CASE Tika Asma

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

1

IDENTITY

Patient

Name : Citra Alhumaira

Birth Date : July 27th 2009

Age : 7 years old

Gender : Female

Address : Jalan Kerja Bakti RT 01/04 Makassar

Nationality : Indonesia

Religion : Islam

Date of admission : January 5th 2016

Date of examination : January 7th 2016

ANAMNESIS

The anamnesis was taken on January 5th 2016, by alloanamnesis (from patient’s mother).

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

Additional complains : Cough, shortness of breath.

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. Patient’s 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 -

2

Varicella -

Diphteria -

Malaria -

Polio -

Enteritis -

Bacillary Dysentry -

Amoeba Dysentry -

Diarrhea -

Thypoid -

Worms -

Surgery -

Brain Concussion -

Fracture -

Drug Reaction -

Birth History

Mother’s 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.

Child’s Birth History

Labor : Hospital

Birth attendants : Doctor

Mode of delivery : pervaginam

Gestation : 38 weeks

3

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 : 5 months old

Food Self : 5 – 6 months old

Sitting : 6 months old

Mental Status : Normal

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

appropriate according to the patient’s 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

4

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 : mild ill

- Awareness : Kompos Mentis

- Pulse : 120 x/min, regular, full, strong.

- Breathing rate : 45x/min

- Temperature : 36,4oC (per axilla)

Antropometry Status

- Weight : 15 kilogram

- Height : 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)

5

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

Lips: moist

Teeth: no caries

Mucous: moist

Tongue: Not dirty

Tonsils: T1/T1, No hyperemia

Pharynx: hyperemia (+)

Neck

Lymph node enlargement (-), scrofuloderma (-)

Thorax :

i. Inspection : symmetric when breathing , retraction +, ictus cordis is visible

ii. Palpation : mass (-), tactile fremitus +/+

iii. Percussion : wheezing on both lungs

iv. Auscultation :

1. Cor : regular S1-S2, murmur (-), gallop (-)

2. Pulmo : vesicular +/+, Wheezing +/+ , Rhonchy +/+

Abdomen :

i. 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

(-)

7

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

iv. Auscultation : normal bowel sound, bruit (-)

Vertebra : 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

5 5 5 5/ 5 5 5 5

5 5 5 5/ 5 5 5 5

Tonus

Hand

Feet

Normotonus / Normotonus

Normotonus / Normotonus

Trophy

Hand

Feet

Normotrophy / Normotrophy

Normotrophy / Normotrophy

Physiologic Reflex

Upper extrimities

Biceps

Triceps

Lower extrimities

+ / +

+ / +

8

Patella

Achilles

+ / +

+ / +

Pathologic Reflex

Upper extrimities

Hoffman

Trommer

Lower extrimities

Babinsky

Chaddock

Oppenheim

Gordon

Schaeffer

- / -

- / -

- / -

- / -

- / -

- / -

- / -

Clonus

Patella

Achilles

- / -

- / -

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/µL 5,000 – 10,000/µL

Hematocrits 40 % 40 – 48 %

Trombocytes 356.000/ µL 150,000 – 400,000/µL

Erythrocytes 4,07 million/µL 4 – 5 million/µL

9

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 ½ (1,25 mg)

- Bisolvon 10 drops

- NaCl 2 cc

PROGNOSIS

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 (-)

10

Phlegm (+)

Breathless (+)

Productive cough (-)

O General condition: Compos mentis.

Heart rate = 115 x/min

Respiratory rate = 35x/min

Temperature = 36,4˚C

Cardio : S1/S2, reguler, no murmur, no gallop

Pulmonary : vesiculer +/+, rhonchi +/+, wheezing +/+

A Asthma Bronchiale

DD/ Bronchiolitis

P - 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 ½ (1,25 mg)

Bisolvon 10 drops

NaCl 1 cc

11

August 7th 2015. Third day of hospitalization.

S Fever (-)

Phlegm (-)

Breathlless (-)


O General condition: Compos Mentis



Temperature = 38.5˚C


Pulmonary : retraction (+) vesiculer +/+, rhonchi +/+, wheezing -/-

A Astha Bronchiale

P - O2 1L/m

IVFD Kaen3B,



Paracetamol syr 3 x 1 cth

12

Ambroxol syr 3 x 1 cth

Inhalation twice a day


Bisolvon 10 drops

NaCl 1 cc

August 8th 2015, Fourth days of hospitalization

S Fever (-)

Phlegm (-)


Breathless (-)

O General condition: Compos mentis.



Temperature = 36˚C


Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/-

A Asthma Bronchiale

P IVFD Kaen3B.



Paracetamol syr 3 x 0,7 cc

Inhalation twice a day


Bisolvon 3 drops

NaCl 1 cc

13

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

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

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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

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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

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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 Structure–function 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

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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.

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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

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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

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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

• Child’s Allergy history- e.g. eczema

• Child’s history of illness to date e.g. frequency of colds

• Child’s symptoms: Severity, frequency and duration of symptoms.

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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 A–B).1

Identification (Evidence A) and avoidance (Evidence B–C) 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 A–B).

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

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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

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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

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If control is not achieved after 1–3 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) 976–997

© 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 airflow 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

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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

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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

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http://www.medscape.com/

http://www.asthma.ca/

CASE Tika Asma

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