ASTHMATIC ATTACK

MIRITI M.D
MASTERS OF CLINICAL MEDICINE; ACCIDENTS AND
EMERGENCY
FACILITATOR: DR SIMBA
DR MBURUGU
 Definition
• Asthma is an airway disease characterized by
chronic inflammation, hyper responsiveness with
exposure to a wide variety of stimuli, and variable
airflow obstruction.
• As a consequence, patients have paroxysms of
cough, dyspnea, chest tightness, and wheezing.
• Asthma is a chronic disease with episodic acute
exacerbations that are interspersed with
symptom-free periods.
• Exacerbations are characterized by a progressive
increase in asthma symptoms that can last minutes
to hours.
 Epidemiology
• In the United States, Asthma is the leading chronic
illness among children (20% to 30%) (NCHS Data
Brief 2012;1).
• The prevalence of asthma and asthma-related
mortality had been increasing from 1980 to the
mid-1990s, but since the 2000s, a stabilization in
prevalence and decrease in mortality has occurred.
• Currently, it is estimated that Asthma affects 1-18%
of the general population in each country. (GINA
Report, 2018) (ISAAC STUDIES) Kenya 10%.
ETIOLOGY:

The fundamental causes of asthma are not completely

understood however a combination of genetic
predisposition with environmental exposure to inhaled
substances and particles that may provoke allergic
reactions or irritate the airways, such as:
– indoor allergens (for example, house dust mites in
bedding, carpets and stuffed furniture)
– Outdoor allergens (such as pollens and pollution and pet
dander, moulds)
– Tobacco smoke
– Chemical irritants in the workplace
– Air pollution.
– Other triggers can include cold air, extreme emotional
arousal such as anger or fear, and physical exercise
 Pathophysiology
• Asthma is characterized by airway obstruction,
hyperinflation, and airflow limitation resulting from
multiple processes:
1. Acute and chronic airway inflammation
characterized by infiltration of the airway wall,
mucosa, and lumen by activated eosinophils, mast
cells, macrophages, and T lymphocytes.
2. Bronchial smooth muscle contraction resulting
from mediators released by a variety of cell types
including inflammatory, local neural, and epithelial
cells.
3. Epithelial damage manifested by denudation and
desquamation of the epithelium leading to mucous
plugs that obstruct the airway.
4. Airway remodeling characterized by the following
findings:
•Sub epithelial fibrosis, specifically thickening of the
lamina reticularis from collagen deposition
•Smooth muscle hypertrophy and hyperplasia
• Goblet cell and submucosal gland hypertrophy and
hyperplasia resulting in mucus hypersecretion
•Airway angiogenesis
•Airway wall thickening due to edema and cellular
infiltration
 DIAGNOSIS
Diagnostic Criteria
• In general, the diagnosis is supported by the presence of
symptoms consistent with asthma combined with
demonstration of variable expiratory airflow obstruction.
• Adequate response to asthma treatment is a valid method
to assist with making the diagnosis.
History
• Recurring episodes of cough, dyspnea, chest tightness, and
wheezing are suggestive of asthma. Symptoms occur most
often at night or early morning, in the presence of potential
triggers, and/or in a seasonal pattern.
• A personal or family history of atopy can increase the
likelihood of asthma.
Physical Examination
•Auscultation of wheezing and a prolonged
expiratory phase can be present on exam,
but a normal chest exam does not exclude
asthma.
•Signs of atopy, such as eczema, rhinitis, or
nasal polyps, often coexist with asthma.
•During a suspected asthma exacerbation,
a rapid assessment should be performed to
identify those patients who require
immediate intervention.
•Respiratory distress and/or peak
expiratory flow (PEF) of <25% of
predicted.
•The presence or intensity of wheezing
is an unreliable indicator of the
severity of an attack.
•Subcutaneous emphysema should
alert the examiner to the presence of a
pneumothorax or
Pneumomediastinum.
Classification of Asthma Exacerbation Severity
Diagnosis: Laboratory Studies
•Routine laboratory tests are not indicated for the diagnosis of
asthma and should not delay the initiation of treatment.
•During an exacerbation, monitor oxygen saturation.
•ABG measurement should be considered in patients in severe
distress or with an FEV1 of <40% of predicted values after
initial treatment.
•A PaO2 <60 mmHg is a sign of severe bronchoconstriction or
of a complicating condition, such as pulmonary edema or
pneumonia.
•Initially, the PaCO2 is low due to an increase in respiratory
rate. With a prolonged attack, the PaCO2 may rise as a result
of severe airway obstruction, increased dead space
ventilation, and respiratory muscle fatigue. A normal or
increased PaCO2 is a sign of impending respiratory failure
and necessitates hospitalization.
Imaging
•Obtaining a chest radiograph is not routinely required
and is performed only if a complicating pulmonary
process, such as pneumonia or pneumothorax, is
suspected or to rule out other causes of respiratory
symptoms in patients being evaluated for asthma.
•Computerized tomography of the chest can be
considered in patients with severe asthma refractory to
treatment to evaluate for alternative diagnosis.

Diagnostic Procedures
•Pulmonary function tests (PFTs) are essential to the
diagnosis of asthma. In patients with asthma, PFTs
demonstrate an obstructive pattern—the hallmark of
which is a decrease in expiratory flow rates.
 Management of Asthma
1 “Relievers”
I. Short-acting bronchodilators
A. β 2-adrenergic agents
B. Anti-cholinergic (Parasympatholytic) agents
2. “Controllers”
1. Corticosteroids
2. Long-Acting bronchodilators
I. β 2 -adrenergic agents
II. Methylxanthines
3. Mast cell stabilizers.
4. Leukotriene inhibitors
5. Anti-IgE monoclonal antibodies
 Treatment - Principles
• Educate parent – triggers, recognize exacerbations,
medication
• Avoidance of exposure to triggers
• Pharmacologic management
– Of acute exacerbations: RELIEVER MEDICATIONS
– Long-term – CONTROLLER MEDICATIONS (for
persistent asthma)
– INHALED ROUTE OPTIMAL FOR MOST DRUGS
• Any persistent form of asthma, controlled more
effectively by suppressing and reversing airway
inflammation than by treating only acute broncho-
constriction and related symptoms
 Pharmacologic Treatment
Two broad types of medication:
I CONTROLLER medications
• Used for persistent forms of asthma
• Used to PREVENT asthma symptoms
• Aim at achieving long-term control
• Are generally anti-inflammatory drugs
• Some immune modulating drugs show promise
II RELIEVER medications
• Used in all classes of asthma
• Used to treat acute asthma symptoms
• Aim at rapidly relieving symptoms, and aborting
the exacerbation
• Are generally rapid acting, short acting beta2
agonists, or anticholinergic drugs
 Treatment of Acute Asthma
exacerbation
Assess severity of the attack (talking, RR, agitation,
ability to breastfeed-infant, pulse oximetry)
• Mild attack: talks normal sentences, SaO2 >95%
• Moderate: phrases, agitated, RR↑, reduced
breastfeeding, SaO2 >91-95%
• Severe: single words, drowsy or confused, RR↑↑,
unable to breastfeed, +/-paradoxical breathing, SaO2
<90%
 Treatment of Acute Asthma
exacerbation
• Give SABA (inhaler + spacer, nebulised) up to 3 treatments in
1 hour (variable delivery to lower airways!)
• Observe at least 3 hours
• If symptoms return in <3hrs, or fail to improve
– add inhaled anticholinergic to SABA
– add oral corticosteroid (OCS)
• If still no improvement, admit to hospital
– give humidified oxygen (nasal canula)
– continue SABA+anticholinergic,
– continue systemic glucocorticosteroid
– consider IV methylxanthines (monitor levels)
– monitor closely
 REFERENCES
• (GINA Report, Global Strategy for Asthma
Management and Prevention,
2018,www.ginasthma.org; National Asthma
Education and Prevention Program Expert Panel
Report 3, 2007,
http://www.nhlbi.nih.gov/guidelines/asthma/asthg
dln.pdf ).
• NCHS Data Brief 2012;1).
• Washington manual of Medical Therapeutics 2014.
www.ketabpedeshki.com
• Basic Paediatric Protocol-2016