Asthma: Kinyua Md. MCM - A & E MKU Facilitator: Dr. Ayunga

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ASTHMA

KINYUA MD.
MCM – A & E
MKU
FACILITATOR: DR. AYUNGA
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)
ETIOLOGY CNT..
• 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:
Acute and chronic airway inflammation characterized
by infiltration of the airway wall, mucosa, and lumen by
activated eosinophils, mast cells, macrophages, and T
lymphocytes.
Bronchial smooth muscle contraction resulting from
mediators released by a variety of cell types including
inflammatory, local neural, and epithelial cells.
Epithelial damage manifested by denudation and
desquamation of the epithelium leading to mucous plugs that
obstruct the airway.
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-Ig E 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:
1. 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, nebulized) 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
ASTHMA COMPLICATIONS
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/asthgdln.Pdfnchs data
brief 2012;1).
• Washington manual of medical therapeutics 2014.
Www.Ketabpedeshki.Com

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