Acute Exacerbation of

Asthma
Dr. Franklin Onyedikachi Ozor
House Officer, Department of Internal Medicine
Federal Teaching Hospital, Lokoja.

November, 2023

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Outline
1. Introduction
2. Epidemiology
3. Pathophysiology of Asthma
4. Aetiology
5. Clinical Features
6. Classification of Asthma
7. Diagnosis
8. Acute Exacerbation of Asthma
9. Management
10.Criteria for ICU admission
11.Criteria for discharge
12.Complications
13.Differentials
14.Conclusion 2
Introduction
• Asthma is a common chronic disease worldwide. It is an inflammatory
disease of the airways characterized by reversible airflow obstruction,
airway narrowing, and bronchial hyperresponsiveness.
• Common triggers include allergens, pollutants, and respiratory infections.

• Patients with poorly controlled asthma develop long-term changes over

time (i.e. with airway remodeling). This can lead to chronic symptoms
and a significant irreversible component to their disease. Many patients
who develop asthma at an older age also tend to have chronic symptoms.

• Asthma exacerbations can be life-threatening and require quick

intervention. By understanding the underlying causes and appropriate
management strategies, we can improve outcomes for patients.
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Epidemiology
• Asthma affects approx. 235 million people worldwide with a global
prevalence of approx. 1-18% in different population groups.
• It is the most common chronic disease in childhood, affecting an
estimated 7 million children in the US.
• Globally mortality is estimated at approx. 1- 10%, with an estimated
100,000 deaths yearly.
• In the USA, approx. 14.6 million persons have Asthma with, 1.8 million
annual ER visits for acute and >5,000 deaths are reported annually.
• In Nigeria, Elegbeleye reported a mortality rate of 6% in LUTH over a 9-
year period (1965–1974).
• Erhabor et al reported a mortality of 4.9% at the OAUTH, Ile-Ife over a
10-year period.
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Pathophysiology
• The pathophysiology of asthma is complex, and involves airway
inflammation, intermittent airflow obstruction and bronchial
hyperresponsiveness.

• The mechanism of inflammation in

asthma may be acute, subacute or
chronic, and the presence of airway
oedema and mucus secretion also
contributes to airflow obstruction
and bronchial reactivity.

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• Varying degrees of mononuclear cell and eosinophil infiltration, mucus
hypersecretion, desquamation of the epithelium, smooth muscle
hyperplasia, and airway remodeling are present.
• Airway hyperresponsiveness or bronchial hyperreactivity in asthma is an
exaggerated response to numerous exogenous and endogenous stimuli.
• The mechanisms involved include direct stimulation of airway smooth
muscle and indirect stimulation by pharmacologically active substances
from mediator-secreting cells such as mast cells or non-myelinated
sensory neurons.
• The degree of airway hyperresponsiveness generally correlates with the
clinical severity of asthma.

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• Antigen presentation by the dendritic cell, with the lymphocyte and
cytokine response leading to airway inflammation and asthma
symptoms.

• T lymphocytes play an important role in the regulation of airway

inflammation through the release of numerous cytokines.

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Aetiology
Factors that can contribute to asthma or airway hyperreactivity
may include any of the following:
• Environmental allergens (eg, house dust mites; animal allergens,
especially cat and dog; cockroach allergens; and fungi)
• Irritants (eg, household sprays, paint fumes)
• Viral respiratory tract infections
• Exercise, hyperventilation
• Gastroesophageal reflux disease
• Obesity
• Environmental pollutants, tobacco smoke
• Occupational exposure
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Aetiology (Cont’d)
• Chronic sinusitis or rhinitis
• Emotional factors or stress
• Perinatal factors (prematurity and increased maternal age; maternal smoking
and prenatal exposure to tobacco smoke; breastfeeding has not been
definitely shown to be protective)
• Aspirin or nonsteroidal anti-inflammatory drug
(NSAID)hypersensitivity, sulfite sensitivity
• Use of beta-adrenergic receptor blockers (including ophthalmic preparations)
• Various high- and low-molecular-weight compounds (eg, insects, plants,
latex, gums, diisocyanates, anhydrides, wood dust, and fluxes; associated
with occupational asthma)
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Clinical Features
Signs and symptoms of asthma include the following:
• Wheezing
• Coughing (chronic, recurrent and episodic)
• Shortness of breath
• Chest tightness/pain
Other non-specific symptoms in infants or young children may be a history
of recurrent bronchitis, bronchiolitis, or pneumonia; a persistent cough with
colds; and/or recurrent croup or chest rattling.

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• Assess the progression of the symptoms; Asthma symptoms worsen at night
• There may be history suggestive of atopy in the patient - allergic
rhinoconjunctivitis (recurrent itching of eyes, redness of eyes, sneezing and
runny nose), atopic eczema (recurrent skin rash), food and/or drug allergy
• There may also be a positive family history of asthma
• Rule out other possible causes - pneumonia (fever, chest pain on inspiration),
foreign body aspiration, pulmonary TB (weight loss, drenching night sweat),
CCF (dizziness, easy fatigability, orthopnea, PND) e.t.c.
• Assess for presence of complications such as exercise intolerance, confusion,
altered sensorium (hypoxia), headache (sinusitis).

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On Examination,
• Patient is acutely ill-looking, in respiratory distress
• There may be signs suggestive of atopy, such as periorbital darkening,
erythematous turbinate, atopic dermatitis
• Respiratory system
• Tachypnea
• Pectus carinatum (in severe acute asthma)
• Tactile fremitus may be reduced
• Percussion note may be hyperresonant
• Presence of widespread rhonchi (may be polyphonic)
• Cardiovascular system
• Patient may be tachycardic
• There may be pulsus parodoxus
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Classification of Asthma
1.Traditional
• Intrinsic/cryptogenic asthma
• Extrinsic asthma
2.Based on phenotype
• Transient early wheezer
• Atopic
• Non-atopic

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3. Based on severity:
Severity Symptoms/day Symptoms/night PEF or FEV1 PEF variability
Intermittent 1/week.
Asymptomatic </= 2/month >/= 80% <20%
between attacks.
Mild >1/week but not daily.
Persistent Attacks may affect >2/month >/= 80% 20-30%
activity.
Moderate Daily attacks with
Persistent exacerbations, < 1/week 60-80% >30%
affecting activity.
Severe Continuous attacks
Persistent throughout the day. Frequent </= 60% >30%
Limited physical
activity.
Diagnosis
1 Oximetry - To check for hypoxemia

2 Pulmonary Function test

• Spirometry for FEV1, FVC (FEV1 /FVC is reduced)
• PEFR - Values < 50% of predicted indicate severe attack.

3 Skin prick test - To determine hypersensitivity to allergens (>2mm is +ve)

4 Chest X-ray
• May show features of hyperinflation in acute attack or severe
persistent asthma
• In first attack, to r/o differentials
• To r/o complications e.g. pneumothorax
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5 Other investigations
• FBC - Shows increased eosinophils count (>4%)
• Serum IgE estimation - increased (>100IU)
• Blood culture to rule out differentials
• E/U/Cr
• Sputum M/C/S
• ABG
• ECG

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Acute Exacerbation of Asthma
Acute severe asthma is a medical emergency characterized by progressive
airway obstruction and hypoxemia that fails to respond to standard
bronchodilator therapy within 30 minutes to 1 hour. It was formerly called
status asthmaticus.
Patients with asthma of any level may have acute episodes, which can be
mild, moderately severe, severe, or characterized by imminent respiratory
arrest.

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1.Mild Episodes
• Patients may be breathless after physical activity, can talk in
sentences and are able to lie flat, and they may be agitated.
• RR is increased, but accessory muscles of respiration are not used.
• HR is <100bpm, and pulsus paradoxus is not present.
• Presence of moderate wheezing, often end-expiratory.
• Rapid forced expiration may elicit wheezing, that is otherwise inaudible
• SpO2 IRA is >95%.
• PEF >/= 70%.

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2. Moderately severe episodes
• Patients are breathless while talking, and infants have feeding
difficulties and a softer, shorter cry.
• In most severe cases, the patient assumes a sitting position.
• RR is also increased, and accessory muscles of respiration are used. In
children, there may also be supraclavicular and intercostal retractions and
nasal flaring, as well as abdominal breathing.
• HR is 100-120bpm, ad pulsus paradoxus may be present (10-20mmHg).
• Loud expiratory wheezing can be heard
• SpO2 IRA is 91-95%
• PEF = 50-69% of best or predicted.
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3. Severe episodes
• Patients are breathless at rest, are not interested in eating, sit upright,
talk in words rather than sentences, and are usually agitated.
• As the severity increases, patient assumes the tripod position.
• RR is often >30cpm. Accessory muscles of respiration are used, and
suprasternal retractions are commonly present.
• HR is >120bpm, and pulsus parodoxus is often present (20-40mmHg).
• Loud biphasic wheezing can be heard.
• SpO2 IRA is <91%.
• PEF = 33-49%

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4. Imminent respiratory arrest
• When children are in imminent respiratory failure, in addition to the
aforementioned symptoms, drowsiness and confusion set in, but
adolescents may not have these symptoms until they are in frank
respiratory failure.
• In status asthmaticus with imminent respiratory arrest, paradoxical
thoracoabdominal movement occurs. There is feeble respiratory
effort (RR < 12cpm).
• Wheezing may be absent (associated with most severe airway
obstruction), and severe hypoxemia may manifest as bradycardia.
Pulsus paradoxus noted earlier may be absent; this suggests
respiratory muscle fatigue.

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• As the episode becomes more severe, profuse diaphoresis
occurs, concomitant with a rise in pCO2 and hypoventilation

• In the most severe form of acute asthma, patients may struggle for
air, act confused and agitated. These are signs of life-threatening
hypoxia.
• With advanced hypercapnia, bradypnea, somnolence and profuse
diaphoresis may be present; almost no breath sounds may be heard
(silent chest); and the patient is willing to lie recumbent.

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Management
• Acute exacerbation of asthma is a medical emergency

• The typical presentation is acute breathlessness and wheeze

• The goals of treatment include:

• To reverse airway obstruction
• To correct hypoxemia
• To prevent or treat complications
• Management involves a quick ABC of resuscitation, with emphasis on A & B.

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Immediate Treatment (SOS)

1 Nebulized Salbutamol 5mg (or Terbutaline 10mg)

Intranasal Oxygen if saturation < 92% (Target is 94-98%).

Usually given as 40-60% by nasal
2 cannula or venturi-type mask to all patients
with hypoxaemia .

IV Hydrocortisone 200mg 6hrly or Prednisolone 40-

3
50mg PO, or both if patient is very ill

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If life-threatening features are present:
1 Inform ICU

2 Give Salbutamol nebulizers every 15 minutes

or 10mg continuously per hour
3 Monitor ECG; watch for arrhythmias

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Add in Ipratropium 0.5mg to nebulizers

5 Give single dose of MgSO4 1.2-2g IV over 20 minutes

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 If improving within 15-30 minutes,
1 Nebulized Salbutamol every 4 hours

2 Prednisolone 40-50mg PO OD for 5-7 days

Monitor peak expiratory flow and O2

saturations, with supplemental O2 if needed.
3 Also monitor ABG

N/B: Antibiotics is indicated only in those with presumptive evidence

of bacterial infection.
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If not improving,
• Refer to ICU for consideration of ventilatory support and
intensification of medical therapy e.g. IV Aminophylline,
IV Salbutamol, IV Terbutaline

Criteria for ICU Admission

1. Altered sensorium
2. Exhaustion, with signs of respiratory muscle fatigue
3. Markedly reduced air entry
4. Increased pCO2 despite treatment
5. No improvement despite adequate treatment
6. Coma
7. Respiratory and/or cardiac arrest
8. Hypotension (Systolic BP < 90mmHg)
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Criteria for Discharge
• PEF >75% of predicted or best
• PEF variability <25%
• On discharge medication for 24hrs
• Inhaler technique checked and recorded
• Treatment with oral and inhaled steroid.
• Own PEF meter and self management plan
• Patient education
• Follow-up at the clinic

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Complications
1. Air leak syndrome
2. Atelectasis
3. Respiratory failure
4. Ventilation-perfusion mismatch
5. Right middle lobe syndrome
6. Cardiac arrest
7. Pneumothorax or pneumomediastinum
8. Hypoxemia with hypoxic ischaemic CNS injury
9. Toxicity from medications

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Differential Diagnoses
1.Acute infective exacerbation of COPD
2.Pulmonary oedema
3.Foreign body aspiration
4.Severe pneumonia
5.Pulmonary embolism
6.Anaphylaxis

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Prevention Strategies and Long-Term
Management
Preventive measures play a crucial role in reducing asthma symptoms
and the risk of exacerbations.
• Avoiding known triggers such as allergens, smoke, and strong odors.
• Regularly monitoring lung function and symptoms to detect early
signs of deterioration.
• Developing an asthma action plan in collaboration with a
healthcare professional.

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Conclusion
Acute severe asthma is a challenging condition that
requires proper diagnosis, prompt treatment, and long-
term management. With appropriate care, individuals
with asthma can live a full and active life.

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