Asthma Case Report Edit Finale Touch! 2003

7/28/2019 Asthma Case Report Edit Finale Touch! 2003

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CASE REPORT

ASTHMA

Presenter : Dicky Yulianda

Day/Date : Tuesday/March 23rd 2010

Supervisor : dr. Rita Evalina, SpA

INTRODUCTION

Asthma is a chronic inflammatory disorder of the airways in which many cells

and cellular elements play a role. The chronic inflammation is associated with airway

hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest

tightness, and coughing, particularly at night or in the early morning. These episodes are

usually associated with widespread, but variable, airflow obstruction within the lung

that is often reversible either spontaneously or with treatment. 1

Asthma is a common chronic disease, causing considerable morbidity. Based on

information collected by the National Center for Health Statistics of the Centers for

Disease Control and Prevention, in 2002, 8.9 million children (12.2%) had been

diagnosed with asthma in their lifetime.2 Up to 80% of children with asthma develop

symptoms before their fifth birthday. Atopy (personal or familial) is the strongest

identifiable predisposing factor. Exposure to tobacco smoke, especially from the

mother, is also a risk factor for asthma.3 In Indonesia, the prevalence of asthma in

children approximately 10% of primary school age, and 6.5% at the junior high school

age. Pathogenesis of asthma is growing rapidly. In the early 60's, the basic pathogenesis

of asthma is bronchoconstriction, then in the 70s developed a chronic inflammatory

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process, whereas the 90's chronic inflammation was accompanied by airway

remodelling.4

Risk factors for asthma include host factors that predispose individuals to or

protect them from developing asthma (genetic predisposition, gender, and race) and

environmental factors that influence thesusceptibility to the development of asthma in

predisposed individuals,precipitate asthma exacerbations and/or cause symptoms to

persist. Exposure to allergens, viral and bacterial infections, diet, tobacco smoke,

socioeconomic status and family size are the main environmental factorsthat influence

the susceptibility to the development of asthma inpredisposed individuals. Exposure to

allergens and viral infections arethe main environmental factors causing exacerbations

of asthma and/or the persistence of symptoms in children.5

The pathophysiology of asthma is complex and involves the following

components: Airway inflammation, Intermittent airflow obstruction amd Bronchial

hyperresponsiveness. The mechanism of inflammation in asthma may be acute,

subacute, or chronic, and the presence of airway edema and mucus secretion also

contributes to airflow obstruction and bronchial reactivity. Varying degrees of

mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the

epithelium, smooth muscle hyperplasia, and airway remodeling are present.6 This

response occurs as a consequence of activation of the epithelialmesenchymal unit,

involving reciprocal activities of growth factors belonging to the fibroblastgrowth

factor, epidermal growth factor, and transforming growthfactor- families.7

Diagnosing asthma in infants and children begins with a review of the patient's

history and physical exam. Symptoms include recurrent wheezing, shortness of breath,

chest tightness, exercise limitation, mucoid vomiting, and chronic day and night cough.

Precipitating factors that trigger these symptoms include viral infections, tobacco

smoke, vigorous exercise, allergen or irritant exposures, breathing cold dry air, aspirin,

aspiration, or acid reflux. The history may also indicate that these symptoms were

improved with the use of inhaled or oral asthma medications but did not improve with

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antibiotics or antihistamine therapy. On physical examination during a symptom-free

interval, asthmatic signs are minimal and may include only a prolonged expiratory time

and a wet-sounding voluntary cough. During acute exacerbations, however, there may

be wheezing with reduced airflow throughout the lung fields, chest hyperinflation,

tachypnea, and the use of accessory muscles.8

Medications used in the treatment of asthma may be divided into two categories:

long-term control medications that are taken regularly and quick-relief medications that

are taken as needed to relieve bronchoconstriction rapidly. Long-term control

medications include anti-inflammatory agents (i.e., corticosteroids, cromolyn sodium,

nedocromil and leukotriene modifiers) and long-acting bronchodilators. Quick-relief

medications include short-acting beta2 agonists, anticholinergics and systemic

corticosteroids.9 Less inflammation typically leads to better asthma control, with fewer

exacerbations and decreased need for quick-reliever asthma medications.9

CASE

WL, a 6 year old girl, was admitted to The Pediatric Department of HAM

Hospital on March 1st 2010 with the main complaint: shortness of breath. This has been

experienced by the patient since last night and has severed since the following morning.

Shortness of breath is associated with weather changes, activities, dusk, cigarette

smoke, and cold weather. A history of shortness of breath was confirmed 2 weeks ago

with the frequency of three times in a month. Attacks are usually preceded by a cold onthe previous day. A history of asthma in family was confirmed. A history of wheezing

was also confirmed. Cough was confirmed experienced by the patient since the last day

accompanied with sputum and usually occurring at night near dawn. Defecation and

urinate were normal.

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History of Previous Disease :

The patient was previously diagnosed with asthma which was confirmed 2 years ago.

History of Previous Medication :

Ambroxol syrup, Salbutamol, Seretide inhaler

Physical examination

On physical examination, the following findings were confirmed.

A girl, with body weight 20 kg, body length was 110 cm, and EID index was

105,3 %, nutritional status was normoweight; body temperature was 36,5C. The level

of consciousness of this patient was alert. There were no pale, icterus, edema, and

cyanosis, but dyspnea was confirmed.

Head : Eye : Light reflexes (+/+), Isochoric pupil, Inferior conjunctiva

palpebral pale (-/-)

Nose : Nostril breathing (+)

Ears and Mouth : Within normal limits

Neck : Lymph node enlargement (-), JVP R-2 cm H2O

Chest : Symmetrical Fusiformic, Retraction (+) epigastrial, suprasternal,

intercostal

HR : 120 bpm, regular, murmur (-)

RR : 45 tpm, regular, rales (-), wheezing (+)

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Abdominal : Soepel

Hepar and lien: were not palpable

Peristaltic was normal

Extremities : Pulse was 120 tpm, regular, normal tone and volume

Working diagnosis: Frequent Episodic of Severe Asthma Attack

Treatment:

- O2 2 L/i nasal cannule

- IVFD D5% NaCl 0,45% 60 gtt/i micro

- Methyl Prednisolon Injection 5mg/6 hours/IV (1st day)

- Nebulization with Combivent 1 amp + NaCl 0,9% 5cc (If Attack was present)

- Daily Diet 1500 Kcal with 40gr Protein

Planning:

- Complete Blood Count

- Blood Gas Analysis

- Blood Glucose ad Random

- Chest X-Ray

Laboratory findings on 1st March 2010

Complete blood count:

- Leucocytes : 21,5 K/uL

- Neutrophil : 18,94 K/uL

- Erythrocytes : 4,97 M/uL

- HGB : 14,7 g/dl

- HCT : 40,6 %

- PLT : 364 fl

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- Manual Differential : Neut/Band/Lymph/Mono/Eosin/Baso : 89/1/7/2/1/0

Arterial blood gas analysis:

- pH : 7,537

- pCO2 : 33,2 mmHg

- pO2 : 154,4 mmg

- Bicarbonate : 27,5

- CO2 total : 28,5

- Base exes : 4,9

- O2 Saturation : 99,2

Chest X-Ray Conclusions on 1st March 2010

Abnormalities of the heart and the lungs were not confirmed

FOLLOW-UP

2nd March 2010

S : Shortness of breath (+), Cough (+)

O: Consciousness was alert, T: 36,8 oC, BW 20 kg



Nose : Nostril breathing (+)

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Ears and Mouth : Within normal limits


Chest : Symmetrical Fusiformic, Retraction (+) epigastrial, suprasternal,

intercostal


RR : 60 tpm, regular, rales (-), wheezing (+)

Abdominal : Soepel





Treatment:



- Methyl Prednisolon Injection 5mg/6 hours/IV (2nd day)

- Aminophylline Injection 6-8 mg/KgBW/Initial in D5% 20cc for 20-30 minutes

160 mg (50 gtt/i micro)

Continue with maintanence dose 0,5-1 mg/KgBW/hour +

9 ml D5%/KgBW/hour10 ml Aminophilin + 90 ml D5%

- Cefotaxime Injection 500mg/8hours/IV (1st day)

- Nebulization with Combivent 1 amp + NaCl 0,9% 5cc /6 hours

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3rd March 2010

S : Shortness of breath (


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- Methyl Prednisolon Injection 5mg/6 hours/IV (3rd day)

- Aminophylline Injection 10 ml + D5% 90ml

4cc/hour- Cefotaxime Injection 500mg/8hours/IV (2nd day)



4th March 2010

S : Shortness of breath (-), Cough (+)

O: Consciousness was alert, T: 36,8 oC, BW 20 kg



Ears Nose and Mouth : Within normal limits


Chest : Symmetrical Fusiformic, Retraction (-)


RR : 28 tpm, regular, rales (-), wheezing (-)

Abdominal : Soepel





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Treatment:



- Methyl Prednisolon Injection 5mg/6 hours/IV (4th day)

- Aminophylline Injection 10 ml + D5% 90ml 4cc/hour

- Cefotaxime Injection 500mg/8hours/IV (3rd day)



The patient was discharged on March 5th 2010.

Patient was given :

o Seretide inhaler 2 x 1 dose

o Dexamethasone tablets 3 x 5 mg (for 3 days)

o Ambroxol tablets 1 x 10 mg

DISCUSSION

Asthma is a chronic inflammatory disorder in the respiratory tract which

involved the cells and cellular elements. Chronic inflammation associated with airway

hyperresponsiveness that cause symptoms of recurrent episodic such as wheezing,

shortness of breath, chest like a compressed, and coughing, particularly at night and

early morning. This episodic associated with airway obstruction broad, varied, and

reversible with or without treatment. Asthma is a chronic respiratory disease

characterized by the inflammatory process that accompanied with the process of

remodelling.1

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Airflow obstruction in asthma is the result of numerous pathologic processes. In

the small airways, airflow is regulated by smooth muscle encircling the airways lumens;

bronchoconstriction of these bronchiolar muscular bands restricts or blocks airflow. A

cellular inflammatory infiltrate and exudates distinguished by eosinophils, but also

including other inflammatory cell types (neutrophils, monocytes, lymphocytes, mast

cells, basophils), can fill and obstruct the airways and induce epithelial damage and

desquamation into the airways lumen. Helper T lymphocytes and other immune cells

that produce pro-allergic, proinflammatory cytokines (IL-4, IL-5, IL-13) and

chemokines (eotaxin) mediate this inflammatory process. Pathogenic immune responses

and inflammation may also result from a breach in normal immune regulatory processes

(regulatory T lymphocytes that produce IL-10 and transforming growth factor [TGF])

that dampen effector immunity and inflammation when they are no longer needed.

Airways inflammation is linked to airways hyperresponsiveness or hypersensitivity of

airways smooth muscle to numerous provocative exposures that act as triggers, as well

as airways edema, basement membrane thickening, subepithelial collagen deposition,

smooth muscle and mucous gland hypertrophy, and mucus hypersecretionall

processes that contribute to airflow obstruction. 2

Although Th-2mediated inflammation is a key therapeutictarget in asthma, its

relationship to altered structure andfunctions of the airways is largely unknown. In

addition toinflammation, asthma is a disorder involving the airway epithelium that is

more vulnerable to environmental injury and respondsto this by impaired healing. This

establishes a chronic woundscenario that is capable of sustaining chronic

inflammation

as well as remodeling. This response occurs as a consequence

of activationof the epithelialmesenchymal unit, involving reciprocal activities of growth factors

belonging to the fibroblastgrowth factor, epidermal growth factor, and transforming

growthfactor- families. The observation that structuralchanges in the airways in

children at or before the onset ofasthma occurs irrespective of inflammation might

suggest thatpremodeling is required before Th-2 inflammatory responses can be

sustained. Once established, altered function of constitutiveairway cells, including

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fibroblasts, smooth muscle, nerves,and the epithelium, provides an abnormal

microenvironment inwhich to generate a separate set of signals that underpin

theacute/subacute inflammation characteristic of asthma exacerbations,triggered by

viruses, pollutants, and allergens.7

The Pathogenesis of Asthma

Intermittent dry coughing and/or expiratory wheezing are the most common

chronic symptoms of asthma. Older children and adults will report associated shortness

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of breath and chest tightness; younger children are more likely to report intermittent,

nonfocal chest pain. Respiratory symptoms can be worse at night, especially during

prolonged exacerbations triggered by respiratory infections or inhalant allergens.

Daytime symptoms, often linked with physical activities or play, are reported with

greatest frequency in children. Other asthma symptoms in children can be subtle and

nonspecific, including self-imposed limitation of physical activities, general fatigue

(possibly due to sleep disturbance), and difficulty keeping up with peers in physical

activities. Asking about previous experience with asthma medications (bronchodilators)

may provide a history of symptomatic improvement with treatment that supports the

diagnosis of asthma.2

The presence of risk factors, such as a history of other allergic conditions

(allergic rhinitis, allergic conjunctivitis, atopic dermatitis, food allergies), parental

asthma, and/or symptoms apart from colds, supports the diagnosis of asthma. During

routine clinic visits, children with asthma commonly present without abnormal signs,

which stresses the importance of the medical history in diagnosing asthma. Some may

exhibit a dry, persistent cough. The chest examination is often normal. Deeper breaths

can sometimes elicit otherwise undetectable wheezing. In clinic, quick resolution

(within 10 min) or convincing improvement in symptoms and signs of asthma with

administration of a short-acting inhaled beta-agonist (SABA) is supportive of the

diagnosis of asthma.2

During asthma exacerbations, expiratory wheezing and a prolonged expiratory

phase can usually be appreciated by auscultation. Decreased breath sounds in some of

the lung fields, commonly the right lower posterior lobe, are consistent with regional

hypoventilation owing to airways obstruction. Crackles (or rales) and rhonchi can

sometimes be heard, resulting from excess mucus production and inflammatory exudate

in the airways. The combination of segmental crackles and poor breath sounds can

indicate lung segmental atelectasis that is difficult to distinguish from bronchial

pneumonia and can complicate acute asthma management. In severe exacerbations, the

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greater extent of airways obstruction causes labored breathing and respiratory distress

manifested as inspiratory and expiratory wheezing, increased prolongation of

exhalation, poor air entry, suprasternal and intercostal retractions, nasal flaring, and

accessory respiratory muscle use. In extremis, airflow may be so limited that wheezing

cannot be heard.2

Penanganan Nasional Asma Anak (PNAA) divided asthma into 3 categories:

mild episodic asthma, frequent episodic asthma and persistent asthma. Basic division is

due to the episodic events of asthma that is more frequently than persistent.10

The Degree of Asthma in Children based onPenanganan Nasional Asma Anak

(PNAA)

Mild Episodic

Asthma

Frequent Episodic

Asthma

Persistent Asthma

Attack Frequency < 1 x/month 1 x/month Frequent

Attack time < 1 week > 1 week Almost throughout

the year, almost no

remission

Attack Intensity Without Symptom Often a symptom Symptom at noon and

night

Activity and

Sleep

Undisturbed Very Disturbed Very Disturbed

Physical

Diagnostic

outside the attack

Normal May Interfere Never be normal

Controller Drugs

(Anti-

Inflammation)

No Need Need Steroid Need Steroid

Lungs Function APE/VEP1 > 80% APE/VEP1 60-80% APE/VEP1 < 60%

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Test (Outside the

Attack

Lungs Function

Variability

> 15% > 30% > 50%

According to the GINA, asthma is divided into: intermittent asthma, mild

persistent, persistent moderate or severe persistent. Meanwhile, according to the

severity of attacks was divided into mild attacks, moderate, severe and the threat of

failing the breath.11

Severity of Asthma Attack (GINA 2008)

Parameter Mild Moderate Severe Respiratory

Arrest Imminent

Breathless Walking

Can lie down

Talking Rest

Talk in

alertness

Sentences

May be

agitated

Phrases

Usually

agitated

Words

Usually

agitated

Respiratory

Rate

Increased Increased Often > 30

min

Paradoxical

Guides to

rates ofbreathing

associated

with

respiratory

distress in

awake

children

Age Normal Rate

< 2 months < 60 x/min

2-12 months < 50 x/min

1-5 years < 40 x/min

6-8 years < 30 x/min

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Accessory

muscles and

suprasternal

retractions

Usually not Usually Usually Paradoxical

thoraco-

abdominal

movement

Wheeze Moderate,

often only end

expiratory

Loud Usually loud Absence of

wheeze

Pulse/min 120 tpm Bradycardia

Guide tolimits of

normal pulse

rate in

children

Infants 2-12 months - Normal Rate < 160x/min

Preschool 1-2 years - Normal Rate < 120x/min

School age 2-8 years - Normal Rate < 110x/min

PEF after

initial

bronchodilato

r % predicted

or % personal

best

Over 80% Approximately

60-80%

< 60%

predicted or

personal best

(100L/min

adults) or

response lasts

< 2 hours

PaO2 Normal > 60mmHg < 60mmHg

Possible

Cyanosis

PaCO2 < 45 mmHg < 45 mmHg > 45 mmHg

Possible

Respiratory

Failure

SaO2 > 95% 91-95%


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The following tests are indicated in the assessment of asthma: 12

Pulmonary function tests (PFTs): These results are not reliable in patients younger

than 5 years. In young children (3-6 y) and older children who are unable to perform

the conventional spirometry maneuver, newer techniques, such as measurement of

airway resistance using impulse oscillometry system, are used. Measurement of

airway resistance before and after a dose of inhaled bronchodilator may help to

diagnose bronchodilator responsive airway obstruction.

o Spirometry: In a typical case, an obstructive defect is present in the form of

normal forced vital capacity (FVC), reduced FEV1, and reduced forced

expiratory flow more than 25-75% of the FVC (FEF 25-75). The flow-volume

loop can be concave. Documentation of reversibility of airway obstruction after

bronchodilator therapy is central to the definition of asthma. FEF 25-75 is a

sensitive indicator of obstruction and may be the only abnormality in a child

with mild disease. In an outpatient or office setting, measurement of the peak

flow rate by using a peak flow meter can provide useful information about

obstruction in the large airways. Take care to ensure maximum patient effort.

However, a normal peak flow rate does not necessarily mean a lack of airway

obstruction.

Bronchial provocation tests: Bronchial provocation tests may be performed to

diagnose bronchial hyperresponsiveness (BHR). These tests are performed in

specialized laboratories by specially trained personnel to document airway

hyperresponsiveness to substances (eg, methacholine, histamine). Increasing doses

of provocation agents are given, and FEV1 is measured. The endpoint is a 20%

decrease in FEV1 (PD20).

Exercise challenge: In a patient with a history of exercise-induced symptoms (eg,

cough, wheeze, chest tightness or pain), the diagnosis of asthma can be confirmed

with the exercise challenge. In a patient of appropriate age (usually >6 y), the

procedure involves baseline spirometry followed by exercise on a treadmill or

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bicycle to a heart rate greater than 60% of the predicted maximum, with monitoring

of the electrocardiogram and oxyhemoglobin saturation. The patient should be

breathing cold, dry air during the exercise to increase the yield of the study.

Spirographic findings and the peak expiratory flow (PEF) rate (PEFR) are

determined immediately after the exercise period and at 3 minutes, 5 minutes, 10

minutes, 15 minutes, and 20 minutes after the first measurement. The maximal

decrease in lung function is calculated by using the lowest postexercise and highest

preexercise values. The reversibility of airway obstruction can be assessed by

administering aerosolized bronchodilators.

Blood testing: Eosinophil counts and IgE levels may help when allergic factors are

suspected.

Chest radiography: Include chest radiography in the initial workup if the asthma

does not respond to therapy as expected. In addition to typical findings of

hyperinflation and increased bronchial markings, a chest radiograph may reveal

evidence of parenchymal disease, atelectasis, pneumonia, congenital anomaly, or a

foreign body. In a patient with an acute asthmatic episode that responds poorly to

therapy, a chest radiograph helps in the diagnosis of complications such as

pneumothorax or pneumomediastinum.

Allergy testing: Allergy testing can be used to identify allergic factors that may

significantly contribute to the asthma. Once identified, environmental factors (eg,

dust mites, cockroaches, molds, animal dander) and outdoor factors (eg, pollen,

grass, trees, molds) may be controlled or avoided to reduce asthmatic symptoms.

Allergens for skin testing are selected on the basis of suspected or known allergens

identified from a detailed environmental history. Antihistamines can suppress the

skin test results and should be discontinued for an appropriate period (according to

the duration of action) before allergy testing. Topical or systemic corticosteroids do

not affect the skin reaction.

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Eosinophilic infiltration, a universal finding, is considered a major marker of the

inflammatory activity of the disease.

Corticosteroids remain the most potent and effective anti-inflammatory agents

available for the management of asthma. They are useful in treating all types of

persistent asthma in patients of all ages. For long-term use, inhaled steroids are

generally preferred over oral steroids because the inhaled agents have fewer systemic

side effects. Oral steroid therapy for long-term control is usually used only to treat

refractory, severe, persistent asthma. The dosages of inhaled corticosteroids depend on

the severity of disease. Most patients can be maintained on two daily doses of the

currently available preparations.Common side effects include cough, dysphonia, throat

irritation and oropharyngeal candidiasis. The likelihood of local side effects, especially

candidiasis, can be reduced if patients use a spacer, rinse their mouth after each use and

use the inhaled steroids less frequently (twice daily rather than four times daily). Higher

dosages may be associated with systemic adverse effects, including adrenal suppression,

osteoporosis and growth delay in children.9

Salmeterol is a long-acting beta2 agonist. Its mechanism of action and side effect

profile are similar to those of other beta2 agonists. Unlike the short-acting agents,

salmeterol is not intended for use as a quick-relief agent. It should not be used as a

single agent for long-term control but instead should be used in combination with

inhaled corticosteroids or other anti-inflammatory agents. Salmeterol is useful in the

management of nocturnal and exercise-induced asthma. The drug is administered in an

MDI in a dosage of two puffs every 12 hours. The inhalation powder formulation,

salmeterol xinafoate, is administered in a dosage of one puff every 12 hours. Several

controlled studies, have found that adding salmeterol to inhaled beclomethasone

dipropionate produces greater improvement in asthma symptoms and less use of rescue

medications than doubling the dosage of inhaled beclomethasone.9

Albuterol is available as an oral extended-release tablet for the long-term control

of asthma. Like salmeterol, this long-acting beta2 agonist is not intended to be used as a

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rescue medication. It is an alternative to sustained-release theophylline or inhaled

salmeterol, especially in patients who have nocturnal asthma despite treatment with

high-dose anti-inflammatory agents. Albuterol is available in 4- and 8-mg tablets. Doses

are taken every 12 hours.9

Theophylline is a methylxanthine bronchodilator with extrapulmonary effects,

including enhancement of respiratory muscle contractility. Theophylline is an old

medication that is being replaced by newer treatment modalities that require less acute

monitoring and have wider margins of safety. Serum levels of theophylline, which is

extensively metabolized by the liver, are markedly affected by a number of variables

including age, diet, disease states, tobacco smoke, and drug interactions, all of which

contribute to the complexity of using this medication. Because of the variability of

theophylline metabolism, as well as a narrow therapeutic index, children using

theophylline must have serum levels monitored periodically with the goal of a serum

concentration of 5 to 20 ug/mL. When compared with b 2-agonists, theophylline has a

slower onset of action and a lower peak effect, making it less suitable for acute therapy.

Unfortunately, theophylline may produce a number of dose-related side effectsincluding gastrointestinal symptoms and possible adverse behavioral effects. Its use as a

first-line drug for persistent asthma has all but disappeared, although it may have a role

in the treatment of severe respiratory failure in status asthmaticus. 8

Short-acting inhaled beta2 agonists are the agents of choice for relieving

bronchospasm and preventing exercise-induced bronchospasm. Selective beta2 agonists,

including albuterol, bitolterol, metaproterenol, pirbuterol and terbutaline, are preferred

to nonselective beta agonists, such as epinephrine, ephedrine and isoproterenol, because

the selective agents have fewer cardiovascular side effects and a longer duration of

action. Inhaled beta2 agonists have a rapid onset of action (i.e., less than five minutes).

Peak bronchodilation occurs within 30 to 60 minutes of administration, and the duration

of action is three to eight hours.Several studies have suggested that chronic daily use of

short-acting beta2 agonists may lead to worsening asthma control and decreased

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pulmonary function, particularly in moderate to severe asthma. Other studies have failed

to demonstrate worsening asthma control but have shown no significant benefit from

the regular daily use of beta2 agonists. In light of current information, regularly

scheduled daily use of short-acting beta2 agonists is not generally recommended. The

frequent use of quick-relief medication (e.g., more than one canister per month)

indicates poor asthma control and the need for increased dosages of long-term control

medications.9

Short-term systemic corticosteroid therapy is useful for gaining initial control of

asthma and for treating moderate to severe asthma exacerbations. The intravenous

administration of systemic corticosteroids offers no advantage over oral administration

when gastrointestinal absorption is not impaired. The recommended outpatient "burst"

therapy for adults is prednisone, prednisolone or methylprednisolone in a dosage of 40

to 60 mg per day taken as one or two daily doses; for children, 1 to 2 mg per kg per day

to a maximum dosage of 60 mg per day. Therapy is continued for three to 10 days or

until symptoms resolve and the patient's PEF improves to 80 percent of his or her

personal best. The oral steroid dosage does not have to be tapered after short-course"burst" therapy if the patient is receiving inhaled steroid maintenance therapy.9

Ipratropium is a quaternary atropine derivative that inhibits vagal-mediated

bronchoconstriction. Although this drug has not been proved to be effective for long-

term asthma management, it may be useful as an adjunct to inhaled beta2 agonists in

patients who have severe asthma exacerbations or who cannot tolerate beta2 agonists.

Ipratropium has few side effects, but inadvertent eye contact can cause mydriasis. 9

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Management of Asthma Attack in Emergency Department (Hospital)14

The prognosis of asthma in childhood is excellent.8 Children with mild asthma

who are asymptomatic between attacks are likely to improve and be symptom-free later

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in life. Children with asthma appear to have less severe symptoms as they enter

adolescence, but half of these children continue to have asthma. Asthma has a tendency

to remit during puberty, with a somewhat earlier remission in girls. However, compared

with men, women have more bronchial hyperresponsiveness (BHR).13

In this case, the diagnosis is established based on historical taking and clinical

examination that lead to asthma. Historical taking gained a shortness of breath which

has endured since this 2-week and history of a cold one day before the attack. History of

the same disease in the family was founded. History of shortness of breath as much as 3

times in the last 1 month. Also note that the patient can not be heavy activities such as

sports.

Patients previously using Seretide inhalers and Salbutamol in treatment. From

the physical examination, retracted epigastrial, intercostal, and suprasternal was

founded, and also nostril breathing and wheezing that can be found in patients with

asthma.

This patient classified with frequent episodic asthma based on frequency of the

attacks that is 3 times in a month with very disturbing activities and time of sleep. The

patient need steroid to relieve the attacks. The patient classified with severe asthma

attack based on several parameter, such as shortness of breath that happened during

sleep, respiratory rate that increased until 45 times per minute, retractions of epigastrial,

suprasternal, and intercostals muscle, heart rate that increased until 120 bytes per

minute.

The patient was given oxygen and combivent nebulization (ipatropium bromide

and albuterol) plus 0.45% NaCl and aminophillyne injection to overcome breathing

problems and provision of methyl prednisolon injection to overcome the inflammation

process. Cefotaxime was also given to this patien in order to resolve the infection

problem. Patients eventually discharged because of shortness of breath had disappeared

and phlegm was reduced.

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These patients should remain controlled as an outpatient to prevent repeated

attacks and the occurrence of airway remodeling through an adequate provison of anti-

inflammatory and a good education to parents and patients about asthma.

Combination therapy can improve lung function tests, asthma symptoms, and

daily activities that ultimately improve the quality of life of children with asthma.

SUMMARY

It has been reported a case of a child with frequent episodic of severe asthma

attack. The diagnosis was established based on historical taking, clinical sign and

symptoms, and physical examination. The prognostic of this patient was good.

Preventive action is very important to do, in order to avoid the factors that trigger

asthma attacks. Needed a long-term and periodically management to deal with or

prevent the occurrence of asthma. The use of controller medication as a precautionary

measure and also a reliever medication as the handling time of the attack were being an

important role. This combination therapy can improve lung function tests, asthma

symptoms and daily activities and ultimately improve the quality of life of children with

asthma.

REFFERENCES

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1. Global Strategy for Asthma Management and Prevention. Global Inisiative for

Asthma. Definition And Overview. 2008. p : 2

2. Liu AH, Covar RA. Childhood Asthma. In: Kliegman RM, Behrman RE, Jenson

HB, Stanton BF.Nelson Textbook of Pediatric 18th ed. Philadelphia, Saunder; 2007.

Chapter 143.

3. Hay WW, Levin MJ. Allergic Disorders: Asthma. Current Diagnosis and treatment

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Asthma Case Report Edit Finale Touch! 2003