treatment may be able to alter the
natural course of the disease.1

21

Education
Asthma education should not be regarded as a single event but rather as a continuous
process, repeated and supplemented at every subsequent consultation. There is general
consensus on the basic elements of asthma education: it should include essential information
about the (chronic/ relapsing) nature of disease, the need for long-term therapy, and the
different types of medication (controllers and relievers). Importantly, education should
highlight the importance of adherence to prescribed medication even in the absence of
symptoms and should involve literal explanation and physical demonstration of the optimal
use of inhaler devices and peak flow meters. Education should be tailored according to the
sociocultural background of the family.1
Trigger avoidance
Asthma symptoms and exacerbations are triggered by a variety of specific and
nonspecific stimuli. It is reasonable that avoidance of these factors may have beneficial
effects on the activity of the disease. The airway pathophysiology mediated through IgE to
inhalant allergens is widely acknowledged; however, not every allergen is equally significant
for all patients. Thus, there is general consensus that sound allergological workup (including
careful history for the assessment of clinical relevance, skin prick testing, and/or specific IgE
measurement) should precede any effort to reduce exposure to the corresponding allergen.1
Pharmacotherapy
The goal of asthma treatment is control using the least possible medications. Asthma
pharmacotherapy is regarded as chronic treatment and should be distinguished from treatment
for acute exacerbations that is discussed separately. In the initial assessment, and especially if
the patient has not received asthma medication before, there is a unique opportunity to
evaluate disease severity. Most guidelines propose the use of severity as the criterion for
selecting the level of treatment at the first assessment. GINA omits this step in this edition,
while PRACTALL suggests that both severity and control can be used.1
After the initial assessment, pharmacological therapy is selected through a stepwise
approach according to the level of disease control. In evaluating control, the differentiation
between current impairment and future risk is considered in NAEPP and GINA. This
additional consideration is important in appreciating the independence of these elements.1

22

If control is not achieved after 13 months, stepping up should be considered, after

reviewing device use, compliance, environmental control, treatment for comorbid rhinitis,
and, possibly, the diagnosis. When control has been achieved for Allergy 67 (2012) 976997
2012 John Wiley & Sons A/S 985 Papadopoulos et al. ICON pediatric asthma at least 3
months, stepping down can be considered.1
Inhaled medication delivery devices.

0 to ~ 5 years pMDI with static-treated spacer and mask (or mouthpiece as soon as the
child is capable of using).1
>~5 years Choice of: pMDI with static-treated spacer and mouthpiece, DPI (rinse or
gargle after inhaling ICS), breath-actuated pMDI (depending on patient ability to use,
preference).1

Nebulizer: second choice at any age

Asthma exacerbations (attacks, episodes)
An exacerbation of asthma is an acute or subacute episode of progressive increase in asthma
symptoms, associated with air- flow obstruction.+1

Asthma exacerbations are of critical importance, as they are associated with high
morbidity, including emergency visits, hospitalizations, and occasional mortality (132, 133).
While detailed criteria for the assessment of severity are proposed (Table 5), there are no
objective criteria for the definition of an exacerbation and/or its differentiation from lack of
23

control. The terminology is variable, and the terms exacerbation, attack, episode, or
seizure (as translated from Japanese) are used almost interchangeably. The optional use of
the adjectives acute and severe suggests that subacute and less severe episodes may also be
within the limits of the concept.1

24

REFERENCES

1. Asthma society of Canada. Asthma in Infants and young Children. 2007. Available on
http://www.asthma.ca. Accessed: August 29th
2. Papadopulous N.G, Arakawa H. Carlsen K.H, et al. International Consensus on (ICON)
pediatric asthma. European Journal of Allergy and Clinical Imunology. P 976-997. 2012
3. Morris M.J. Asthma Clinical Presentation. 2015. Available on http://www.medscape.com.
Accessed: August 29th. 2015

25