This document discusses acute severe asthma, an exacerbation of asthma characterized by persistent dyspnea that does not resolve with usual bronchodilator therapy. It covers the epidemiology, pathophysiology, clinical presentation, management, and differentials of acute severe asthma. Management involves relieving airflow obstruction with oxygen, bronchodilators, and corticosteroids. Patients not improving or deteriorating require intensive care admission for close monitoring. Acute severe asthma is a medical emergency but has a good outcome with prompt treatment.

1. by Dr. EMMANUEL NIMROD
10/25/2023 1

2. • Introduction
• Epidemiology
• Risk factors
• Pathophysiology
• Clinical presentation
• Management
• Differentials
• Conclusion
• References
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3. • Asthma is a chronic inflammatory disorder of the
airways, characterised by episodic dyspnoea, cough,
wheezing, and chest tightness that may resolve either
spontaneously or with treatment
• Acute severe asthma is an asthmatic exacerbation
characterised by persistent dyspnoea that is not
relieved by the usual standard therapy with
bronchodilators within 30 mins to 1 hour.
• An acute asthmatic attack that is severe enough to
persist, despite the patient’s optimum use of his/her
conventional medication.
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4. • It also described a clinical pattern of acute
asthmatic attack that requires high dose of
Inhaled corticosteroids and another control
medication for it to remain controlled or any
asthma that persists despite this therapy.
• It is synonymous with, and has largely replaced,
the old term status asthmaticus.
• Medical emergency
• The commonest respiratory emergency in clinical
practice.
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5. • Over 300million individuals are affected
• Global prevalence range between 1 and
18%
• Global mortality rate more than 250,000
annually.
• MR in Nigeria is 4.9% (Erhabor & Adigun)
• More than 75% of hospital admissions and
mortalities due to asthma are potentially
preventable.
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6. Non modifiable
 Age
 Gender
 Genetic and epigenetic factors
 Race
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7. Modifiable
 Occupation
 Obesity
 Smoking
 Infections
Co morbidities e.g severe sinusitis, OM,
GERD
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8. • Bronchospasm
• Edema and inflammation
• Mucus production
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9. • Multifactorial
• Type 1 hypersensitivity reaction that occurs
in two stages:
o exposure to innocuous agents and
sensitization
o Subsequent exposure and reaction
a. Early acute bronchospastic response
b. late inflammatory response
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10. • Both processes have in common air flow
limitation.
• Inspiration is an active process while expiration
is passive (4:1).
• Air trapping: hyperinflation of the lungs
increased intra-alveolar pressure.
• Compartmentalization into slow and fast
• V/Q mismatch
• Compensatory response: increased respiratory
drive, initial respiratory alkalosis and a later
acidosis.
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11. • Bronchospasm
• Edema and inflammation
• Mucus production
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13. Symptoms and signs depend on the severity of the
disease.
In majority of patients
• Prolonged exposure to allergen or respiratory
infection preceding the acute exacerbation
• History of rapid increase in the daily use of
bronchodilators to control acute symptoms.
• Early warning signs of nocturnal symptoms of
cough, wheeze, chest tightness and dyspnoea,
which are progressive and poorly responsive to
bronchodilators.
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15. At presentation the patient may be
• Dyspnoeic/tachypnoeic: >22cpm
• Tachycardic: >110bpm
• Unable to complete sentences.
On examination
• There is Widespread wheezes on auscultation,
and a peak-flow reading less than 50% of
expected or patient’s known best reading. SpO2
less than 92%.
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16. Early Patient assessment
The goals of management is
a. To relieving the severe airflow obstruction
b. To restore normal lung function,
c. To correct hypoxaemia, arrest any life-
threatening complications, and prevent
future relapses.
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17. • Acute severe asthma is a medical
emergency, and should be approached
using the ABC of resuscitation.
• Airway
• Breathing
• Circulation
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18. • Oxygen therapy
Oxygen given at high doses and flow rates helps to prevent tissue
hypoxia, corrects pulmonary hypertension, and enhances
bronchodilation. It should be given as 35–60% of O2 by nasal prongs
or face mask until hypoxaemia is corrected
• B2-agonist
Short-acting inhaled B2-agonists are the drugs of choice to treat
acute severe asthma via an oxygen-driven nebuliser which ensures
that large volumes of B2-agonist are delivered directly into the
airways. When not available, a metered dose inhaler with a spacer
device can be used.
(albuterol) It has an onset of action of 5 min and duration of action of
6 h. Other drugs used include terbutaline and fenoterol.
Long-acting drugs are not recommended for emergency treatment.
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19. • Corticosteroids
asthma is an inflammatory disease and the
bronchospasm of acute asthmatic attack is
due to an inflammatory condition, steroids
are central in the management of acute
severe asthma
IV hydrocortisone 100–200 mg every 6
hours and /or prednisolone 30–60 mg
should be started.
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20. • Theophylline/aminophylline
should only be for those patients not responding to
standard therapy. Loading dose of 6 mg/kg over 15–30
min should be followed by an infusion of 0.5 mg/kg/h.
Ipratropium bromide
is a selective bronchodilator with slow onset of action
(1.5–2 h), it is not used as a first-line attack in acute
severe asthma. However, In patients who show marked
side-effects when given maximal doses of B-agonist, or
who do not respond to its therapy, adding ipratropium
bromide is a reasonable option – given in a nebulised
form at a dose of 6-hourly
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21. Antibiotics: in patient whose trigger is
suspected to be bacterial infection.
Oxygen saturation should be monitored
regularly.
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22. • Patients require monitoring closely
throughout the period of admission. This
should include clinical, physiological, and
serial blood gases monitoring. The PEF
should be measured every 15–30 min
after starting treatment until the patient is
stable.
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23. • Patients with evidence of severe airway obstruction who improve
minimally or deteriorate despite therapy should be admitted to an
ICU.
• This includes patients with
a. Worsening respiratory distress/respiratory arrest
b. Altered mental status/coma
c. Low SPO2 <90%,
d. PaO2 < 8 kPa (60 mmHg) and falling,
e. PaCO2 > 6 kPa (45 mmHg) and rising despite oxygen
supplementation or rising hypercabia
f. Hypotension with systolic B.P <90mmHg
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24. • Medical history This will include determining
• the time of onset and severity of symptoms
(especially compared with previous
exacerbations),
• all current medications, prior hospitalizations, and
emergency department admission.
• Medication compliance and symptoms control
• Attempts should be made to uncover the cause of
the recent exacerbations. Common causes include
exposure to extrinsic antigens, severe viral
respiratory infections, inadequate or incorrect
medications, exercise, emotions, drugs (such as
aspirin, NSAIDS, beta-blockers), seasonal
variations, etc.
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25.  Basic investigations
 Blood gas analysis
 Pulse oximetry
 Chest radiography
 Specific investigations
Lung function test
 PEFR
 Spirometry-FEV1, FEV25-75, FVC, FEV/FVC
 Provocation test- Exercise test, methacholine/histamine
 Others: exhaled nitric oxide (FeNO)
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26. Complications in the management of severe
asthma include:
• Respiratory failure
• Pneumothorax due to rupture of bullae
• Hypokalaemia, which can occur as a result
of hyperventilation
• Drug related complications
• Hypotension
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27. • Cardiac failure
• Pneumonia
• Chronic bronchitis
• Gastro esophageal reflux disease
• Foreign body aspiration
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28. • The outcome from acute severe asthma is
generally good.
• Death is fortunately rare but a
considerable number of deaths occur in
young people and many are preventable.
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29. • Acute asthmatic attack is a medical
emergency, which has a good outcome if
treated promptly.
• Failure to recognise the severity of an
attack by the physician or the patient,
contributes to delay in delivering
appropriate therapy and to under-
treatment, which can lead to death.
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30. • Kumar and Clark Clinical Medicine 9th
edition
• Davidson Principle and practice of
medicine 22nd Edition
• Journal of acute severe asthma 2021
• Erhabor Adigun et al 2012 on status
asthmaticus
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