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1

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.

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Differentials
Acute Inhaled Bronchiectasi
pulmonary COPD
edema Foreign body s

Points towards: Cough, Points towards: Cough,


Points towards:
Wheeze, SOB, Purulent SOB,Wheeze Purulent Points towards:
sputum sputum Cough, SOB,
SOB, Wheeze
Wheeze

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
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WHAT IS ASTHMA?

Asthma is a heterogeneous disease, usually


characterized by chronic airway inflammation.
It is defined by the history of respiratory symptoms
such as wheeze, shortness of breath, chest tightness
and cough that vary over time and in intensity,
together with variable expiratory airflow limitation.

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MAKING THE INITIAL DIAGNOSIS

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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?

Empiric treatment with YES NO YES


ICS and prn SABA
Review response
Consider trial of treatment for
Diagnostic testing most likely diagnosis, or refer
within 1-3 months for further investigations

GINA 2022, Box 1-1 (4/4) Treat for ASTHMA Treat for alternative diagnosis
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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

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History and family history

• Respiratory symptoms in childhood


• History of allergic rhinitis or eczema
• Family history of asthma or allergy

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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’)

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Asthma flare-ups
(exacerbations)

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ASTHMA FLARE-UPS (EXACERBATIONS)

Exacerbations of asthma are episodes characterized by a progressive increase in


symptoms of shortness of breath, cough, wheezing or chest tightness and progressive
decrease in lung function,

They represent a change from the patient's usual status that is sufficient to require a
change in treatment.

Exacerbations may occur in patients with a pre-existing diagnosis of asthma or


occasionally as the first presentation of asthma

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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??

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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

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Managing exacerbations in acute care settings For adult >12 years old

INITIAL ASSESSMENT Are any of the following present?


A: airway B: breathing C: circulation Drowsiness, Confusion, Silent chest

NO
YES

Further TRIAGE BY CLINICAL STATUS Consult ICU, start SABA and O2,
according to worst feature and prepare patient for intubation

MILD or MODERATE SEVERE

Talks in phrases Talks in words


Prefers sitting to lying Sits hunched forwards
Not agitated Agitated
Respiratory rate increased Respiratory rate >30/min
Accessory muscles not used Accessory muscles being used
Pulse rate 100–120 bpm Pulse rate >120 bpm
O2 saturation (on air) 90–95% O2 saturation (on air) < 90%
PEF >50% predicted or best PEF ≤50% predicted or best

Short-acting beta2-agonists Short-acting beta2-agonists


Consider ipratropium bromide Ipratropium bromide
Controlled O2 to maintain Controlled O2 to maintain
saturation 93–95% (children 94-98%) saturation 93–95% (children 94-98%)
Oral corticosteroids Oral or IV corticosteroids
Consider IV magnesium
Consider high dose ICS

If continuing deterioration, treat as


severe and re-aassess for ICU

ASSESS CLINICAL PROGRESS FREQUENTLY


MEASURE LUNG FUNCTION
in all patients one hour after initial treatment

FEV1 or PEF 60-80% of predicted or FEV1 or PEF <60% of predicted or


personal best and symptoms improved personal best,or lack of clinical response
SEVERE
MODERATE
Continue treatment as above
Consider for discharge planning and reassess frequently

GINA 2022, Box 4-4 (1/4) 14


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Treatment in acute care settings such as the emergency department

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

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II. Inhaled short-acting beta2-agonists
• Administered frequently by pMDI with a spacer
• No evidence to support the routine use of intravenous beta2-agonists

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III. Systemic corticosteroids
In all but the mildest exacerbations
Should be administered within 1 hour of presentation

Use of systemic corticosteroids is particularly important in the emergency department if:


• Initial SABA treatment fails to achieve lasting improvement in symptoms
- The exacerbation developed while the patient was taking OCS
• A history of previous exacerbations requiring OCS

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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

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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.

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• 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.

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Other treatments

V. Ipratropium bromide ( Atorvent)


Moderate-severe exacerbations : SABA and ipratropium, a short-acting anticholinergic
Greater improvement in PEF and FEV1 compared with SABA alone

VI. Aminophylline and theophylline ( not recommended)


Intravenous route not be used, in view of poor efficacy and safety profile, and the greater
effectiveness and relative safety of SABA.

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VII. Magnesium (Intravenous)
• FEV1 <25–30% predicted at presentation
• Not responding to initial treatment
• Persistent hypoxemia
A single 2 g infusion over 20 minutes

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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.

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Reviewing response of treatment
• Clinical status
• Oxygen saturation
• Lung function

Deterioration despite intensive bronchodilator and corticosteroid treatment  re-evaluated


for transfer to the intensive care unit

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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.

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ABG RESULTS

ABGs revealed worsening lactataemia and metabolic decompensation

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Cont..Treatment and course

• Mr. X received repeated doses of 5 mg nebulised salbutamol provided


by the ambulance crew.
• In the emergency department, he received nebulised bronchodilators,
parenteral steroids and magnesium.
• A sepsis care bundle was instituted (intravenous co-amoxiclav,
intravenous fluids, blood culture, hourly urine output) because of the
lactataemia and he was moved to a monitored bed in the acute
medical unit, with instructions to staff to carry out overnight medical
review.

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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.

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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.

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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.
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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.

His persistently elevated respiratory rate was compensation for the


lactataemia. It is at this point that peak flow measurements are crucial. If,
as expected, they showed improvement, it would make it very unlikely that
the situation was caused by a worsening of his asthma.

Peak flow assessment remains a cornerstone of the assessment of asthma


exacerbations. Instead, in this case, the decision was taken to escalate
treatment (table 1), leading to further metabolic derangement confusion
over the diagnosis and potential harm to the patient (figure 1).

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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

Categories of asthma medications


The pharmacological options for long-term treatment of asthma fall into the following
three main categories.
• Controller medications:
Regular maintenance treatment

• Reliever (rescue) medications


As-needed relief of breakthrough symptoms
Short-term prevention of exercise-induced bronchoconstriction

• Add-on therapies for patients with severe asthma


Persistent symptoms and/or exacerbations despite optimized treatment with high dose controller
medications (usually a high dose ICS and a LABA) and treatment of modifiable risk factors.
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ASTHMA MEDICATIONS: ADULTS
Classified as controllers or relievers
1. Relievers are medications used on an as-needed basis that act quickly to reverse
bronchoconstriction and relieve its symptoms.
They include:
● Rapid-acting inhaled β2-agonists(Salbutamol)
● Systemic glucocorticoids ( IV Hydrocortisone, T.Prednisolone)
● Anticholinergics antimuscarinic (SAMA) (ipratropium bromide-Atorvent)

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ASTHMA MEDICATIONS: ADULTS

2. Controllers are medications taken daily on a long-term basis to keep asthma under

clinical control chiefly through their antiinflammatory effects.

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They include:
1. Inhaled glucocorticosteroids
2. Leukotriene modifiers ( Monteluekast)
3. Long-acting inhaled β2-agonists (use in combination with inhaled glucocorticosteroids)-
Symbicort( Formoterol + Budesonide)

4. Theophylline ( Phosphodiesterase inhibitor)


5. Cromones
6. Anti-IgE-Omalizumab
7. Systemic glucocorticoids

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8. Other controller therapies (Methotrexate, cyclosporin, gold, troleandomycin
(macrolide)
9. Allergen-specific immunotherapy

Spiriva inhalation powder cap 18 mcg (18 mcg)


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ASTHMA MEDICATIONS: ADULTS

1. Inhaled glucocorticosteroids (IGC)


• Currently the most effective anti-inflammatory medications for the treatment of
persistent asthma
• Hydrofluoroalkanes suspension (HFAs); less oral deposition but increase risk of
systemic side-effects
• Ciclesonide, only activated in the lungs and no need for spacer

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Low, medium and high dose inhaled corticosteroids Adults and adolescents (≥12 years)

• This is not a table of equivalence,


but of estimated clinical
comparability
• Most of the clinical benefit from
ICS is seen at low doses
• High doses are arbitrary, but for
most ICS are those that, with
prolonged use, are associated with
increased risk of systemic side-
DPI: Dry powder inhaler
HPA: Hydrofluoroalkanes suspension : effects

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