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Acute Exacerbation of Asthma
Acute Exacerbation of Asthma
I CAN’T
BREATH
References
2022 GINA Report, Global Strategy for Asthma Management and Prevention
https://ginasthma.org/2022-gina-report-global-strategy-for-asthma-management-and-prevention/
• The patient,Mr X a 66-year-old man, with UL bronchial asthma, atrial
fibrillation (AF) had a 3-day history of worsening cough, wheeze and
shortness of breath that was not relieved by his salbutamol inhaler.
He had purulent sputum but neither fever, chest pain nor
haemoptysis. no measuring of his peak flow. He had an admission for
an asthma exacerbation 15 years prior, but never required admission
to intensive care. He had never smoked. He took warfarin in addition
to his salbutamol.
Case Report • On examination, he was able to speak full sentences, but was using
his accessory muscles to aid respiration.
• RR : 23 breaths/min spo2: 95% under Npo2 2L/min, HR 104 bpm and
he was normotensive and euvolaemic.
• Auscultation of the chest revealed a bilateral polyphonic wheeze. The
remainder of the examination was normal.
• A clinical diagnosis of acute infective exacerbation of bronchial
asthma was made.
2
Differentials
Acute Inhaled Bronchiectasi
pulmonary COPD
edema Foreign body s
Points against:
SOB is not severe, No Points against: Not a Points against:
chest pain, No swelling smoker, Points against:
Cough onset not No hemoptysis, No
in feet and feet,
sudden chest pain, No
finger clubbing
3
WHAT IS ASTHMA?
4
MAKING THE INITIAL DIAGNOSIS
5
Patient with
respiratory symptoms
Are the symptoms typical of asthma?
NO
YES
Detailed history/examination
for asthma
History/examination supports
asthma diagnosis?
Further history and tests for
NO alternative diagnoses
Clinical urgency, and
YES Alternative diagnosis confirmed?
other diagnoses unlikely
Perform spirometry/PEF
with reversibility test
Results support asthma diagnosis?
Repeat on another
NO
occasion or arrange
NO
YES other tests
Confirms asthma diagnosis?
GINA 2022, Box 1-1 (4/4) Treat for ASTHMA Treat for alternative diagnosis
6
Diagnosis of asthma
The diagnosis of asthma should be based on:
A history of characteristic symptom patterns
Evidence of variable airflow limitation, from bronchodilator reversibility testing or other
tests
Document evidence for the diagnosis in the patient’s notes, preferably before starting
controller treatment
It is often more difficult to confirm the diagnosis after treatment has been started
7
History and family history
8
Diagnosis of asthma – physical examination
• Physical examination in people with asthma
• Often normal
• The most frequent finding is wheezing on auscultation, especially on forced expiration
• Wheezing may be absent during severe asthma exacerbations (‘silent chest’)
9
Asthma flare-ups
(exacerbations)
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ASTHMA FLARE-UPS (EXACERBATIONS)
They represent a change from the patient's usual status that is sufficient to require a
change in treatment.
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What trigger
asthma Viral
Poor respiratory
Allergen
adherence infection
Outdoor
exposure
to ICS
Food allergy grass pollen)
air pollution
( dust,
exacerbation??
12
A history of near-fatal asthma requiring intubation and mechanical ventilation
Factors
that Hospitalization or emergency care visit for asthma in the past year
increase Currently using or having recently stopped using oral corticosteroids (a marker of event
severity)
the risk Not currently using inhaled corticosteroids
of Over-use of SABAs, especially use of more than one canister of salbutamol (or equivalent)
asthma- monthly
A history of psychiatric disease or psychosocial problems
related
death Poor adherence with asthma medications and/or poor adherence with (or lack of) a
written asthma action plan
Food allergy in a patient with asthma
13
Managing exacerbations in acute care settings For adult >12 years old
NO
YES
Further TRIAGE BY CLINICAL STATUS Consult ICU, start SABA and O2,
according to worst feature and prepare patient for intubation
I. Oxygen
To achieve arterial oxygen saturation of 93–95%
By nasal cannulae or mask
Severe exacerbations
• Controlled low flow oxygen therapy
• Pulse oximetry to maintain saturation at 93–95%
• Better than with high flow 100% oxygen therapy
Not to withheld oxygen therapy if pulse oximetry not available
Once stabilized, consider weaning off oxygen using oximetry
16
II. Inhaled short-acting beta2-agonists
• Administered frequently by pMDI with a spacer
• No evidence to support the routine use of intravenous beta2-agonists
17
III. Systemic corticosteroids
In all but the mildest exacerbations
Should be administered within 1 hour of presentation
18
Route of delivery: oral administration as effective as intravenous
At least 4 hours to produce a clinical improvement
Intravenous corticosteroids:
• Too dyspneic to swallow
• Patient vomiting
• Patients requiring non-invasive ventilation or intubation
Dosage: daily doses of OCS equivalent to 50 mg prednisolone as a single morning dose,
or 200 mg hydrocortisone in divided doses, are adequate for most patients (Evidence B).
Duration: 5- and 7-day courses as effective as 10- and 14-day courses
Oral dexamethasone for 2 days can also be used but there are concerns about metabolic side-effects if it is continued beyond 2 days.
No benefit in tapering the dose of OCS, either in the short term or over several weeks
19
IV. Inhaled corticosteroids
Within the emergency dept. high dose ICS given within the first hour after
presentation reduces the need for hospitalization in patients not receiving
systemic corticosteroid
High-dose ICS
• Well tolerated, Cost being a significant factor
Patients admitted to hospital for an asthma exacerbation should continue on, or be
prescribed, ICS-containing therapy.
20
• On discharge home: patients should be prescribed ongoing ICS-
containing treatment since the occurrence of a severe exacerbation
is a risk factor for future exacerbations and ICS-containing
medications significantly reduce the risk of asthma-related death or
hospitalization
• SABA-only treatment of asthma is no longer recommended.
21
Other treatments
22
VII. Magnesium (Intravenous)
• FEV1 <25–30% predicted at presentation
• Not responding to initial treatment
• Persistent hypoxemia
A single 2 g infusion over 20 minutes
23
VIII. Antibiotics (not recommended)
Unless there is strong evidence of lung infection (e.g. fever or purulent sputum or radiographic evidence of
pneumonia).
Aggressive treatment with corticosteroids should be implemented before antibiotics are considered.
24
Reviewing response of treatment
• Clinical status
• Oxygen saturation
• Lung function
25
Cont..Investigation
• Mr X's chest radiograph was normal.
• The white cell count was 11.3 (neutrophils 7.8, eosinophils 0.03×109/L) and C reactive
protein was 6 mg/dL. Renal function, serum electrolytes and liver enzymes were normal.
Troponin was 8 ng/L. International normalized ratio was 2.2.
• Arterial blood gas (ABG) at admission (table 1) revealed type 1 respiratory failure and a
compensated metabolic acidosis, with a serum lactate of 5.6 mmol/L.
• Peak flow measurements were not taken.
• ECG showed AF with a controlled ventricular rate.
26
ABG RESULTS
27
Cont..Treatment and course
28
Cont…
• He was reviewed 4 h and 6 h after admission. His respiratory rate
remained elevated at 24/min but his oxygen saturations had improved
to 99%. His heart rate was 105 bpm and he remained normotensive.
Urine output was over 150 mL/h.
• Peak flows were not recorded. Aminophylline infusion was prescribed
and intravenous fluids were sped up. Nebulised salbutamol was
continued.
29
Cont.
• After a further 2 h, he developed orthopnoea and worsening
hypoxaemia but his wheeze had improved.
• Clinically, he was thought to have pulmonary oedema, probably
precipitated by an acute coronary syndrome.
• Repeat ECG showed sinus tachycardia without ST changes. Repeat
troponin was 40 ng/L. His chest radiograph was unchanged.
Aminophylline and salbutamol were stopped.
• He was treated with fondaparinux, clopidogrel and a glyceryl trinitrate
infusion.
30
Cont..
• At 10 h after admission, the patient showed signs of clinical improvement.
His lactate had fallen to 5.9. Over the next few hours, his oxygen was
weaned off and a serum lactate level was recorded at 3.3 mmol/L.
• A diagnosis of salbutamol-induced lactic acidosis and acute exacerbation of
asthma was made.
• He was given prednisolone and a corticosteroid/long-acting β-2 agonist
inhaler.
• Troponin fell to 24 ng/L and treatment for acute coronary syndrome was
stopped. Echocardiogram showed a left ventricular ejection fraction of 65%,
no regional wall motion abnormalities and no valvular pathology. He was
discharged after 24 h.
31
Summary
The patient took a high frequency of inhaled salbutamol from a metre-
dosed inhaler at home and had nebulised treatment before his first ABG,
resulting in the high initial value (table 1). He was clinically stable, without
signs of sepsis, making type A lactataemia unlikely.
32
Causes of lactic acidosis
Isaac BT, McLellan T, Samuel J, Yung B. Conundrum in an asthma exacerbation. BMJ Case Rep. 2016 May 10;2016:bcr2016214360. doi: 10.1136/bcr-2016-214360. PMID:
27166007; PMCID: PMC4885350.
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Assessment of asthma
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ASTHMA MEDICATIONS
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ASTHMA MEDICATIONS: ADULTS
2. Controllers are medications taken daily on a long-term basis to keep asthma under
40
They include:
1. Inhaled glucocorticosteroids
2. Leukotriene modifiers ( Monteluekast)
3. Long-acting inhaled β2-agonists (use in combination with inhaled glucocorticosteroids)-
Symbicort( Formoterol + Budesonide)
41
8. Other controller therapies (Methotrexate, cyclosporin, gold, troleandomycin
(macrolide)
9. Allergen-specific immunotherapy
43
Low, medium and high dose inhaled corticosteroids Adults and adolescents (≥12 years)
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