CASE REPORT

ASTHMA
Presenter Day/Date Supervisor : Dicky Yulianda : Tuesday/March 23rd 2010 : 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

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 the susceptibility 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 factors that influence the susceptibility to the development of asthma in predisposed individuals. Exposure to allergens and viral infections are the 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 fibroblast growth factor, epidermal growth factor, and transforming growth factor- 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

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 on the 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.

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 Chest : Lymph node enlargement (-), JVP R-2 cm H2O : Symmetrical Fusiformic, Retraction (+) epigastrial, suprasternal, intercostal HR : 120 bpm, regular, murmur (-) RR : 45 tpm, regular, rales (-), wheezing (+)

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 Complete Blood Count Blood Gas Analysis Blood Glucose ad Random Chest X-Ray

Planning:

Laboratory findings on 1st March 2010 Complete blood count: Leucocytes Neutrophil Erythrocytes HGB HCT PLT : 21,5 K/uL : 18,94 K/uL : 4,97 M/uL : 14,7 g/dl : 40,6 % : 364 fl

Manual Differential

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

Arterial blood gas analysis: pH pCO2 pO2 Bicarbonate CO2 total Base exes : 7,537 : 33,2 mmHg : 154,4 mmg : 27,5 : 28,5 : 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 Head : Eye : Light reflexes (+/+), Isochoric pupil, Inferior conjunctiva palpebral pale (-/-) Nose : Nostril breathing (+)

Ears and Mouth : Within normal limits Neck Chest : Lymph node enlargement (-), JVP R-2 cm H2O : Symmetrical Fusiformic, Retraction (+) epigastrial, suprasternal, intercostal HR : 100 bpm, regular, murmur (-) RR : 60 tpm, regular, rales (-), wheezing (+) Abdominal : Soepel Hepar and lien: were not palpable Peristaltic was normal Extremities : Pulse was 100 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% 50 gtt/i micro 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/hour 10 ml Aminophilin + 90 ml D5% Cefotaxime Injection 500mg/8hours/IV (1st day) Nebulization with Combivent 1 amp + NaCl 0,9% 5cc /6 hours

Daily Diet 1500 Kcal with 40gr Protein

3rd March 2010 S : Shortness of breath (<<), Cough (+) O: Consciousness was alert, T: 36,8 oC, BW 20 kg Head : Eye : Light reflexes (+/+), Isochoric pupil, Inferior conjunctiva palpebral pale (-/-) Ears Nose and Mouth : Within normal limits Neck Chest : Lymph node enlargement (-), JVP R-2 cm H2O : Symmetrical Fusiformic, Retraction (-) HR : 110 bpm, regular, murmur (-) RR : 32 tpm, regular, rales (-), wheezing (+) Abdominal : Soepel Hepar and lien: were not palpable Peristaltic was normal Extremities : Pulse was 110 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% 50 gtt/i micro

Methyl Prednisolon Injection 5mg/6 hours/IV (3rd day) Aminophylline Injection 10 ml + D5% 90ml 4cc/hour Cefotaxime Injection 500mg/8hours/IV (2nd day) Nebulization with Combivent 1 amp + NaCl 0,9% 5cc /6 hours Daily Diet 1500 Kcal with 40gr Protein

4th March 2010 S : Shortness of breath (-), Cough (+) O: Consciousness was alert, T: 36,8 oC, BW 20 kg Head : Eye : Light reflexes (+/+), Isochoric pupil, Inferior conjunctiva palpebral pale (-/-) Ears Nose and Mouth : Within normal limits Neck Chest : Lymph node enlargement (-), JVP R-2 cm H2O : Symmetrical Fusiformic, Retraction (-) HR : 98 bpm, regular, murmur (-) RR : 28 tpm, regular, rales (-), wheezing (-) Abdominal : Soepel Hepar and lien: were not palpable Peristaltic was normal Extremities : Pulse was 98 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% 50 gtt/i micro Methyl Prednisolon Injection 5mg/6 hours/IV (4th day) Aminophylline Injection 10 ml + D5% 90ml 4cc/hour Cefotaxime Injection 500mg/8hours/IV (3rd day) Nebulization with Combivent 1 amp + NaCl 0,9% 5cc /6 hours Daily Diet 1500 Kcal with 40gr Protein

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 therapeutic target in asthma, its relationship to altered structure and functions of the airways is largely unknown. In addition to inflammation, asthma is a disorder involving the airway epithelium that is more vulnerable to environmental injury and responds to this by impaired healing. This establishes a chronic wound scenario that is capable of sustaining chronic inflammation as well as remodeling. This response occurs as a consequence of activation of the epithelialmesenchymal unit, involving reciprocal activities of growth factors belonging to the fibroblast growth factor, epidermal growth factor, and transforming growth factor- families. The observation that structural changes in the airways in children at or before the onset of asthma occurs irrespective of inflammation might suggest that premodeling is required before Th-2 inflammatory responses can be sustained. Once established, altered function of constitutive airway cells, including

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fibroblasts, smooth muscle, nerves, and the epithelium, provides an abnormal microenvironment in which to generate a separate set of signals that underpin the acute/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 on Penanganan Nasional Asma Anak (PNAA) Mild Episodic Asthma Attack Frequency Attack time < 1 x/month < 1 week Frequent Episodic Asthma 1 x/month > 1 week Frequent Almost throughout the year, almost no remission Attack Intensity Without Symptom Often a symptom Symptom at noon and night Activity and Sleep Physical Diagnostic outside the attack Controller Drugs (AntiInflammation) Lungs Function APE/VEP1 > 80% APE/VEP1 60-80% APE/VEP1 < 60% No Need Need Steroid Need Steroid Normal May Interfere Never be normal Undisturbed Very Disturbed Very Disturbed Persistent Asthma

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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 Breathless Mild Walking Can lie down Talk in alertness Sentences May be agitated Increased Phrases Usually agitated Increased Age < 2 months 2-12 months 1-5 years 6-8 years Words Usually agitated Often > 30 min Normal Rate < 60 x/min < 50 x/min < 40 x/min < 30 x/min Paradoxical Moderate Talking Severe Rest Respiratory Arrest Imminent

Respiratory Rate Guides to rates of breathing associated with respiratory distress in awake children

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Accessory muscles and suprasternal retractions

Usually not

Usually

Usually

Paradoxical thoracoabdominal movement

Wheeze

Moderate, often only end expiratory <100 tpm Infants Preschool School age Over 80%

Loud

Usually loud

Absence of wheeze Bradycardia

Pulse/min Guide to limits of normal pulse rate in children PEF after initial bronchodilato r % predicted or % personal best PaO2

100-200 tpm 2-12 months 1-2 years 2-8 years Approximately 60-80%

>120 tpm

- Normal Rate < 160x/min - Normal Rate < 120x/min - Normal Rate < 110x/min < 60% predicted or personal best (100L/min adults) or response lasts < 2 hours < 60mmHg Possible Cyanosis

Normal

> 60mmHg

PaCO2

< 45 mmHg

< 45 mmHg

> 45 mmHg Possible Respiratory Failure

SaO2

> 95%

91-95%

<90%

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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 FEV 1, 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 beta 2 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 beta 2 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 effects including 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 longterm asthma management, it may be useful as an adjunct to inhaled beta 2 agonists in patients who have severe asthma exacerbations or who cannot tolerate beta 2 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 antiinflammatory 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 Pediatrics 19th ed. The McGraw-Hill Companies Inc. 2009. Chapter 36 4. Kartasasmita CB. Epidemiologi Asma Anak. In: Rahajoe NN dan Supriyatno B. Buku Ajar Respirologi Anak 2008 Edisi pertama. Jakarta: IDAI. 2008. p: 71 5. Pocket Guide For Asthma Management and Prevention In Children. Global Inisiative for Asthma. A Six Program to Manage and Control Asthma. 2008. p : 4 6. Sharma GD. Asthma. Overview. Department of Pediatrics. University Medical Center. 2009 Available at: http://emedicine.medscape.com/article/296301-overview [Accessed March 2010]
7. Holgate ST, Holloway J. Epithelial Mesenchymal communication in the

pathogenesis of chronic asthma. The Proceedings of the American Thoracic Society (2004) p1:93-98. Available at http://pats.atsjournals.org/cgi/content/short/1/2/93 [Accesed March 2010] 8. Ross MH. Asthma. In: Rudolph CD, Rudolph AM. Rudolph Pediatrics 21st edition. The McGraw-Hill Companies Inc. 2002. Chapter 23.8 9. Gross KM, Ponte CD. New Strategies in the Medical Management of Asthma. American Phamily Physician. West Virginia University School of Medicine. 1998. Available at: http://www.aafp.org/afp/980700ap/gross.html [Accessed March 2010]. 10. Melinda H. Diagnosis Asma Pada Anak. In: Buku Ajar Respirologi Anak 2008 Edisi pertama. Jakarta: IDAI; 2008. p 109

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11. Pocket Guide For Asthma Management and Prevention In Children. Global Inisiative for Asthma. What is known about Asthma?. 2008. p : 25 12. Sharma GD. Asthma. Differential Diagnose and Workup. Department of Pediatrics. University Medical Center. 2009 Available at: http://emedicine.medscape.com/article/1000997-diagnosis [Accessed March 2010]. 13. Sharma GD. Asthma. Follow up. Department of Pediatrics. University Medical Center. 2009 Available at: http://emedicine.medscape.com/article/296301-overview [Accessed March 2010]. 14. Supriyanto B and Makmuri MS. Serangan Asma Akut. In: Buku Ajar Respirologi Anak 2008 Edisi pertama. Jakarta: IDAI; 2008. p 132

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