Asthma Flashcards

1
Q

DEFINITION

A
  1. Most common chronic childhood disease and the major cause of hospitalisation for children.
  2. It is a common chronic inflammatory condition affecting the airways and displays a varied phenotypic picture.
  3. At present we have no cure for asthma !!

4.Paediatric asthma represents a lifelong problem, although modern and optimal treatment do offer a good disease control.

5.Recently, paediatric asthma has been reported as a major risk factor for COPD in adult life.

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2
Q

DEFINITION ‘

A

There is no universally accepted definition of asthma but:
1. reversible airway obstruction
2. airway hyperresponsiveness
3. chronic inflammation
→ are key features

It is a chronic disease with:
- repeated attacks of airway obstruction
- intermitent symptoms of responsiveness to triggering factors such as allergens,smoke, exercise, viral infections

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3
Q

PREVALENCE

A

1.Asthma prevalence has increased during the last 2 decades

2.It is causes considerable morbidity and healthcare utilisation

3.High frequency of sleep disturbance due to asthma/ absence from school/ limitation of activities.

4.Asthma is associated with reduced growth of lung function( lung function at a young age is a determinant of lung function in adult life).

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4
Q

EPIDEMIOLOGY

A

1.Worldwide , 1-30% / some countries having come through the epidemic and others still experiencing increasing prevalence.

2.Are more common in boys compared to girls / female predominance after puberty

3.Asthma is more common in younger children and although symptoms apparently resolve in many, episodic wheeze recurs in adulthood in approximately 25%

4.Asthma is associated with allergic conditions such as- eczema, hay fever and food allergy → but most allergic individuals do not have asthma and approximately 20% of children with asthma - are not allergic !!

5.Strong hereditary component to asthma( identical twins are more concordant for asthma compared to fraternal twins)

6.There is no single asthma gene( aprox 20 genes each making a modest contribution towards asthma risk,and these differ between populations)

7.Genetic predisposition in combination with environmental exposures occuring at certain critical times →often in the first 2 years of life→ are implicated in asthma causation.

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5
Q

ETIOLOGY (1)

A
  1. Highest prevalence of asthma in Western countries , including UK, Australia, New Zeeland and USA ,suggesting an association between asthma and a„Westernized lifestyle“
    2.A number of related hypotheses have been proposed including the hygiene and dietary hypotheses/

3.The hygiene hypothesis being proposed - exposure to infections contracted from older siblings during early life - or to live on a farme when they exposure to different allergen – may protect against the development of allergy

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6
Q

ETIOLOGY (2)

A

1.the dietary hypothesis – an excess of dietary oxidant or lack of dietary antioxidants(vit E,C) in maternal diet during pregnancy lead to increased asthma

2.Reduced birth weight , antenatal exposures to paracetamol or products of tobacco smoke ,place exposures in early life as crucial to asthma causation
(many children with asthma are initially symptomatic in preschool years)

3.Sedentary lifestyle, obesity,indoor and outdoor air quality- may also be related to asthma causation

4.Changes in outdoor air quality (increasing concentrations of fine particulates, ozone, sulphur dioxide and oxides of nitrogen)-are associated with increased presentation of children with acute asthma

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7
Q

ETIOLOGY (3)

A

80% - asthma exacerbations in primary care are associated with viral upper respiratory tract infections- predominantly due to rhinovirus (common cold virus)

There is substantial literature/ studies to support the role of early respiratory infection in the later development of asthma → the common cold viruses are implicated

Exposure to allergens wich include house dust mite , cat ,dog and grasses are also associated with increased risk for acute asthma exacerbation

Precipitants for acute asthma symptoms in children include :
- viral upper
- respiratory tract infections,
- change in the weather,
- poor air quality,
- allergen exposure and exercise

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8
Q

PATHOPHYSIOLOGY

A

Asthma- chronic inflammatory airway disease characterised by:

  1. reversible airway obstruction
  2. bronchial hyperresponsivenes (BHR)

Chronic inflammation is often characterised by:
- eosinophilic activity
- allergic inflammation

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9
Q

Bronchial obstruction is a result of:

A
  • bronchial muscle constriction (acting particularly through the β receptors)
  • mucosal oedema
  • increased airway secretios (resulting from airway inflamation)
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10
Q

PATHOPHYSIOLOGY
All contribute →

A

reduced airway flow → reduced lung function→classical symptom →wheezing + dyspnea + cough.

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11
Q

Reversibility of the bronchial obstruction may occur:

A
  • spontaneously
    or
  • with bronchodilator( particularly β agonists)
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12
Q

Airway inflammation

A

in asthma is generally considered to be eosinophilic

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13
Q

Allergen exposure

A

may lead to a break in natural tolerance – triggering alergic
inflammation – with an allergen-specific immune response involving T and B lymphocytes

The adaptative immune system classically involves T cellular responses to antigens or allergens ,with production of specific IgE antibodies from B-cell,adapts to environmental challenges

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14
Q

Pathophysiology of allergens

A

binds to the high-affinity receptor for IgE (on the antigen presenting cells)– that facilitate presentation to T-cells – IgE is synthesised in the presence of interleukins(Ils – IL4,IL13) + other cytokines

Allergic inflammation – is characterised by a T-helper cell(Th) type 2 cascade involving Th2 cytokines + other immune mediators

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15
Q

Viral infections

A

important triggers of symptoms and exacerbations of asthma in childhood( many children with viral wheeze may later not have asthma)

Recent studies suggest that respiratory viruses, like human rhinovirus – play a role in triggering the immune system
( mechanisms are currently not known, but cycles of inflammation, with repeated insults - the inflammatory
resolution becomes less complete with prolonged periods of pathological changes – may progress to deterioration in respiratory function/ remodelling )

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16
Q

PATHOPHYSIOLOGY
atopic asthma

A

There is accumulating evidence that interaction between respiratory viral infection and atopy is important in the cause and pathogenesis of atopic asthma

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17
Q

Bronchial hyperresponsiveness + airway remodelling

A

Some research are suggested that allergic sensitisation precedes
rhinovirus-induced wheezing !!

BHR is a common / but not obligate feature of childhood asthma

BHR presents as a general liability to develop symptoms by exposure to various physiological or environmental stimuli (exercise is a classical childhood asthma symptom trigger)

Airway remodelling is less clear, particularly as to when it starts and what elicits the process ( lung function reductions in older children are likely to reflect structural changes in the airway)

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18
Q

DIAGNOSIS
Classical symptoms are:

A

-wheeze

  • cough (particularly at night or during exertion)
  • dyspnea
  • chest tightness
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19
Q

For diagnosis asthma we neeed

A
  1. history taking
  2. physical examination
  3. lung pulmonary function testing
  4. objective documentation of reversible bronchial obstruction
  5. allergy and bronchial hyperresponsiveness(BHR) - testing
  6. assesing airway inflammation whenever possible
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20
Q

DIAGNOSIS
In all children ask about:

A

1.wheezing, cough

2.Specific triggers - passive smoker,pets, humidity,mold and dampness, respiratory infections, cold air exposure, exercise/ activity, cough after laughing / crying

3.Altered sleep paterns:awakening, night cough, sleep apnea

4.Exacerbatios in the past year

5.Nasal symptoms: running,itching, sneezing, blocking

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21
Q

DIAGNOSIS
In infants ask about :

A

1.Noisy breathing, vomiting with cough

2.Retractions, changes in respiratory rates

3.Difficulty with feeding (poor sucking, grunting sounds)

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22
Q

DIAGNOSIS

In children(˃ 2 yr) ask about:

A

1.Shortness of breath day/ night

2.Fatigue( decrease in playing compared to peer group, increased irritability)

3.Complaints about „ not feeling well“

4.School absence/ poor school performance

5.Reduced frequency or intensity of physical activity

6.Avoidance of other activities, e.g visits to friends with pets

7.Specific triggers :sports, PE classes ,exercise, activity

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23
Q

DIAGNOSIS

In children(˃ 2 yr) ask about:

A

1.Shortness of breath day/ night

2.Fatigue( decrease in playing compared to peer group, increased irritability)

3.Complaints about „ not feeling well“

4.School absence/ poor school performance

5.Reduced frequency or intensity of physical activity

6.Avoidance of other activities, e.g visits to friends with pets

7.Specific triggers :sports, PE classes ,exercise, activity

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24
Q

DIAGNOSIS

In children(˃ 2 yr) ask about:

A

1.Shortness of breath day/ night

2.Fatigue( decrease in playing compared to peer group, increased irritability)

3.Complaints about „ not feeling well“

4.School absence/ poor school performance

5.Reduced frequency or intensity of physical activity

6.Avoidance of other activities, e.g visits to friends with pets

7.Specific triggers :sports, PE classes ,exercise, activity

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25
Q

DIAGNOSIS

In children(˃ 2 yr) ask about:

A

1.Shortness of breath day/ night

2.Fatigue( decrease in playing compared to peer group, increased irritability)

3.Complaints about „ not feeling well“

4.School absence/ poor school performance

5.Reduced frequency or intensity of physical activity

6.Avoidance of other activities, e.g visits to friends with pets

7.Specific triggers :sports, PE classes ,exercise, activity

25
Q

DIAGNOSIS

In children(˃ 2 yr) ask about:

A

1.Shortness of breath day/ night

2.Fatigue( decrease in playing compared to peer group, increased irritability)

3.Complaints about „ not feeling well“

4.School absence/ poor school performance

5.Reduced frequency or intensity of physical activity

6.Avoidance of other activities, e.g visits to friends with pets

7.Specific triggers :sports, PE classes ,exercise, activity

25
Q

DIAGNOSIS

In children(˃ 2 yr) ask about:

A

1.Shortness of breath day/ night

2.Fatigue( decrease in playing compared to peer group, increased irritability)

3.Complaints about „ not feeling well“

4.School absence/ poor school performance

5.Reduced frequency or intensity of physical activity

6.Avoidance of other activities, e.g visits to friends with pets

7.Specific triggers :sports, PE classes ,exercise, activity

26
Q

PHYSICAL EXAMINATION

A

Is nearly normal between exacerbations
In all children check for the following

  • Clubbing
  • Chest shape- hyperinflation suggests poorly controlled disease
  • Symetry and degree of chest expansion
  • Nature of the breath sounds
  • Presence of crepitations
  • Presence of prolonged expiratory phase to the breathing cycle
  • Presence of wheeze

if the wheeze is heard – a bronchodilator should be given and its effect noted

27
Q

Clinical features of moderate exacerbation of asthma

A

Breathless, but able to complete whole sentences(able to talk)
PEF ˃ 50-75% of predicted
Respiratory rate ˂ 30 breaths / min
Oxygen saturation – usually ˃ 92%
Pulse ˂ 110/min
Chest signs- expiratory wheeze,prolonged expiratory phase,crackles( rales) and rhonchi can sometimes be heard

28
Q

Clinical features of severe exacerbation of asthma

A

Sitting forward,anxious,nasal flaring, unable to complete sentences

PEF: 33- 50% of predicted
Respiratory rate ˃ 30breaths / min
Oxygen saturation – usually ˃ 90%
Pulse ˃ 110/min
Chest signs- expiratory and inspiratory wheeze, rales,use of accessory
muscle,chest retractions(suprasternal ,intercostal); decreased breath
sounds in some of the lung fields( regional hypoventilation owing to airways obstruction !)

Combination of segmental crackles + poor breath sounds can indicate lung segmental atelectasis

29
Q

Clinical features of life-threatening exacerbation of
asthma

A

Exhausted, confused, unable to speak, cyanosed,or comatose, poor respiratory effort

  • PEF ˂ 33% of predicted
  • Poor effort, low respiratory rate
  • Oxygen saturation ˂ 90%
  • Bradycardya, arrhythmias
  • Silent chest
30
Q

INVESTIGATIONS

A
  1. History and examination
  2. If the diagnosis is not in doubt and the symptoms are mild, no investigation are required !!!

3.In other situation spirometry may be helpful / but most children with asthma will have normal spirometry between exacerbations / mild exacerbations

  1. Children with active post-viral cough / reactive airway disease- will have normal spirometry and this finding can help prevent unnecessary treatment !
  2. Using home peak-flow recordings and symptom diaries over a month can be helpful if the family is sufficiently motivated to make the twice daily measurements
31
Q

PULMONARY FUNCTION TESTING
Spirometry

A

1.Forced expiratory airflow measures are helpful in diagnosing /monitoring asthma

2.Is indicated in all children with suspected asthma, ˃5- 6 years of age

3.Involves the patient performing a forced respiratory manoeuvre,which measures FEV1(forced expiratory volume in 1 second), FVC (forced vital capacity),and FEV1/ FVC ratio

4.Most asthmatic children will have normal spirometry

5.FEV1/ FVC ratio ˂ 0,8 indicates significant airflow obstruction

6.The guidelines cutoff criteria of FEV1˂ 80% and ˂ 60% of predictive for moderate and severe asthma, are controversial for children with asthma,many of whom can have near normal or even supra normal airflow, despite having the other hallmarks of moderate to severe disease !

32
Q

PULMONARY FUNCTION TESTING

A

Such measures of airflow alone are not diagnostic for asthma,because
numerous other conditions can cause airflow reduction.

|Lung function tests can help to confirm the diagnosis of asthma and determine disease severity |

Bronchodilator response to an inhaled β-agonist is greater in asthmatics vs non-asthmatics an improvement in FEV1˃ 12% or ˃ 200 ml –is consistent with asthma !!

33
Q

PULMONARY FUNCTION TESTING
Bronchoprovocation challenges

A

can be helpful in diagnosing/optimizing
asthma management; asthmatic airways are hyperresponsive and more
sensitive to inhaled methacoline,histamine,cold or dry air

the degree of BHR to these exposures correlates with asthma severity and
airway inflammation !

Bronchial challenge tests tend to be reserved for research purposes in
specialized centres !

34
Q

PULMONARY FUNCTION TESTING

Exercise challenges(testing)

A

aerobic exertion or running for 6-8 min can help to identify children with exercise –induced bronchospasm

Exercise often provokes airflow obstruction in untreated or inadequately
treated asthmatics

In asthmatics FEV1 decreases during or after exercise by ˃15%;the onset of
exercise –induced bronchospasm is usually within 15 min after / can
spontaneously resolve within 30-60 min

Exercise challenges can induce severe asthma exacerbations in at-risk
patients!

35
Q

PULMONARY FUNCTION TESTING
Peak expiratory flow(PEF)

A

monitoring devices provide a simple and inexpensive
home –use tool to measure airflow and can be helpful

Monitoring PEF daily to

PEF variation ˃ 20% is consistent with asthma /suggests poorly controlled
asthma

assess objectively airflow as an indicator of asthma
control / PEFmonitoring should be started by measuring morning and evening for several weeks for patients to determine a personal best, and to correlate PEF value with symptoms! |

36
Q

ALLERGY TESTING
Skin prick test

A

Skin prick tests or serum – specific IgE assays, have a limited role in the
diagnosis or management of asthma !

The tests have a false positive rate of around 15%

A negative test usually rules out allergic sensitization of the airways to the
allergen tested

Demonstrating allergic sensitization does provide a rationale for allergen
avoidance !

37
Q

Measuring exhaled nitric oxide (FENO)

A

|marker of inflammation in asthma confirm the diagnosis |

NO is produced in the epithelial cells of the bronchial wall;
NO production increases during eosinophilic inflammation and is elevated in patients with asthma

Repeated measurements in the same child may also be predictive of an
imminent deterioration of asthma control !

FENO – has not been established as useful for ruling in or ruling out a diagnosis of asthma

38
Q

OTHER INVESTIGATIONS

A
  1. Oesophgeal pH study – to investigate possible GOR
  2. Brochoscopy – to exclude an abnormal airway anatomy, tuberculosis,
  3. tracheobrochomalacia; to collect lavage fluid for analysis (eosinophil and neutrophil cell counts and culture)
  4. Sweat test, genetic test (to exclude CF)
  5. Serum IgG, IgA, IgM and specific antibody responses to vaccinations (as a screen for immune deficiency)
  6. HRCT of the chest – to identify any unexpected bronchiolitis obliterans or bronchiectasis
  7. Nasal brush biopsy for cilial evaluation (to exclude PCD)
  8. Aspergillus IgE and IgG (precipitin) - which may indicate ABPA
  9. Total IgE - atopy
  10. Sputum culture / cough swab – to identify persistent endobronchial infection or aspergilus
39
Q

Management

Aims of asthma management:

A

**To achieve and maintain clinical control **
To control symptoms, allowing normal levels of activity, undisturbed sleep full school attendance

To prevent exacerbations !

To maintain normal lung function

To use the minimum therapy necessary with minimum adverse events

40
Q

GINA definition of controlled asthma:

A
  1. No (twice or less/ week) daytime symptoms
  2. No nocturnal symptoms / awakening because of asthma
  3. No (twice or less/week) need for reliever medication / rescue treatment
  4. No limitations of daily activities / exercise
  5. Normal or near normal lung function (FEV1, PEF) results

Increased use, especially daily use of reliever medication, should be taken as
an **indicator of deteriorating control **and the need to re-assess
management

41
Q

Management

Future risk to the patient includes

A

Loss of control

Risk of exacerbations

Accelerated decline in lung function

Side effects of treatment

42
Q

GINA – guidelines suggest 3 asthma control levels:

A

Controlled

Partly controled

Uncontroled

Asthma control is measured by symptoms scores and not PEF / spirometry

43
Q

GINA guide step up / step down in asthma treatment –

A

is a working schema, it enables physicians to assess asthma control systematically and adjust treatment acordingly

In patients with uncontroled asthma – step up treatment should be considered

44
Q

Before stepping up treatment, need to check:

A

Adherence to treatment
Inhaler tehnique
Ongoing exposure to triggers
Comorbidity (allergic rhinitis, obesity, GOR)
Is it Asthma?
Step down should be considerd if are well controlled for 3-6 months !

45
Q

ASTHMA MEDICATION

Medications to treat asthma can be classified:

A

controllers and relievers

46
Q

CONTROLLERS

A

are medication taken daily on a long term basis to keep asthma
under clinical control chiefly through their antiinflammatory effects

They icludes:
1. Inhaled glucocorticosteroids(ICS)
2. Systemic glucocorticosteroids(CSS)
3. Leukotriene modifiers
4. Long-acting inhaled β2-agonists(LABA) in combination with ICS
5. Sustained-release theophylline
6. Cromones
7. Anti-IgE; anti interleukin 5R, 4R

ICS- ARE THE MOST EFFECTIVE CONTROLLERS MEDICATIONS
CURRENTLY AVAILABLE

47
Q

RELIEVERS

A

are medications used in an as-needed basis that act quickly to
reverse bronchoconstriction and relieve its symptoms

They includes:
- Rapid acting inhaled β2 agonists
- Inhaled anticholinergics
- Short-acting theophilline
- Short acting oral β2 agonists

Asthma treatment can be adminstered in different ways:
- Inhaled
- Orally
- Injection

48
Q

ASTHMA MEDICATION

Advantage of inhaled therapy

A

Drugs are delivered directly in to the airways

Higher local concentration

Less risk of systemic side effects

49
Q

SIDE EFFECTS OF ICS

A
  1. High dose ICS of ˃ 800 micrograms/day (beclometasone equivalent) can be associated with adrenal suppression
  2. Temporary reduction in the growth velocity commonly occurs with ICS, but there is no effect on the final height, with long-term use of ICS at standard doses ≤ 400 micrograms/day
  3. Bone mineral density (BMD) may be reduced following the long term use of high dose ICS ! ( teenager)
  4. High dose ICS or incorect inhaler tehnique may also associated with a hoarse voice/oral candida
50
Q

ASTHMA MANAGEMENT

Non pharmacological approaches

A

The preventive measures recommended include allergen avoidance from birth, avoidance of tobacco smoke and encouragement of breastfeeding (primary prevention in high-risk infants)

There is no evidence of sustained benefit for any of the alternative
therapies:homeopathy,herbal medicines, breathing techniques,acupuncture, hypnosis,dietary manipulation

**Allergen avoidance is important **
**Vit D **– recent research has shown that vit D has an important role in the modulation of the immune system response ( an epidemiological study sugested that low concentration of vit D in children with asthma is associated with more severe symptoms, frequent exacerbations,reduction in lung function and an increase in medication use)

51
Q

Why not treat with SABA alone?

A

**Inhaled SABA has been first-line treatment for asthma for 50 years **
Asthma was thought to be a disease of bronchoconstriction

Role of SABA reinforced by rapid relief of symptoms and low cost

1.Regular use of SABA, even for 1–2 weeks, is associated with increased AHR, reduced bronchodilator effect, increased allergic response, increased eosinophils (e.g. Hancox, 2000; Aldridge, 2000)

2.Can lead to a vicious cycle encouraging overuse

3.Over-use of SABA associated with 🡩** exacerbations** and
🡩 mortality (e.g. Suissa 1994, Nwaru 2020)

4.Starting treatment with SABA trains the patient to regard it as their primary asthma treatment

5.The only previous option was daily ICS even when no symptoms, but adherence is extremely poor

6.GINA changed its recommendation once evidence for a safe and effective alternative was available

52
Q

ASTHMA MANAGEMENT

Anti IgE – TREATMENT – OMALIZUMAB-

A

is a monoclonal human antibody that
can **antagonize the role of IgE **in the pathogenesis of allergic asthma

-IT CAN BE CONSIDERED AS AN OPTION IN CHILDREN

IgE mediated sensitisation(one or more allergen)

Is a treatment for patient with **moderate - severe allergic asthma **and with elevated serum levels of IgE( 76 – 3000UI/ML)

With chronic symptoms / uncontrolled

Recurrent severe asthma exacerbations

Resistance to high doses of ICS and LABA

In step 4 - 5 , for children ˃ 6 yr

53
Q

Hospital management of acute asthma exacerbation
Mild attack

A

Oxygen via a face mask/nasal canula (if SpO2 ˂ 94%)
Salbutamol MDI+spacer – 2 puffs
re-assess after 30 min

If not improved give 2 puffs salbutamol
**Oral prednisolone 2mg/kg **(max 40mg) daily for 3 days
Re-assess, repeat salbutamol up too 4 hourly, as needed

54
Q

Hospital management of acute asthma exacerbation

Moderat attack

A

**Nebulised salbutamol **0,1-0,15 mg/kg, max 2,5 mg for ˂ 5 years / otherwise 5 mg

Re-assess after 10 -30 min

If not improved give nebulized salbutamol (+/- ipratropium bromide)

Re-assess after 10 -30 min

If not improved give nebulized salbutamol (+/- ipratropium bromide)

Oral prednisolone 2mg/kg (max 40mg) daily for 3 days

If they remain wheeze-free after 3 hours of observation they can be discarged

55
Q

Hospital management of acute asthma exacerbation

Life-threatening asthma or failure to respond to nebulized therapy

A

1.High – fllow face mask oxygen to maintain saturations ˃ 94%

  1. Nebulised salbutamol 0,1-0,15 mg/kg, max 2,5 mg for ˂ 5 years / otherwise 5 mg; as often as needed

3.Attach cardiac monitor

4.**Methyl-prednisolone **2 mg/kg iv/im, bolus, then 0,5 mg/kg every 6 h or prednisone/prednisolone 2mg/kg po every 24 h

5.Re-assess after 3 h to take effect

6.Methylxanthines (aminophylline) iv/pev continuous

7.If air movement is still poor – epinephrine: 0,01 ml/kg sc/im (1:1000 max dose 0,5 ml), every 15 min up to three doses

56
Q

Hospital management of acute asthma exacerbation

Life-threatening asthma or failure to respond to nebulized therapy

For sick children with asthma responding poorly to treatment may be helpful:

A
  1. Salbutamol infusion
  2. Terbutaline sc
  3. Magnesium sulfate iv/im
  4. A helium and oxygen mixture
  5. Noninvasive positive pressure ventilation
  6. Intubation – indications include deteriorating mental status, severe hypoxemia, respiratory or cardiac arrest
57
Q

Before a child goes home
Discharge can be considered when:

A

Bronchodilators taken by an MDI + spacer are needed no more frequently than 4 hourly

SaO2 ˃ 94%

The inhaler technique has been assessed as satisfactory

A written asthma management plan should be provided + including any
adjustment to regular prophylactic therapy

58
Q

DIAGNOSIS

Diagnosing asthma – may be a challenging, particularly in infants and preschool children

A

Asthma – is not a single disease,is a compilation of diseases presenting as a
syndrome / or a collection of symptoms

Most cases of asthma – start in childhood !

The severity and number of obstructive episodes in early childhood appear to be predictors for later on- going childhood asthma

Several phenotypes of asthma have been described

The asthma –like clinical presentations - often reffered to as wheezy disorders in children, are common prior to signs or documentation of allergic markers / although nonallergic childhood asthma is common in many areas!