• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Wheezing and noisy breathing seminar

Wheezing and noisy breathing seminar



to differentiate b/w wheezing and stridor....lead to know to make clinical dx for asthma, croup, laryngomalacia, epiglottis...there many noisy breathing....our focus wheezing n stridor....

to differentiate b/w wheezing and stridor....lead to know to make clinical dx for asthma, croup, laryngomalacia, epiglottis...there many noisy breathing....our focus wheezing n stridor....



Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.


11 of 1 previous next

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment
  • rapid swelling (edema) of the dermis, subcutaneous tissue,[1]mucosa and submucosal tissues with assso. With nervous system involvement

Wheezing and noisy breathing seminar Wheezing and noisy breathing seminar Presentation Transcript

  • Wheezing & Noisy Breathing• Presenter: Azizah MajidMuhammad Naqib BajuriNoor Azwa SulaimanNoor Afifah Abd Rahman
  • Content• Anatomy of respiratory system• Stridor• Epiglottitis• Laryngomalacia• Croup• Wheezing• Bronchiolitis• Asthma• Pneumonia
  • A
  • ..
  • Stridor abnormal, high-pitched sound produced by turbulentairflow through a partially obstructed airway at the level of the supraglottis, glottis, subglottis, and/or trachea.externally audible sound associated with respiration (Itoccurs when a normal respiratory volume of air movesthrough narrowed airways, which results in the normal laminar flow becoming turbulent) * signifies partial airway obstruction. a symptom, not a diagnosis or disease, & the underlying cause must be determined
  • Depending on its timing in the respiratory cycle. Inspiratory • laryngeal obstruction stridor expiratory • tracheobronchial stridor obstruction. Biphasic • a subglottic or glottic stridor anomaly. In addition to a complete history and physical, as well as other possible additional studies, most cases require flexible and/or rigid endoscopy to adequately evaluate the etiology of stridor.
  • Common Causes of Stridor Croup Tracheitis Acute, Febrile Epiglottitis Retropharyngeal abscess ACUTE Foreign body Acute, Thermal injury to airway Afebrile Angioneurotic edema LaryngomalaciaCHRONIC Vascular anomalies Adenotonsillar hyperplasia
  • Life-threatening Causes of Stridor Usually Febrile Usually Afebrile• Epiglottitis • Foreign body• Retropharyngeal • Angioneurotic edema abscess • Neck trauma• Tracheitis • Neoplasm (compressing trachea) • Thermal injury
  • IntroductionAcute inflammation in the supraglottic region oforopharynx with inflammation of epiglottis,vallecula, arytenoids and aryepiglottic fold.Due to its place in the airway, swelling of thisstructure can interfere with breathing, andconstitutes a medical emergency. Infection cancause the epiglottis to obstruct or completelyclose off the windpipe.
  • Epidemiology• Greater prevalence in countries without HiB immunization• Occur most commonly in children aged 1-6 years
  • • Bacterial infection of the epiglottis, most often: Haemophilus influenzae type B• Some cases are attributable to Streptococcus pneumoniae, Streptococcus agalactiae, Staphylococcus aureus, Streptococcus pyogenes, Haemophilus influenzae, and Moraxella catarrhalis.• Viral infection: Herpes simplex virus, candida (immunocompromised pt) & Aspergillus.
  • PathophysiologyMicroorgansim colonize the pharynges throughrespiratory transmission from intimate contact Penetrate mucosal barrier Invading the bloodstream and causing bacteremia and seeding of the epiglottis and surrounding tissues Acute onset of inflammatory edema of epiglottis. Edema rapidly progresses to involve the aryepiglottic folds, the arytenoids, and the entire supraglottic larynx This may cause the throat structures to push the epiglottis backward-- continued inflammation and swelling of the epiglottis, complete blockage of the airway may occur, leading to suffocation and death.
  • Signs and symptoms• This dramatic, potentially lethal condition is charac: by an acute potentially fulminating course of high fever, sore throat,dyspnea, & rapidly progressing respiratory obstruction.• Healthy child suddenly develops a sore throat & fever. Within a several hours, the patient : toxic, swallowing is difficult, & breathing is labored. Drooling is usually present & the child may have the tripod position.• Stridor is a late finding & suggests near complete airway obstruction. Complete obstruction of the airway &death if adequate treatment is not provided.• The early symptoms - insidious but rapidly progressive, & swelling of the throat may lead to cyanosis and asphyxiation.
  • Diagnosis• confirmed: direct inspection by direct fibreoptic laryngoscopy, (carried out in controlled environment like an operating room) although this may provoke airway spasm. (“cherry red” swollen epiglottis and arytenoids ) . Tx should not be delayed for this test to be carried out.• Classic radiographs of a child who has epiglottitis show the “thumb sign• If epiglottitis is suspected, attempts to visualise the epiglottis using a tongue depressor are strongly discouraged.• Other test: FBC, pulse oximetry, throat culture (per nasal swab) (after stabilizing breathing)
  • Normal epigottis “Thumb sign”
  • The most likely differential diagnostic candidates are croup, peritonsillar abscess, and retropharyngeal abscess. On CT imaging, the "halloween sign" describe a normal thickness epiglottis. It can safely excluded the acute epiglottitis.CT imaging show"halloween sign"
  • Management• Transferred directly to ICU – intubation (nasogastric tube & nasotracheal tube)tube removed 24H.• IV Antibiotic – eg: cefuroxime (after airway is secured& given for 3-5days• Tracheostomy – severe• In addition, patients should be given antibiotics, such as second- or third-generation cephalosporins, either alone or in combination with penicillin or ampicillin for streptococcal coverage.• If allergy to penicillins is present, Co-trimoxazole or clindamycin is an alternative. In household contacts of any unvaccinated child infected with H. influenzae, rifampicin is used as prophylaxis
  • ComplicationsPatients may develop Pneumonia lymphadenopathy septic arthritis Pulmonary Meningitis Empyema oedema Pneumothorax Death (asphyxia)
  • Comparison of a normal pediatric airway (bottom) andairway from a child who died from epiglottitis (top).
  • Prognosis• The prognosis is good for patients with epiglottitis whose airways have been secured & the mortality rate is <1% in these patients• However, mortality rates as high as 10% can occur in children whose airways are not protected by endotracheal intubation
  • • Definition  An abnormal high-pitched or low-pitched sound heard-either by unaided human ear or through stethoscope-mainly during expiration  Occur as a results of narrowing of airways - Bronchospasm - Increased secretion - Retention of sputum
  • 2 patterns of wheezing1) Transient early wheezing2) Persistent and recurrent wheezing
  • Transient early wheezing• Preschool children• Virus-associated wheeze aka viral wheeze and wheezy bronchitis• Result from small airways to narrow and obstruct d/t inflammation and immune response to viral infection• l/t episodic nature, triggered by viruses cause common cold
  • • Have decreased lung function from small diameter• Risk factor – Maternal smoking during and/or after pregnancy – Not related from family hx of asthma and allergy• More common in males usually resolves by 5 years of age
  • Persistent and recurrent wheezing• Both preschool and school-aged• Frequent wheeze triggered by many stimuli• Presence of IgE to common inhalant allergens such as house dust mite, pollens, pets• Associated persistence of wheezing beyond preschool years
  • • Recurrent wheezing associated with evidence of allergy to one or more inhaled allergens termed as atopic asthma• Have persistent sxs and decreased lung fx.• Associated with other atopic disease such as eczema, rhinoconjunctivitis and food allergy; more common with family hx
  • Causes of recurrent wheeze• Transient early wheeze• Atopic asthma (Ig-mediated)• Non-atopic asthma• Recurrent aspiration of feeds• Inhaled foreign body• Cystic fibrosis• Recurrent anaphylaxis in child• Cong. abnormality of lung, airway or heart• Idiopathic
  • ……
  • • Common respiratory illness especially in infants aged 1-6 months old• 90% aged 1-9 m (rare after 1 year of age)• Throughout the year, cyclical periodicity with annual peaks occur in Nov, Dec, Jan• Majority of children with viral bronchiolitis has mild illness – About 1% require hospital admission
  • • Respiratory syncytial virus (RSV) is pathogen in 80% of cases.• Others human metapneumovirus, parainfluenza virus, rhinovirus, adenovirus, influenza virus & Mycoplasma pneumoniae• Dual infection with RSV and human metapneumovirus assoc. with severe bronchiolitis
  • Clinical Features• Coryzal sxs precede by dry cough & increase breathlessness• Feeding difficulty• Recurrent apnoea• High risk factor – Premature develop bronchopulmonary dysplasia – Cyctic fibrosis – Congenital heart disease
  • • Age < than 3 months• Toxic – looking• Moderate/Severe Chest recession• Central cyanosis• Wheeze• Crepitations on auscultation• Feeding Difficulty• Apnoea• Oxygen saturation <93%• High risk group
  • Investigations• Full blood count• Respiratory viruses identified by PCR analysis of nasopharyngeal secretions• Chest X-ray unnecessary but if performed shows hyperinflation of lungs d/t small airways obstruction, air trapping & focal atelectasis• Pulse oximetry to measure & monitor arterial oxygen saturation continously• Blood gas analysis performed in severe cases to identify hypercarbia
  • • General Measures  Assessment respiratory status and oxygenation  Maintained above 93% arterial oxygenation  Monitor sign of respiratory failure• Nutrition & Fluid theraphy  Feeding by nasogastric tube  Intravenous fluids with severe respiratory distress, cyanosis, apnoea
  • • Pharmacotheraphy  Inhaled ß2-agonist  A trial of nebulised ß2-agonist  Given in oxygen  May be considered in infants with viral bronchiolitis  Corticosteroid - may be tried in severe case  Antiviral agent - Ribavirin is the only for RSV bronchiolitis  Antibiotics - to all infants with :  Recurrent apnoea & circulatory impairment  Possibility of septicaemia  Acute clinical deterioration  High WBC  Progressive infiltrative changes on CXR
  • • Mist, antibiotics, steroids and nebulised bronchodilators such salbutamol or ipratropium not been shown to reduce severity and duration of illness
  • Prognosis• Most infants recover from acute infection within 2 weeks• Half will have recurrent episodes of cough & wheeze• Usually by adenovirus infection, may result in permanent damage to airways (bronchiolitis obliterans) but rarely
  • Prevention• Monoclonal antibody to RSV (palivizumab, given monthly by intramuscular injection) reduce no. of admissions in high-risk preterm infants.• Good hand hygiene needed to prevent cross infection to other infants because RSV is highly infectious.
  • DEFINITION A viral infection of the upper and lower respiratory tract leading to erythema and edema of the tracheal walls and narrowing of the subglottic region. A result of inflammation of the larynx, trachea and bronchilaryngotracheobronchitis
  • EPIDEMIOLOGY ages of 6 months - 3 years  peak at 2 years
  • ETIOLOGY  Pathogen most common: parainfluenza virus (74%), (types 1, 2 and 3). others :  Respiratory Syncytial Virus,  Influenza virus types A and B,  Adenovirus,  Enterovirus,  Measles,  Mumps  Rhinoviruses rarely :  Mycoplasma pneumoniae  Corynebacterium Diptheriae.
  • PATHOGENESIS VIRAL INFECTION INFLAMMATION Lower airway wheezing Vocal cord and pharynxswellinghoarseness of voice Trachea redness+swelling barking cough Subglottis, tracheaedemainspiratory stridor RESPIRATORY FAILURE
  • CLINICAL FEATURES HISTORY  PHYSICAL  Low grade fever, cough EXAMINATION and coryza for 12-72 hours, followed by:  Sign of respiratory  Increasingly bark-like distress cough and hoarseness.  Stridor  Stridor that may occur when excited, at rest or both.  Respiratory distress of varying degree.  Symptoms are acute onset and worse at night
  • video
  • DIAGNOSIS a clinical diagnosis Assessment of severity Clinical Assessment of Croup (Wagener) Severity  Mild: Stridor with excitement or at rest, with no respiratory distress.  Moderate: Stridor at rest with intercostal, subcostal or sternal recession.  Severe: Stridor at rest with marked recession, decreased air entry and altered level of consciousness.
  • DIFFERENTIAL DIAGNOSIS Epiglottitis Bacterial tracheitis Retropharyngeal abscess Foreign body
  • INVESTIGATION1. Studies show that it is safe to visualise the pharynx to exclude acute epiglotitis, retropharyngeal abscess etc.  In severe croup, it is advisable to examine the pharynx under controlled conditions, i.e. in the ICU or Operation Theatre.2. Pulse oximetry is helpful but not essential3. Arterial blood gas :not helpful because the blood parameters may remain normal to the late stage. The process of blood taking may distress the child4. A neck Radiograph is not necessary, unless the diagnosis is in doubt, such as in the exclusion of a foreign body.
  • X-ray May be essential to exclude differential diagnoses Lateral view  Thickening of pre-tracheal soft tissue – retropharyngeal abscess  Air at pharynx-croup: d/t subglottic edema  Thumb sign: epiglottitis AP view  Angulation of trachea  Steeple –shaped trachea: croup-subglottic edema
  • Management1. Indications for Hospital admission  Moderate and severe viral croup.  Age less than 6 months.  Poor oral intake.  Toxic, sick appearance.  Family lives a long distance from hospital; lacks reliable transport.2. Antibiotics are not recommended unless bacterial super-infection is strongly suspected or the patient is very ill.3. IV fluids are not usually necessary except for those unable to drink.
  • MedicationCorticosteroid (oral, IM,IV) Nebulised adrenaline  Moderate to severe  For all grade (mild croup to severe)  Onset within 30  Onset after few mins hours  diminished after  Dexamethasone ~2h Anti-inflammatory  Rebound effect of effect lasted up to symptoms may 72 hrs occur
  • CLINICAL EXAMPLE 9-month old baby was admitted to pediatric ward with complaint of acute onset of noisy breathing which is associated with fever, barking cough and hoarseness. He also had history of coryzal symptoms like sneezing and cough for 2 days. He cannot suck well like previously because of nasal blockage. Immunization is up to date. Smoking history is present in his father. Provisional diagnosis: croup Points for:  Acute onset of noisy breathing  Fever  Barking cough  Hoarseness
  • EPIDEMIOLOGY Congenital anomaly of larynx an isolated finding in the otherwise healthy infant or may be associated with other neurologic disorders such as cerebral palsy Although laryngomalacia is typically thought of as occurring only in infants, it is occasionally observed in older children and adults.  Neurologically impaired children (i.e., those with cerebral palsy) with poor pharyngeal control  Exercise-induced laryngomalacia results when enough inspiratory force occurs during exercise to draw the aryepiglottic folds into the larynx, partially obstructing the glottis
  • ANATOMICAL LOCATION The anatomic abnormality causing the supraglotttic obstruction of laryngomalacia varies among infants.1. anterior prolapse of the mucosa overlying the arytenoid cartilages (57%)-most common2. short aryepiglottic folds that tether the epiglottis posteriorly (15%),3. posterior collapse of the epiglottis (12%),4. combination of these findings (15%)
  • On inspiration, the epiglottic folds collapse into the airway. The lateral tips of the epiglottis are also collapsing inward (arrow)Progressive airway obstructionon inspiration.Note omega-shaped epiglottis
  • CLINICAL FEATURES Stridor  inspiratory,  low-pitched  exacerbated by any exertion: crying, agitation, or feeding.  results from the collapse of supraglottic structures inwards during inspiration.  Symptoms usually appear within the first 2 wk of life and increase in severity for up to 6 mo, although gradual improvement can begin at any time. Laryngopharyngeal reflux is commonly associated with laryngomalacia. high prevalence of gastroesophageal reflux disease (GERD)
  • DIAGNOSIS The diagnosis is confirmed by outpatient flexible laryngoscopy When the work of breathing is moderate to severe, chest radiographs are indicated. Because 15-60% of infants with laryngomalacia have synchronous airway anomalies, complete bronchoscopy is undertaken for patients with moderate to severe obstruction.
  • MANAGEMENT Expectant observation  suitable for most infants because most symptoms resolve spontaneously as the child and airway grow. Laryngopharyngeal reflux is managed aggressively severe obstruction that surgical intervention is unavoidable  (patients with apparent life-threatening events, cor pulmonale, cyanosis, failure to thrive) endoscopic supraglottoplasty can be used to avoid tracheotomy.
  • Contents• Introduction• Epidemiology• Causes• Pathogenesis• Clinical features• Diagnosis• Investigation• Management
  • Introduction…• There is no single definition for pneumonia. It is a clinical illness defined in terms of symptoms and signs, and its course. WHO defines pneumonia in terms of febrile illness with tachypnoea for which there is no apparent cause.
  • – Bronchopneumonia : which is a febrile illness with cough, respiratory distress with evidence of localised or generalised patchy infiltrates on chest x-ray– lobar pneumonia : which is similar to bronchopneumonia except that the physical findings and radiographs indicate lobar consolidation.– Community acquired pneumonia (CAP) : signs and symptoms of pneumonia in a previously healthy child due to an infection which has been acquired outside hospital
  • Epidemiology…• Acute respiratory infections namely pneumonia cause up to 5 million deaths annually among children less than 5 years old in developing nations.• Of the estimated total of 12.9 million deaths globally in 1990 in children under 5 years of age, over 3.6 million were attributed to acute respiratory infections mostly due to pneumonia. This represents 28% of all deaths in young children and places pneumonia as the largest single cause of childhood mortality.• In Malaysia the prevalence of ARI in children below the age of five years is estimated to be 28% - 39.3%
  • Causes…• A specific aetiological agent cannot be identified in 40% to 60% of cases. Viral pneumonia cannot be distinguished from bacterial pneumonia based on a combination of clinical findings.• The majority of lower respiratory tract infections that present for medical attention in young children are viral in origin such as respiratory syncytial virus, influenza, adenovirus and parainfluenza virus. One helpful indicator in predicting aetiological agents is the age group as shown in table.
  • • Risk factors for developing pneumonia:  low weight for age  lack of breast feeding  failure to complete immunization  presence of coughing sibling (s) at home  overcrowding in bedroom
  • Pathogenesis…• When bacteria infects the pulmonary lobes, the lungs produce mucus that fills the alveolar sacs.• In turn, this causes a condition known as consolidation which occurs when the lungs fill with mucus, reducing air space.• The reduction in air space makes breathing difficult causing shortness of breath and labored or shallow breathing.
  • Clinical features…• Symptoms : – Fever – Difficulty in breathing – Cough – Lethargy – Poor feeding – Localized chest, abdominal, neck pain
  • • Signs: – Tachypnea – Nasal flaring – Chest indrawing – Chest hyperinflation and wheeze – (early) diminished breath sound, scattered crackles and rhonci over affected side – (effusion, empyema, pyopneumothorax) dullness on percussion and breath sound markedly diminished – Lag in respiratory excursion on affected side – Abdominal distension may be prominent because of gastric dilation from swallowed air or ileus – Liver may seem enlarged because of downward displacement of diaphragm
  • Diagnosis…• The clinical diagnosis of pneumonia has traditionally been made using auscultatory findings such as bronchial breath sounds and crepitations in children with cough.• However, the sensitivity of auscultation has been shown to be poor and varies between 33 %- 60% with an average of 50 % in children.• Tachypnoea is the best single predictor in children of all ages. Measurement of tachypnoea is better compared with observations of retractions or auscultatory findings.
  • • It is nonetheless important to measure respiratory rate accurately. Respiratory rate should be counted by inspection for 60 seconds.• However in the young infants, pneumonia may present with irregular breathing and hypopnea.
  • Investigation…1. Chest radiograph – Chest radiograph is indicated when clinical criteria suggests pneumonia. It will not identify the aetiological agent. However the chest radiograph is not always necessary if facilities are not available or the pneumonia is mild2. Complete white blood cell and differential count – This test may be helpful as an increased white blood count with predominance of polymorphonuclear cells may suggest bacterial cause. However, leucopenia can either suggest a viral cause or severe overwhelming infection.
  • 3. Blood culture – Blood culture remains the non-invasive gold standard for determining the precise aetiology of pneumonia. However the sensitivity of this test is very low. Positive blood cultures are found only in 10% to 30% of patients with pneumonia. Even in 44% of patients with radiographic findings consistent with pneumonia, only 2.7% were positive for pathogenic bacteria.4. Culture from respiratory secretions – It should be noted that bacteria isolates from throat swabs and upper respiratory tract secretions are not representative of pathogens present in the lower respiratory tract. This investigation should not be routinely done.
  • 5. serology tests – serological studies should be performed in children with suspected atypical pneumonia as Mycoplasma pneumoniae, Chlamydia, Legio nella and Moxarella catarrhalis are difficult organisms to culture.6. Other tests – Bronchoalveolar lavage is usually necessary for the diagnosis of Pneumocystis carini infections primarily in immunosuppressed children. It is only to be done when facilities and expertise are available. If there is significant pleural effusion diagnostic, pleural tap will be helpful.
  • Management…• Assessment of severity of pneumonia **• Assessment of oxygenation – The best objective measurement of hypoxia is by pulse oximetry --> avoids the need for ABG
  • • Criteria for hospitalization – <3 months old regardless severity – Fever(>38.5), refusal to feed and vomiting – Fast breathing with/without cyanosis – Associated systemic manifestation – Failure of previous antibiotic – Recurrent pneumonia – Severe underlying disorder
  • • Antibiotic therapy – Depends on age, severity, radiographic findings, local epidemiology of pathogens, sensitivity and resistance of organism • Staphylococcal infection : cloxacillin • Streptococcus pneumonia : penicillin, cephalosporin • Atypical pneumonia : macrolides (erythromycin, azithromycin) • Severe CAP : 2nd or 3rd generation cephalosporin and macrolides• Supportive therapy – Fluids  should not overhydrated (ADH ususally increase in severe pneumonia) – Oxygen  maintain SPO2 >95% – Analgesic and temperature control  PCM – Chest physiotherapy  assist removal tracheobronchial secretion
  • • Outpatient management – Fast breathing but no chest indrawing – Oral antibiotics – Advice to return in 2 days or earlier if child getting worse
  • Introduction…• Def : chronic airway inflammation leading to increase airway responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night and early morning
  • Causes…• Bronchial asthma triggers may include: – Smoking and secondhand smoke – Infections such as colds, flu, or pneumonia – Allergens such as food, pollen, mold, dust mites, and pet dander – Exercise – Air pollution and toxins – Weather, especially extreme changes in temperature – Drugs (such as aspirin, NSAID, and beta-blockers) – Food additives (such as MSG) – Emotional stress and anxiety – Singing, laughing, or crying – Perfumes and fragrances – Acid reflux
  • Pathogenesis… Environmental Bronchial Bronchial factors + genetic hyperactivity + inflammation predisposition trigger factors Edema, Symptoms: cough,bronchoconstriction wheezing, chest Airway narrowing , excess mucus tightness, production breathlessness
  • Clinical features…• Symptoms: – Shortness of breath – Tightness of chest – Wheezing – Excessive coughing or a cough that keeps child awake at night• In acute episode: – Breathless during rest – Not interested in feeding – Sit upright – Talk in words (not sentences) – Usually agitated
  • • Findings during a severe episode include the following: – Respiratory rate is often greater than 30 breaths per minute – Accessory muscles of respiration are usually used – Suprasternal retractions are commonly present – The heart rate is greater than 120 beats per minute – Loud biphasic (expiratory and inspiratory) wheezing can be heard – Pulsus paradoxus is often present (20-40 mm Hg) – Oxyhemoglobin saturation with room air is less than 91%
  • Investigations…• Lung function test increased functional residual capacity• Peak expiratory flow rate (PEFR)  >5 y/o• Bronchodilator reversibility test  improved 10-15% after inhalingbronchodilator)• Skin prick test  to diagnose the atopy• Chest x-ray  usually normal -TRO other conditions
  • The radiographic changes of asthma are those ofoverexpansion (flat diaphragm, square chest shape)
  • Managements…• Bronchodilator therapy  Inhaled B2 agonist are most commonly used and most effective bronchodilators.  Short acting(relievers): salbutamol or terbutaline (effective for 2-4hr)  Long acting (LABAs): salmaterol (12hr)  They are not used in acute asthma and should not be used with inhaled corticosteroid  Useful in exercise induced asthma
  • • Inhaled corticosteroid  Most effective inhaled prophylactic therapy.  Decreases airway inflammation, resulting in decrease symptoms, asthma exacerbations and bronchial hyperactivity  It can produced systemic side effects, including impaired growth, adrenal suppression and altered bone metabolisms, when high doses are used• Add-on therapy  Leukoriene receptor antagonist (montelukast); can also be used in older children when symptoms are not controlled by the addition of the LABA  Slow-release oral theophylline is an alternative; but incident of side effects (vomiting, insomnia, headaches, poor concentration) -not commonly used in children-
  • • Other therapy  Oral prednisolone  Anti-IgE therapy (omalizumab)  Antibiotics – most are of no value in the absence of bacterial infection>> recent data suggest that macrolides antibiotic (erythromycin) may have specific role in asthma management  Antihistamine – useful in the treatment of allergic rhinitis• Allergen avoidance and other pharmacological measures  Avoid allergens  Allergen immunotherapy is effective for treating atopic asthma  Parents to avoid smoking in the house
  • References…• Illustrated textbook of paediatrics, 4th edition• Paediatric protocols for Malaysian hospital• Clinical practice guidelines (CPG)
  • Thank youvery muchh for your kind attention ^__^