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LEARNING OBJECTIVES
By the end of this unit the participants will be able to
– Discuss the definition and clinical characteristics of asthma
– Review the signs and symptoms of asthma
– Discuss current asthma epidemiology
– Explain current asthma pathogenesis
– Assess and diagnose asthma using clinical criteria
– Demonstrate competence in the clinical assessment of
suspected case of asthma including case history and clinical
examination
– Demonstrate correct use of a peak expiratory flow meter and
interpret the results.
DEFINITION OF ASTHMA:
– 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.
• GINA 2020
– Symptoms are associated with variable expiratory airflow,
i.e. difficulty breathing air out of the lungs due to:
• Bronchoconstriction (airway narrowing)
• Airway wall thickening
• Increased mucus
Asthma Epidemiology
o One of the most common disease worldwide.
o Most common chronic disease in children.
o Worldwide:
 334 million people currently suffer from asthma,
 Prevalence rates are increasing.
 250,000 deaths each year
 Over 80% of asthma deaths occur in low and middle-income
countries
•
Asthma Global Report 2019
Asthma Epidemiology
– The prevalence of asthma in affluent countries
 has risen over the last 30 years but
 now appears to have stabilized,
 with 10 - 12% of adults and 15% of children affected by the
disease.
– In developing countries where
 the prevalence of asthma had been much lower,
 there is a rising prevalence,
 associated with increased urbanization.
Asthma in Ethiopia
o The prevalence of asthma is estimated between 1.5-3.0% of the
population (3 million people)
o 10 x prevalence of TB.
o According to the latest WHO data ( 2018):
 Asthma deaths in Ethiopia reached 4,485 or 0.73% of
total deaths.
 Age adjusted death rate 8.35/100,000 population
 Ethiopia ranks #61 in the world in terms of asthma
deaths.
Asthma in Ethiopia
– ISAAC Study :In Ethiopia, larger community-based prevalence studies
done among school children in Addis Ababa, Jimma and Gondar
 Prevalence of asthma was between 2 % and 4 %.
 The 12-month prevalence of self-reported wheezing was found to be 10.7%
and 16.2% in Addis Ababa and Gondar respectively.
– Asthma prevalence was lower in rural compared to urban areas.
– Use of ICS /Combination therapy in Ethiopia study;
 4% in Jimma University Hospital
 32% in Tikur Anbessa Hospital.
– The Asthma Control rate was only 28.6% in patients from Jimma
University Hospital.
Definition of Severe Asthma
o There is no universally accepted definition of severe asthma.
o Severe asthma is not a single disease as evidenced by the
variety of clinical presentations, physiologic characteristics,
and outcomes.
o 5-10% of all asthmatics may have severe disease.
o Severe asthma is responsible for up to 50% of the total asthma
related health care costs.
Definition of severe
Asthma
Severe Asthma
Consequence of severe asthma
Comorbidity in severe asthma
Cause of Asthma
– Heterogeneous disease with interplay between genetic
and environmental factors
– Several risk factors that predispose to asthma have
been identified
– These should be distinguished from triggers, which are
environmental factors that worsen asthma in a patient
with established asthma
Risk factors and Triggers involved in Asthma
Pathogenesis & Pathophysiology of Asthma
– Airflow limitation in asthma is recurrent and caused by
a variety of changes in the airway
– These include: Bronchoconstriction, Airway edema,
Airway hyperresponsiveness
– Airway hyper-reactivity (AHR) – the tendency for
airways to narrow excessively in response to triggers
that have little or no effect in normal individuals – is
integral to the diagnosis of asthma and appears to be
related to airway inflammation as shown in the figures
below.
Current Paradigm of Asthma Immunology
Pathogenesis of Asthma
Genetic Predisposition Environmental Factors
Pathophysiology of Asthma
Asthma Diagnosis
– History
 Paroxysms of cough, wheezing, difficulty of breathing and
chest tightness
 History of allergic diseases( Rhinitis, eczema)
 Family history of Asthma
– Physical examination(Respiratory distress, Wheezing..)
– Pulmonary Function test(PEAK flow /Spirometry
– Positive allergy test
– Increased IgE
– CBC, CXR, Sputum examination for excluding infection
and complication
Diagnosis of asthma –
symptoms
Increased probability that symptoms are
due to asthma if:
Decreased probability that symptoms
are due to asthma if:
 More than one type of symptom
(wheeze, shortness of breath,
cough, chest tightness)
 Symptoms often worse at night or
in the early morning
 Symptoms vary over time and in
intensity
 Symptoms are triggered by viral
infections, exercise, allergen
exposure, changes in weather,
laughter, irritants such as car
exhaust fumes, smoke, or strong
smells
 Isolated cough with no other
respiratory symptoms
 Chronic production of sputum
 Shortness of breath associated
with dizziness, light-headedness
or peripheral tingling
 Chest pain
 Exercise-induced dyspnoea with
noisy inspiration (stridor)
Asthma Diagnosis-Physical Examination
– Physical examination in people with asthma
 Often normal
 The most frequent finding is wheezing on auscultation, especially
on forced expiration
– Wheezing is also found in other conditions, for example:
 Respiratory infections (Viral)
 COPD
 Upper airway dysfunction
 Endobronchial obstruction
 Inhaled foreign body
– Wheezing may be absent during severe asthma
exacerbations (‘silent chest’)
Diagnosis of asthma in Ethiopia based on level of
care
Divided in to two levels:
 Asthma diagnosis at Primary Health Care unit
 Asthma Diagnosis at General Hospital and Above level
Diagnosis of asthma at Primary
Health Care Unit
Asthma diagnosis at PHC unit
PEAK Expiratory Flow Meter in Asthma Diagnosis
– USE OF PEAK EXPIRATORY FLOW METER IN ASTHMA
 Peak expiratory flow (PEF) meters are handheld devices designed
as personal monitoring tools.
 Currently WHO recommend to use PEF for diagnosis of asthma in
LMIC where there is no spirometry services
 A peak flow meter measures how fast air can be blown out of the
lungs.
 NB: PEAK flow may under diagnose asthma
USE OF PEAK EXPIRATORY FLOW METER IN ASTHMA
Figure 1a: Example of hand held
Peak flow meter
Figure 1b: How to Measure PEF
using a peak flow meter
Figure 1c. Calculating percentage
reversibility of PEFR
USE OF PEAK EXPIRATORY FLOW METER IN
ASTHMA
– A change in PEF of at least 20%, is accepted as being
consistent with asthma.
– PEF values less than 200 L/min indicate severe airflow
obstruction.
 PEF can establish peak flow variability, quantify asthma severity,
and provide both patient and clinician with objective
measurements on which to base treatment decisions.
 It is affordable means of support in the diagnosis of asthma in the
primary health care level.
 The standard however in the diagnosis of asthma is with the
support of spirometry.
Asthma Diagnosis at General Hospital and
Above level
– Features to make the diagnosis of Asthma as
mentioned above
– Evidence of variable expiratory airflow limitation
– Document that variation in lung function is greater
than in healthy people
– The standard however in the diagnosis of asthma is
with the support of spirometry
Spirometry
– Spirometry performed at least once documenting
 Ratio of Forced Expiratory Volume in the first second (FEV1)
to Forced Vital Capacity (FVC)(FEV1/FVC) is below 70% (below
the limit of normal)
 An increase of FEV1 by > 200ml and > 12% from the base line
value after inhaling a bronchodilator
 FEV1 increases by more than 12% and 200ml from baseline (in
children, by >12% of the predicted value) after 4 weeks of anti-
inflammatory treatment
– In occasions where spirometry test is normal but the
patient has the typical symptoms, bronchial challenge
test can exclude the diagnosis of asthma.
Spirometry
– A fall in FEV1 from baseline of ≥20% with standard
doses of methacholine challenge performed in a
controlled setting demonstrates variability in
expiratory airflow limitation which could not be
evidenced by office spirometry test.
– The other safer alternative is trial of treatment and
asses the change in FEV1 post treatment.
– Increase of FEV1 by 12% and 200 ml from baseline after
4 weeks of anti-inflammatory treatment, outside of
recent respiratory illnesses, confirms significant
variability.
Spirometry
Figure 2; Office Spirometry
Machine
Asthma diagnosis at General
Hospital & above
Case study 1 (30 min)
• A 25 years old house wife presented with recurrent five
months history of night time and morning productive
cough of whitish sputum associated with low grade
fever and running nose in the last three days.
Discussion points:
• What additional information would you like to get?
• Possible differential diagnosis?
• How do you make the diagnosis of this case?
Summary:
– Asthma is a major cause of illness and death in Ethiopia and the rest of the
world.
– Asthma causes symptoms of wheezing, coughing and shortness of breath.
– There is usually a life long history of asthma, or at least a history from
childhood.
– Asthma is often associated with allergies or allergic conditions such as allergic
rhinitis or eczema.
– The symptoms of asthma are usually variable. The variation may be within the
day, from day to day or depending on the seasons.
– Asthma is a often clinical diagnosis in low & middle in come countries (LMIC).
– In the absence of spirometry test peak flow meter can be used as diagnostic
test for asthma in primary health care setup.
Summary:
– Asthma is a chronic disease causing inflammation of the
airways with an unknown cause.
– Asthma requires long term treatment to control the chronic
inflammation in the airways.
– If asthma inflammation is not controlled the airways
become hypersensitive and to become narrowed.
– The asthma patient can have exacerbations which cause
wheezing, coughing, breathlessness and chest tightness.
– Infections, allergens, irritants and exercise can all trigger
asthma exacerbations.
We would like to thank
Dr Amsalu Bekele, Dr Rahel Argaw, Dr Hanan Yusuf and Dr
Tewodros Haile for preparing this powerpoint
MANAGEMENT OF ASTHMA IN ADULTS
AND ADOLESCENTS ≥ 12 YEARS OF AGE
Learning objectives
– By the end of this unit, the learner should be
able to:
 Describes the goals of asthma management
 Assess severity of asthma
 State criteria for diagnosis of severe asthma
 Describe means of minimizing or avoiding
precipitating factors
 List the main groups of asthma medications
 Describe asthma management based on control
 Describe the supportive care for acute severe
asthma management
 Identify patient who need referral to specialist.
Goal of Asthma Management
– Avoid troublesome symptoms during the day and
night
– Need little or no reliever medication
– Have productive, physically active lives
– Have normal or near-normal lung function
– Avoid serious asthma flare-ups (also called
exacerbations, or severe attacks).
Goal of Asthma Management
– Achieving these goals requires a partnership
between patient and their health care providers
 Ask the patient about their own goals regarding their
asthma. Shared decision-making is associated with
improved outcome
 Good communication strategies are essential
 Consider the health care system, medication availability,
cultural and personal preferences and health literacy
 Take every opportunity to assess patients,
particularly when they are symptomatic or after
a recent exacerbation
Asthma control
– Asthma control –Has two main domains
 Assessment of symptom control over the last 4 weeks
 Assessment of risk factors for poor outcomes
Assessment of Asthma control
(In the Past 4 weeks)
1. Symptom control
assessment
Level of asthma symptom control
 In the past 4 weeks, he/she
had:
Well Partly
controlled
Uncontrolled
 Daytime asthma symptoms for
more than twice/week?
 Yes No
none 1-2 of
these
3-4 of
these
 Any activity limitation due to
asthma?
 Yes No
 Reliever needed* more than
once a week?
 Yes No
 Any night waking or night
coughing due to asthma?
 Yes No 
Asthma
Control
Inflammation
Direct or Indirect
Lung
Function
Utilization of
Healthcare
Resources
Functional
Status
Missed Work
and/or School
Patient Self-Report
of Control
Daytime
Symptoms
Nighttime
Awakenings
Use of a
“Quick Relief”
Inhaler and/or
Nebulizer
How should control be measured in asthma?
Adapted with permission from Chipps BE, Spahn JD. J Asthma. 2006;43:567-572.
Assessment of risk factors for poor outcomes
(In the past 12 months)
2. Assessment of risk factors for poor outcomes
Risk factors for exacerbations
 Uncontrolled asthma symptoms
Additional risk factors, even if the patient has few symptoms
 High SABA use (≥3 canisters/year)
 Having ≥1 exacerbation in last 12 months
 Incorrect inhaler technique and/or poor adherence
 Smoking
 Obesity, chronic rhinosinusitis, pregnancy, blood eosinophilia, low
socioeconomic status, depression, anxiety
Risk factors for fixed airflow limitation include
 Lack of Inhaled Corticosteroid (ICS) treatment, smoking, occupational
exposure, mucus hypersecretion, preterm birth, low birth weight.
Risk factors for medication side effects include
 Frequent Oral corticosteroid (OCS) use, high dose and /or potent ICS,
some drugs that decrease steroid metabolism, poor inhaler technique
Principles of asthma management
1. Asthma management of patients not on
treatment or for first time presenters
– For patients presenting with acute symptoms, follow
the algorithm for management of asthma
exacerbation
– For patients with indolent but variable symptoms
once the diagnosis is confirmed, assess for any risk
for poor outcome
– Patients with any risk factor for poor outcome are
eligible to start higher dose of controller therapy and
based on response/control of asthma, treatment
Principles of asthma management
cont…
2. Management of asthma among patients on
pharmacologic treatment
– Assess for asthma control in each visit and
determine asthma severity based on the level of
step needed to control the symptoms
• Mild asthma – Control achieved with step 1 or 2
medications
• Moderate asthma – Step 3 management is required to
control asthma
• Severe asthma- Steps higher than 3 are needed for
control
– Reassess for risk factor for poor outcome
Asthma management for Adults and Adolescents 12
years and above at PHC in Ethiopia
Step 1. Low dose inhaled Beclometasone 100µg
taken whenever Inhaled Salbutamol (SABA) is
needed.
Step 2a. Standing dose of daily Beclometasone
inhaler 100µg (1 puff) BID plus Salbutamol puff
when needed.
Step 2b. Standing dose of daily Beclometasone
inhaler 200µg (2 puffs ) BID plus Salbutamol puff
when needed.
If total daily dose of Beclometasone is more than
During initial presentation
• Start in step 1
– Symptoms less than twice per month
• Start with Step 2
– Symptoms twice a month or more, but less than
daily
Asthma management for Adults and Adolescents
above 12 years
at General hospital & above in Ethiopia
Steps 1 and 2 – Refer management for PHC
Step 3. Standing dose of Low dose Budesonide - Formoterol
combination (160/4.5µg) one puff BID
OR
Standing Medium dose of Beclomethasone 400µg (4 Puffs of
100µg) BID alone
OR
Low dose Beclomethasone 200µg (2 puffs) BID + Monteleukast
10mg po daily
OR
Low dose Beclomethasone 200µg (2 puffs) BID +Theophylline
10mg/kg
Asthma management at General hospital
& above in Ethiopia
Step 4. Medium dose Budesonide- Formoterol
combination (160/4.5µg) two puffs BID
OR
High dose Beclomethasone 600µg puffs BID (200µg
of beclomethasone 3 puffs BID) + Monteleukast or
Theophylline
Step 5. High dose Budesonide-Formoterol
combination
(160/4.5µg) three puffs BID
OR
During initial presentation
• Start with Step 3 if :
– Symptoms most days, or waking with asthma
once a week or more
• Start with step 4 if :
– Symptoms most days, or waking with asthma
once a week or more, and low lung function
Reliever Therapy
• The preferred reliever therapy for those on
standing dose of Budesonide- Formoterol is the
use of the same combination of low dose ICS-
formoterol (SMART) as-needed based.
• Maximum Total Daily dose of Formoterol should
not exceed 72μg.
• Alternative reliever is Salbutamol puff as needed
Asthma control
– Follow the continuous control-based asthma
management cycle:
–Assess symptom control + risk factors
–Adjust treatment (pharmacological and non-
pharmacological)
–Review the response: symptoms,
exacerbations, side effect
Reviewing Response and Adjusting
treatment
 Stepping up asthma treatment;
 Sustained step-up, for at least 2-3 months if
asthma poorly controlled;
 Short-term step-up, for 1-2 weeks, e.g. with viral
infection or allergen;
 Day-to-day adjustment;
 For patients prescribed low-dose ICS/formoterol
maintenance and reliever regimen
 Stepping down asthma treatment;
 Consider step-down after good control
maintained for 3 months.
 Find each patient’s minimum effective dose
that controls both symptoms and
exacerbations without the development of
adverse effects.
 Stopping ICS often leads to potentially
dangerous worsening of asthma.
Asthma medication and common side
effects
– SABAs- Short acting beta agonists bronchodilators
 Should be the main therapy only during acute
exacerbations but
 NOT recommended as a stand-alone therapy except in
pediatric age group
– LABAs- Long acting beta agonists
 Provide bronchodilation for up to 12 hours after a single
dose.
 Salmeterol and formoterol are the LABAs available for
asthma in combination with ICS.
 Formoterol has similar duration of action with salmeterol but
bronchodilation with formoterol is significant within minutes
of inhalation, maximal within 2 hours
Cont…
– Inhaled Corticosteroids (ICS)
 Preferred, first-line controller agents for all patients
especially for those at risk for poor outcome
 Most patients with asthma don’t need high dose, at a
group level, most of the benefit is obtained at low
dose.
 Have few side effects at standard treatment doses.
 Local side effects include oral candidiasis, dysphonia,
reflex cough and bronchospasm.
 High dose ICS and long-term use of oral steroids
predisposes to systemic side effects which includes
adrenal suppression, osteoporosis, skin thinning, easy
bruising, diabetes, hypertension, infections, glaucoma
Theophylline
 Provides mild bronchodilation in asthmatic patients. Has
also weak anti-inflammatory and immunomodulatory
properties
 Theophylline use needs to be monitored closely owing to
 The medication’s narrow therapeutic-toxic range,
 Individual differences in metabolism, and
 The effects of many factors on drug absorption and
metabolism.
 At therapeutic doses, potential adverse effects include
 Insomnia, aggravation of dyspepsia ,GERD, and urination
difficulties in men with prostatic hyperplasia.
 Dose-related toxicities include :
Leukotriene antagonist(LTRA)
– Leukotriene receptor antagonists (LTRA) are less
effective than ICS particularly for exacerbations.;
– Used as add on for
 Patients who experience intolerable side-effects from
ICS; or
 For patients with concomitant allergic rhinitis.
– Before prescribing montelukast (adult dose 10 mg
once daily), health professionals should counsel
Inhaled corticosteroids (ICS) and Combinations for
Adults and adolescents (≥12 years)
Inhaled corticosteroid Total daily dose (mcg)
Low Medium High
Beclomethasone
dipropionate (HFA)
200–500 500–1000 >1000
Fluticasone/salmeterol
(DPI)
100/50 250/50 500/50
Budesonide (DPI) 200-400 400-800 >800
Mometasonefuroate
(HFA-pMDI)
200-400  400
NB: DPI-Dry Powder inhaler, MDI -Metered dose inhaler CFC-Chloroflourocarbon
HFA-Hydroflouroalkane
*When Budesonide/formoterol is prescribed as maintenance and reliever therapy, the
maximum recommended dose of formoterol in a single day is 72 mcg.
Non-Pharmacological Strategies and Interventions
for asthma management
– Reduce indoor air pollution by cooking outside or
using smokeless cooking stoves
– Avoid allergens that the patient is sensitive to
– Avoidance of tobacco smoke exposure
– Occupational asthma
– Encourage Physical activity
– Avoid medications that may worsen asthma
– Remediation of dampness or mold in homes
Patients with poor asthma control should be
assesses for the following
– Reasons for poor adherence and misunderstanding
the difference between relievers and controllers
– Poor inhaler technique
– Exposure to trigger factors at home and work
– Presence of gastro-esophageal acid reflux disease
(GERD)
– Rhinitis and sinusitis
– Use of medications that may aggravate asthma such
as aspirin, non-steroidal anti-inflammatory drugs and
ß blockers
– Other medical conditions mimicking asthma symptoms
(e.g. cardiac disease).
Case study 2 (30 min)
• A 30 years old man came with history of cough for 1 month.
The cough is Productive of whitish sputum and phlegm in
the morning, it is worse at night, day and better during the
day. He feels shortness of breath during the day when he
goes upstairs. His mother is asthmatic. He is a banker and
used to have sneezing and running nose whenever he
counts money. He has no night Sweating, weight loss, or
fever no chest pain, no pedal Edema, or Orthopnea.
Physical findings show no distress but has wheezing in the
chest bilaterally.
• What is the most likely diagnosis? Differentials?
• How do you classify the severity of patient?
• How do you manage this patient?
Summary
– Asthma is a chronic inflammatory disorder of the
airway, persistent asthma is most effectively
controlled with daily long-term control medication
directed toward suppression of airway inflammation.
– A stepwise approach to pharmacologic therapy is
recommended to gain and maintain control of
asthma in both the impairment and risk domains.
– Asthma treatment should contain appropriate
controller medicines with as needed reliever.
• We would like to thank
– Dr. Amsalu Bekele, Dr Hanan Yusuf, Dr Tewodros
Haile and Dr Rahel Argaw for preparing this
powerpoint
Definition
• 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, i.e. they
represent a change from the patient's usual status
that is sufficient to require a change in treatment.
• Definition based on combination of symptom, clinical
findings and lung function is more objective in
assessing severity.
• A minority of patients perceive airflow limitation
poorly and can experience a significant decline in
lung function change in symptoms. This especially
affects patients males with a history of near fatal
asthma.
Assessment of risk
The prevention of exacerbations is the most
important aim for patients with asthma and
healthcare professionals.
In order to achieve this aim, it is important to
plan the re-assessment of asthma patients and
treatment adjustments because of the immediate
risks (i.e. acute respiratory failure, death) and
future risks (recurrence of exacerbations, decline
in lung function, and side-effects of treatments)
• Factors which are associated with exacerbation
1) the level of asthma control,
2) asthma severity based on ERS/ATS definition,
3) lung function,
4) the presence of comorbidities,
5) the psychosocial status (to assess the ability to seek
help in case of clinical worsening),
6) previous history of near fatal attacks and
7) response to treatment.
• Such factors seem important in guiding treatment
decisions and, importantly, decisions regarding
hospitalizations.
Triggers of exacerbation
• Indoor allergens
– House dust mites in bedding, coach roach eggs
carpet, stuffed furniture, pollution and pet dander
• Outdoor allergen
– Pollen, molds
• Tobacco smoke
• Chemical irritants in workplace
• Cold air and physical exercise
• Certain medications, such as aspirin, NSAID
Classification of asthma severity &
management
• Mild
• Moderate
• Severe
• Very severe
DEGREE OF
SEVERITY SYMPTOMS AND SIGNS INITIAL PEF (OR FEV1) CLINICAL COURSE
Mild Dyspnea only
with activity
(assess
tachypnea in
young children)
PEF ≥ 70 percent of
predicted or personal
best
Usually treated at home
Prompt relief with inhaled
short-acting beta2 agonist
Possible short course of
oral systemic
corticosteroids
Moderate Dyspnea
interferes with or
limits usual
activity
O2 saturation
90-95%
PEF 50-69 percent of
predicted or personal
best
Usually requires office or
emergency department
visit
Relief from frequent
inhaled short-acting
beta2 agonist
Oral systemic
corticosteroids; some
symptoms last for one to
two days after treatment
begins
Self management of exacerbation
• Severe exacerbations are potentially life threatening
and their treatment requires careful assessment and
monitoring by health care professionals.
• A careful written asthma action plan helps patients to
recognize and respond appropriately to worsening of
symptoms.
• The criteria for initiating an increase in controller
medication will vary from patient to patient.
Asthma action plan
ICS-Formoterol
• For patients with mild asthma prescribed as-needed
combination low dose ICS-formoterol, increasing the
as-needed doses of ICS-formoterol when asthma
worsens reduces the risk of severe exacerbations
requiring OCS by 2/3rd compared to SABA-only
treatment. However the benefit is achieved when
initiated at the early stage of worsening asthma.
ICS
• For patients with maintenance-only ICS containing
treatment should generally be increased if asthma
symptoms are interfering with normal activities, or
PEF has fallen by >20% for more than 2 days.
Possible options
– Temporarily doubling ICS dose (delay of 5-7 days
may contribute to failure)
– Age >16 years quadrupling ICS dose can reduce
use of OCS.
OCS
Short course of 40 mg prednisolone for 5 days with
instructions can be tried if:
– Fail to respond to an increase in reliever and
controller medication for 2-3 days
– Deteriorate rapidly or who have a PEF or FEV1< 60%
of their personal best or predicted value.
– Have a history of sudden severe exacerbations.
Follow up after outpatient
management
• Ideally before ceasing oral corticosteroids if prescribed.
• Maintenance controller treatment can generally be
resumed at previous levels 2-4 weeks after
exacerbation, unless the history suggests that the
exacerbation occurred on a background of long-term
poorly controlled asthma.
• In this situation use this opportunity to train inhaler
technique, check adherence and provide additional
asthma education.
• After checking technique and adherence a step up in
First Line Therapy at PHC
1. Prednisolone 30-40 mg per day for five days for
adults initiated within one hour of presentation
AND
2. Salbutamol four- six puffs by metered dose
inhaler and by spacer every 20 minutes for one
hour
3. Oxygen supplementation if saturation is below
90%.
Second Line treatment at
General Hospital and above
• Increase frequency of dosing via metered dose inhaler
and spacer or give salbutamol by continuous
nebulization at 5-10 mg per hour.
• Add nebulized ipratropium, if available
• Continue steroid therapy
• IV magnesium sulfate (2g infused over 20 minutes)
• IV theophylline or Aminophylline
Review
• Patient’s response after discharge (within a week)
• Patient’s understanding of the cause of their
asthma
• Modifiable risk factors for asthma
• Understanding of correct uses of medications
• Adult and adolescent patients with more than 1-2
exacerbations per year despite more than Step 3
therapy should be referred to a specialist.
Part II Asthma education
Goals of asthma education
• An explanation of the nature of asthma and its
inflammatory basis
• A description of the different classes of drugs
and their purpose in treatment (i.e. as-needed
“relievers” and regular “controllers”)
• Advice on prevention strategies (allergen,
irritant, and tobacco smoke avoidance)
• How to recognize worsening asthma and how and
when to implement their action plan
• In some patients, particularly those requiring
stabilization or patients who have had a recent
exacerbation or deterioration, the use of a PEF
meter and chart.
• The correct choice and use of inhalers and the
opportunity to practice under supervision
INHALER USE FOR ASTHMA
MANAGEMENT
• An inhaler is a medical device used for delivering
medication into the body via the lungs. It is mainly
used in the treatment of asthma and chronic obstructive
pulmonary disease. The two most common forms are:
– Metered-dose inhaler
– Dry powder inhalers (Accuhalers and turbuhalers)
• Some of the types of inhalers include: Autohalers
(Breath Activated aerosol devices), Nebulizers mists
and nasal inhalers
• Most patients (up to 80%) cannot use their inhaler
correctly. This contributes to poor symptom
control and exacerbations. To ensure effective
inhaler use.
• Choose the most appropriate device for the
patient before prescribing, check in haler
technique at every opportunity, correct using
physical demonstrations, paying attention to
incorrect steps and confirm that you have
checklists.
Metered-dose inhaler (MDIs)
• The medicine is in a small canister, inside a plastic
case. When the inhaler is pressed, a measured dose
of medicine comes through the mouthpiece.
• MDIs require good technique and coordination by
pressing down on the inhaler and breathing in at the
same time.
• Because using the inhaler correctly can be
difficult, spacer devices are recommended for use
with MDIs. The spacer is attached to the MDI to
make it easier to use the inhaler and get more
medicine into the lungs
A. How to use Metered Dose Inhaler
• Remove the cap and check the mouthpiece is clean
and free of objects.
• Shake the inhaler four or five times
• Holding the inhaler upright with your thumb on the
base, breathe out as far as comfortable
• Place the mouthpiece in your mouth; closing your lips
around it to form a good seal - do not bite
• Start to breathe in slowly; press down firmly on the
top of the canister to release a dose; while continuing
to breathe in slowly and deeply
• Removing the inhaler from your mouth; hold your
breath for about 10 seconds, or as long as is
comfortable.
• Breathe out gently away from your inhaler
mouthpiece
• For a second dose, wait approximately 30 seconds
before repeating steps 2-7
• Replace the cap
Dry Powder Inhaler (DPI)
• Dry powder inhalers are handheld devices that deliver
medication to the lungs and airways as you inhale
through it.
• Examples of dry powder inhalers include: Turbuhaler;
Accuhaler; Handihaler; Ellipta inhaler and Breezhaler.
The common forms available in Ethiopia are Turbuhaler
(eg.Symbicort) and Accuhaler (eg.Seritide)
B. How to use Accuhaler® (Dry powder inhaler-
DPI)
• Check dose counter.
• Open cover. (Use thumb grip)
• Hold the casing of the Accuhaler® in one hand while
sliding the thumb grip away until a click is heard
• Holding your Accuhaler® with the mouthpiece towards
you slide the lever away from you until a click is heard.
This makes the dose available for inhalation and moves
the dose counter on.
• Holding the inhaler horizontally, breathe out
as far as comfortable
• Place the mouthpiece in your mouth; closing
your lips around it to form a good seal - do
not bite
• Breathe in as strongly and deeply as possible
• Removing the inhaler from your mouth;
hold your breath for about 10 seconds, or as
long as is comfortable
• Breathe out gently away from your inhaler
mouthpiece
• To close the Accuhaler®, slide the thumb
grip back towards you as far as it will go
until it clicks.
Turbuhaler (DPI)
• Since the turbuhaler is a breath-activated
device, to use the turbuhaler properly, you
must be able to breathe in deeply. Adults
and children 7 years of age and older
should be able to use the turbuhaler.
C. How to use Turbuhaler (DPIs )
1. Open: unscrew and remove the cap. Hold the
turbuhaler upright.
2. Load the dose: twist the base anticlockwise and then
back in the other direction until you hear a click. Your
turbuhaler is now loaded with one dose of medicine
3. Breathe out: breathe out, away from the turbuhaler. Do
not blow directly into the turbuhaler.
4. Inhale your dose: place the mouth piece in your mouth
and form a seal with your lips. Breathe in deeply. Remove
the turbuhaler and hold your breath for up to 10 seconds.
5. Close: replace the cap and twist until it is on
properly.
6. Cleaning and storing your turbuhaler: wipe
the mouthpiece with a clean dry tissue. Do not
wash the mouthpiece or allow it to get wet when
cleaning. Keep the cap on when not in use. The
device may clog if exhaled or dribbled into or if
stored in an area of high humidity with the cap
off or unsealed.
Common problems when using a turbuhaler
• To get the most benefit, it is important to use the
correct technique. Here are a few common
problems:
• Not holding your turbuhaler upright (vertical)
while loading the dose.
• Covering the air inlets with your lips.
• Breathing in through your nose instead of your
mouth.
• Shaking the inhaler to see how much is left.
• Storing your turbuhaler in a damp place with the
cap off.
• How to use Spacers
• If patient unable to use an inhaler correctly, add a spacer
to increase drug delivery to the lungs, especially if using
inhaled corticosteroids. This may also reduce the risk of
oral candida.
• Clean the spacer before first use and every second week:
remove the canister and wash spacer with soapy water.
Allow it to drip dry. Avoid rinsing with water after each
use.
• Spacers are not commonly available in Ethiopia so a
plastic water bottle. See figure below.
• To modify a 500ml plastic bottle for use as an effective
spacer
How to use a bottle spacer
Use a modified 500ml plastic bottle in a similar way to
a conventional spacer
Case study 3 (30 min)
• The above patient returns back after 2 weeks with Shortness of
breath, fever and cough productive of yellowish sputum appears to
be in distress with difficulty of speaking, his RR was 30, pulse was
100/mt and BP-130/80mmhg and T-37.5, He has no wheezing and
difficult to hear the breath sounds, heart beatare normal and no
murmur, no gallop, no pedal edema. He appears weak and
occasionally confused.
• What is the diagnosis?
• What are the abnormal findings in this patient?
• What do these abnormal findings imply?
• Classify the severity of asthma?
• What are the steps of management?
• We would like to thank
Dr Hanan Yusuf, Dr Tewodros Haile,
Dr Amsalu Bekele and Dr Rahel Argaw for
preparing this powerpoint
Diagnosis and management of
asthma in children under the
age of five years
Learning objective
• Identifying asthma in children
• Prenatal risk factors of asthma
• Algorithm in identifying asthma in under five
years of age child at PHC and General Hospital
• Steps Asthma Management
• Assessing asthma control in preschool children
• Preparing locally made spacer out of plastic
bottles bottle
109
What is asthma in preschool children ?
• Wheezing or coughing that occurs with exercise,
laughing or crying, and symptoms in the absence of
apparent respiratory infection
• History of other allergic disease (eczema or allergic
rhinitis), allergen sensitization or asthma in first-
degree relatives
• Clinical improvement during 2–3 months of
controller treatment, and worsening after cessation
110
Prenatal Risk factors for Asthma
111
• Family history of atopic disease
• Maternal smoking and asthma
• Environmental pollution (especially tobacco smoke and
indoor biomass exposure),
• Nutrition
• Maternal stress
• Use of antibiotics
• Birth by caesarean section
Sources: ISAAC Publications
Impact of asthma
• Uncontrolled asthma is associated with
– missed school days
– repeated hospitalization
– risk of airway remodeling
– general poor quality of life in the affected children
113
114
115
Steps Asthma Management
116
Pharmacologic management
117
Low, medium and high ICS doses: children 6-
11 years
GINA 2020, Box 3-6B
DPI: dry powder inhaler; HFA: hydrofluoroalkane propellant; pMDI: pressurized metered dose inhaler (non-CFC); * see product information
This is NOT a table of equivalence. These are suggested total daily doses for the
‘low’, ‘medium’ and ‘high’ dose treatment options with different ICS.
118
Low, medium and high ICS doses: children
5 years and younger
GINA 2020, Box 3-6B
This is NOT a table of equivalence. These are suggested total daily doses for the
‘low’ dose treatment options with different ICS.
119
BDP: beclometasone dipropionate; DPI: dry powder inhaler; HFA: hydrofluoroalkane propellant; pMDI: pressurized metered dose
inhaler (non-CFC)
Assessing asthma control in preschool children
120
…Cont
Watch patients inhaler
technique, check adherence .
Remove potential risk
factors : Assess and
manage risk factors
Refer to specialist for
confirmation of asthma
If asthma is confirmed
escalate the steps of
treatment
121
Inhalation technique for preschool children
• Use spacers with face mask, in all
children less than five years of age
• Locally prepared plastic bottle based
spacers can be used.
• Clean the spacers with detergents
without rinsing it at least every 2 weeks.
• Tight seal should be created between
mask and face during inhalation and
cleaning face
• Mouth rinse after steroid administration
should be practiced regularly
122
Constructing locally made spacers
1. Wash the bottle with soap and water and air dry
for a minimum of 12 hours to reduce
electrostatic charge on the interior plastic.
2. Make a wire mould similar in size and shape to
the mouthpiece of the MDI.
3. Heat the mould and hold in position on the
outside of the base of the plastic bottle until the
plastic begins to melt (~10 seconds). Rotate the
mould 180% and reapply to the bottle until the
mould melts through to make a hole.
4. While the bottle is still warm, insert the MDI
into the hole to ensure a tight fit between the
MDI and bottle spacer.
Prime initially with 10 puffs of
the medicine to reduce
electrostatic charge on the walls
123
Summary
• Asthma in under five children is recognized
using symptoms rather than lung function tests.
• Genetics, environmental , perinatal risk factors
are identified .
• Inhaled corticosteroids are the backbone of
asthma management in under five years of age
• Locally made spacer is effective in delivering
inhaled drugs for asthma symptom control .
124
• We would like to thank
– Dr. Rahel Argaw, Dr Hanan Yusuf, Dr Tewodros
Haile and Dr Amsalu Bekele for preparing this
powerpoint
LEARNING OBJECTIVES:
The participant will be able to:
• Describe the epidemiology, risk factors and pathogenesis of
COPD
• Describe the diagnostic approach in COPD
• Define COPD screening tools
• Explain strategies for prevention of COPD
• Manage COPD
Definition
A common, preventable and treatable disease characterized by
-Persistent respiratory symptoms and
-Airflow limitation that is due to
>Airway and/or alveolar abnormalities
>Usually caused by significant exposure
to noxious particles or gases
Outline
 Definition, Epidemiology, risk factors & pathogenesis
 Clinical manifestations
 Diagnosis and initial assessment
 Preventive strategies
 Management of stable COPD
Definition
• Chronic bronchitis
Clinically defined condition with chronic cough and phlegm
Small airways disease
A condition in which small bronchioles are narrowed
• Emphysema
Anatomically defined condition
Characterized by destruction and enlargement of the lung alveoli
COPD
Epidemiology
• NCDIs
-Major public health problem in Ethiopia
accounting for an estimated
-52% of the total annual mortality
-46% of total national disease burden (DALY’s lost) in
2016
• Based on Global Burden of Diseases Study 2016
CRDs contribute to
-2.5% of the deaths due to NCDs
Epidemiology
Third leading cause of death in the world
 Estimated 384 million cases of COPD globally with estimated
prevalence of 12%
More than 3 million people died of COPD in 2016 accounting for
6% of all deaths globally
Burden is projected to increase because of continued exposure to
COPD risk factors and aging of the population
Prevalence of COPD is higher in smokers and ex-smokers compared
to non-smokers
Higher in ≥ 40year group compared to those < 40 years of age
Higher in men than in women
The prevalence of COPD is not precisely known even though
hospital based studies show it is probably fairly common in Ethiopia
Underdiagnoses in COPD
Epidemiology
STEPS Survey indicated
-Prevalence of current smokers to be 4.2% of adults
GATS
-29.3% (6.5 million) were exposed to environmental tobacco smoke
(ETS) in their workplace in the past 30 days
-Overall, 12.6% (8.4 million) of adults were exposed to ETS
at home
-60.4% in bars and nightclub
-31.1% in restaurant
-19.7% in government buildings
-11.4% in public transportation
-7.0% in health-care facilities
Epidemiology
Shisha use
Indoor air pollution due to biomass fuel use
Industrialization and urbanization -exposure to particulate
matter are rising
Whereas,
Availability of services for CRDs is very low at 45% in
Health facilities
Among those facilities mean readiness was only 55% based
on SARA 2016 report
Risk factors
PATHOGENESIS AND PATHOPHYSIOLOGY OF COPD
• The chronic air flow limitation caused by a mixture of small
air ways diseases (e.g. Obstructive bronchiolitis) and
parenchymal destruction(emphysema), the relative
contributions of which of which vary from person to person
• COPD is characterized by:
– Airflow limitation and gas trapping
– Gas exchange abnormalities
– Mucus hypersecretion
– Pulmonary hypertension
Noxious particles
and gases
Lung inflammation
Host factors
COPD pathology
Proteinases
Oxidative stress
Anti-proteinases
Anti-oxidants
Repair mechanisms
CHANGES IN LUNG
VOLUMES
Note: This is a simplified diagram of FEV1 progression over time. In reality, there is tremendous heterogeneity in the rate of decline in FEV1
owing to the complex interactions of genes with environmental exposures and risk factors over an individual’s lifetime
[adapted from Lange et al. NEJM 2015;373:111-22].
Clinical
manifestations
Symptoms of COPD
– Cough(usually the first symptoms)
– Sputum production
– Chronic and progressive dyspnea
– Wheezing and chest tightness
– Others – including fatigue, weight
loss, anorexia, syncope, rib
fractures, ankle swelling,
depression, anxiety
Physical examination in COPD
– The respiratory examination is
the most important examination
when assessing a COPD patient
– Even in quite severe disease
there may be no physical
findings in a COPD patients
– Chest auscultation may
demonstrate bilateral wheeze or
crackles
DIAGNOSIS OF COPD
Pathways to diagnosis of COPD at primary health care
Pathways to diagnosis of COPD at General hospital
& above
© 2020 Global Initiative for Chronic Obstructive Lung Disease
CLINICAL SCREENING OF COPD
• Spirometry is required to make the diagnosis of COPD
• Clinical criteria can be used to determine probability of COPD
in the absence of spirometry
• The COPD Population Screener™ (COPD-PS™)
Easy-to-use
Validated tool designed to identify patients at risk for COPD
About the score:
Score 5-10 — High risk of COPD
Score 0-4 — Low risk of COPD
Confirmation of COPD diagnosis requires spirometry.
Management of COPD
• An effective COPD management plan includes
four components:
1. Assess and monitor disease
2. Reduce risk factors
3. Manage stable COPD
4. Manage exacerbations
Initial assessment
 The goals of COPD assessment are to determine
-Level of airflow limitation
-Impact of disease on the patient’s health status
-Risk of future events (such as exacerbations, hospital admissions, or
death)
in order to guide therapy
 Concomitant chronic diseases occur frequently in COPD patients
 Cardiovascular disease
 Skeletal muscle dysfunction
 Metabolic syndrome
 Osteoporosis
 Depression
 Anxiety
 Lung cancer
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
Pharmacologic treatment of COPD in Ethiopia
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2019 Global Initiative for Chronic Obstructive Lung Disease
© 2019 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
© 2020 Global Initiative for Chronic Obstructive Lung Disease
COPD PREVENTIVE
STRATEGIES
• The following are strategies to prevent COPD:
– Reduce indoor air pollution
• Smokeless cooking stoves
• Cooking in a well-ventilated room
• Cooking meals outside the house
•
– Smoking cessation-counseling
• Smoking cessation has the greatest capacity to influence the
natural history of COPD
• If effective resources and time are dedicated to smoking
cessation, long-term quit success rates of up to 25% can be
achieved
Case study 4 (30 min )
• A 45yearold woman from rural village has noticed a persistent,
occasionally productive cough for the past 6 months. The cough is worse
whenever she spends the day at her home while cooking where is exposed
to the smoke of the wood fire. She finally decides to visit the health
center. Her husband and she never smoked cigarettes.
• The cough has been present for almost a year. She has no fever or chills.
She does admit to more shortness of breath when she walks for long
distance over the past six months.
• Physical examination was normal findings.
• Discussion points:
• What further questions do you want to ask?
• What differential diagnoses do you consider?
• At this point, what further investigations do you think would be
appropriate?
• What would be the best option to improve her symptoms and slow
progression?
Summary
– COPD is characterized by chronic cough, dyspnea, wheezing and
sputum production
– Caused by exposure to inhaled pollutants, almost always smoke from
either domestic fires or tobacco smoking
– Rhonchi, decreased intensity of breathe sounds, and prolonged
expiration on physical examination
– Airflow limitation on pulmonary function testing that is not fully
reversible and is most often progressive
– Occurs later in life, usually older than 35 years old
– Prevention involves decreasing exposure to tobacco and avoiding
indoor air pollution
• We would like to thank
– Dr. Tewodros Haile, Dr. Aschalew Worku, Dr
Amsalu Bekele, Dr Hanan Yusuf and Dr Rahel
Argaw for preparing this powerpoint
COPD Exacerbation
Outline
• Definition & causes
• Differential diagnosis
• Classification of severity
• Indications for hospitalizations
• Management of severe exacerbations
• Indications for MICU admission, NIV & IMV
• Discharge criteria and recommendations for
follow up
Definition
• An exacerbation of COPD is a sustained
worsening of the patient's condition, from the
stable state and beyond normal day-to-day
variations that is acute in onset and may
warrant additional treatment in a patient with
underlying COPD.
• Exacerbations are infrequent in early COPD
and are largely a feature of moderate-to-severe
disease.
COPD exacerbation
• Negatively affects a patient’s quality of life
• Accelerates the rate of decline of lung
function
• Associated with significant mortality,
particularly in those requiring
hospitalizations
Main Causes of COPD Exacerbations
• Bacterial and viral infections
• pollution events
• cold weather
• interruption of regular treatment
© 2020 Global Initiative for Chronic Obstructive Lung Disease
Classification of severity of COPD exacerbations
• Mild: treated with antibiotics but no systemic
corticosteroid. Absence of respiratory failure.
• Moderate: treated with parenteral corticosteroids with or
without an antibiotic. Absence of respiratory failure.
• Severe: Type 1 respiratory failure with hypoxaemia but
no carbon dioxide retention or acidosis.
• Very severe & Life-threatening: Type 2 respiratory
failure, decompensated with acidosis and carbon
dioxide retention.
© 2019 Global Initiative for Chronic Obstructive Lung Disease
Potential indications for hospitalization
assessment*
Management of severe but not life threatening
exacerbations*
What are the indications to add antibiotics
• Three cardinal symptoms-increase in dyspnea,
sputum volume and sputum purulence
• Signs of pneumonia
• Mechanical ventilation
Key points for the management of exacerbations
Indications for medical intensive care unit
admission*
Indications for Noninvasive mechanical ventilation
(NIV)
Indications for Invasive mechanical ventilation
Discharge criteria
Recommendations for follow up
Case study 4
• A 45 year old woman from rural area has noticed a mild, occasionally
productive cough for the past 3-4 months. The cough is worse whenever
she spends the day at her home while cooking where is exposed to the
smoke of the wood fire.
• She finally decides to visit you at the health center. Her husband and she
never smoked cigarette.
• The cough has been present for almost a year. She has no fever or chills.
She does admit to more shortness of breath when she walks for long
distance over the past six months.
• Physical examination was normal findings.
• Discussion points
– 1- What further questions do you want to ask ?
– 2- What differential diagnoses do you consider?
– 3-At this point, what further investigations do you think
would be appropriate?
– 4-What would be the best option to improve her symptoms
and slow progression?
Answers
1- What further questions do you want to ask ?
-characteristic of cough intermittent or persistent?
-cough with phlegm or productive?
-nigh sweating, fever or weight loss?
2- What differential diagnoses do you consider?
Tuberculosis
Bronchial asthma
Bronchiectasis
Lung cancer
COPD
3-At this point, what further investigations do you think would be appropriate?
Chest x ray, Sputum AFB, ESR, CBC
Lung function studies: flow meter and spirometer and response to salbutamol
4-What would be the best option to improve her symptoms and slow progression?
• Reduce exposure to Smoking (outdoor cooking)
• Behavioral change communication
• Nutrition and regular treatment of chest infection etc…
• Bronchodilator treatment
• Exercise to improve exercise tolerance and quality of life
• Home oxygen treatment and morphine depending on the advance of disease
We would like to thank
• Dr. Tewodros Haile, Dr Hanan Yusuf, Dr Amsalu Bekele
and Dr Rahel Argaw for preparing this powerpoint
Cardiovascular Risk Assessment for
Health Professionals In Ethiopia
March 2021
Unit 1: INTRODUCTION
• CVDs :
– are number one cause of death globally
– 17.9 million people deaths from CVDs in 2016, (
31% of all global deaths).
– 80% occur in low- and middle-income countries,
often in people less than 60 years of age.
– CVDs are rising alarmingly in Ethiopia on top of
already existing CVDs like Rheumatic heart
diseases, cardiomyopathy and cor-pulmonale.
Introduc..
• CVDs are preceded by longtime exposure to single or
combined risk factors which can be modifiable or non-
modifiable.
• Continuing exposure to these risk factors leads to further
progression of cardiovascular diseases which include one or
more of the following:
– Coronary artery disease (CAD) manifested by fatal or nonfatal
myocardial infarction (MI), angina pectoris, and/or heart failure
– Cerebrovascular disease manifested by fatal or nonfatal stroke
and transient ischemic attack
– Peripheral artery disease manifested by intermittent
claudication and critical limb ischemia
– Aortic atherosclerosis and thoracic or abdominal aortic
aneurysm
Introduc..
• Early identification, control and avoidance of the
modifiable risk factors can significantly reduce or retard
the progression of cardiovascular diseases .
• Control of the risk factors before development of CVDs
is the most cost effective and applicable intervention
especially for low income countries likes Ethiopia.
• Several attempts were made globally and nationally
for the control of these risk factors for reducing
development of cardiovascular diseases.
Introduc…
Single versus Multiple Risk factors
approach
Previous guidelines did not take into consideration some
important facts:
• that multiple risk factors are responsible for cardiovascular
disease,
• that risk factors and determinants of heart attacks and
strokes are very similar, and, therefore, prevention
approaches are similar.
The new guidelines integrate the management of multiple risk
factors e.g. raised blood pressure, raised cholesterol, and
raised blood sugar and tobacco use.
Introduction..
• Multiple risk factor-interventions targeting individuals with
high baseline cardiovascular risk are cost effective especially
in low income countries like ours.
• Though the presence of one risk factor may increase the
chance of having future CV event, this chance of developing
CVDs is variably influenced by the presence or absence of
other risk factors.
• Therefore treatment decision of the single risk factor is
better made on the analysis of the combined effect of the total
risk factor than the sole magnitude of the single risk factor.
Unit 2.CARDIOVASCULAR RISK
ESTIMATION
Current components of management of individual
CV risk factors for prevention of atherosclerosis and
CVD include :
– CV risk assessment.
– Treatment of those at high risk for disease.
– Management adjusted to patient’s total risk of CHD or
CVD; the higher the risk, the greater the intensity of
management.
– Employment of a range of interventions to address
risk factors for CVD
CV Risk Estimation..
• No single absolute test or score used to predict the
future development of CVDs.
• A general estimate of the relative risk for CVD can be
approximated by counting the number of traditional
risk factors present in a patient
• The increased risk of CVD resulting from multiple risk
factors is frequently greater than simply additive.
• Hence we need a more precise estimation of the
absolute risk for a first CVD event desirable when
making treatment recommendations for a specific
individual.
CV risk Estimation…
• The total risk approach relies on risk prediction scores
derived from large epidemiologic cohort studies involving
diverse groups of individuals with risk factors but with no
CVDs at baseline.
• Score are developed after long years of follow up
• These prediction scores have been developed and validated
primarily in high-income countries and subsequently
adapted to other populations after re-calibration
• The World Health Organization (WHO) and the
International Society of Hypertension (ISH) recently
developed a set of CV risk prediction charts for use in all
regions of the world
CV Risk Estimation..
• The first WHO risk prediction chart was developed in
2007 and recent update was made in 2019.
• The world was divided into 21 GBD regions and
Ethiopia is represented by the Eastern Sub-saharan
African Region.
• It was suggested by the WHO working group of CV risk
prediction chart that each country should adapt the
risk chart to its national context.
• It is with this basis that the national CV working group
developed this risk charts to be used in Ethiopia.
Case Study
• Case study 1 – A 40 year old smoker was
evaluated at health center and had a BP of
130/85 and has no history or physical findings of
previous stroke, heart failure, MI or diabetes
mellitus.
• The second case was a 50 years nonsmoker with
BP of 120/80 with no history or findings of stroke,
heart failure, and diabetes mellitus but was
diagnosed to have myocardial infarction 5 years
ago.
Case study..
• Q. 1.List the cardiovascular risk factors in
these patients.
• 2. How do compare future cardiovascular
risk of these two patients? Which one has
higher risk and why?
• 3. For which patient WHO risk prediction
chart is applicable?
Unit 3:
WHO CV RISK CHARTS:
1. Definitions of terms:
• CV risk: in the WHO risk assessment CV risk
refers to the chance of having fatal or nonfatal
heart attack or stroke in the next 10 years with
the current risk profile of the patient.
• CV risk factors are any biologic or
environmental conditions known to increase
the inherent risk/chance of having CV event.
They are classified into modifiable and non-
modifiable risk factors.( See Table below)
CV risk Factors
Defini..
• Cardiovascular disease (CVD): is manifested
cardiovascular event (stroke, heart attack,
peripheral arterial or aortic disease).
• Risk chart: is collection of tables of risk estimates
with different types and levels of risk factors.
• Primary Prevention: This is control of risk factors
before cardiovascular disease develops.
• Secondary Prevention: Prevention of further
occurrence or progression of previous
cardiovascular disease.
2. Types of WHO risk charts
• WHO risk charts were developed for
estimation of the chance of future
cardiovascular event in those individuals who
never had cardiovascular diseases.
• It does not apply for patients who have
already developed cardiovascular diseases.
• There are two types of WHO risk charts based
on availability of laboratory facility to measure
blood glucose and cholesterol levels
Laboratory-based WHO CVD risk
charts
• These are CVD risk charts that include measurements
of total cholesterol and information on diabetes
mellitus .
• The laboratory-based CVD risk charts should be used
for treatment decisions.
• This is the indicated risk chart in a setting where
laboratory facilities and human and financial resources
are accessible.
• These charts will facilitate health providers to initiate
an intervention and treatment regimen, and to
implement an appropriate follow-up plan based on the
patient’s total risk status.
Parameters needed for Lab Based
WHO Risk Chart
• The variables needed for using this chart are as follows:
History:
• Age: specific numbers between 40 to 74 years. The risk prediction
doesn’t apply for age category out of the specified range
• Smoking: current smoking
• Sex: Male OR Female
• Diabetes: Yes OR No. If history of diabetes is not known OR there is
no blood sugar determination facility; then risk assessment should
be done using the other risk prediction chart (non-laboratory based
charts)
Physical Examination
• Blood Pressure: measured value of the systolic blood pressure
Laboratory parameters for Lab Based
WHO Risk Chart
1. Blood sugar: to diagnose diabetes
2. Total cholesterol: Measured valves of total
cholesterol.
– In most of the Ethiopian Laboratories, total
cholesterol is in mg/dl units; but the risk
prediction score applies values in mmol/l units.
– The cholesterol value in mg/dl should be
multiplied by 0.02586 before applying the value
for risk prediction.
B.Non-laboratory-based WHO risk
charts
• Many low-resource settings have limited testing
facilities or limited financial and physical capacity
for biochemical measurements (e.g. blood sugar
determination and cholesterol assays).
• WHO CVD risk (non-laboratory-based) charts can
be used to predict total CVD risk without
information on total cholesterol and diabetes.
• In most primary health care facilities of Ethiopia,
laboratory facilities exist to diagnose diabetes
either with fasting or random blood glucose
levels.
Non Lab..
• If the patient is not diabetic, the non- laboratory based
WHO risk chart correlates well with laboratory based
risk chart when a 10 % cut of point is used as high risk.
• The non-laboratory-based WHO CVD risk charts are
aimed at stratification in low-resource communities
and office settings and can be used for decisions
regarding referral.
• Patients diagnosed to have diabetes and non-diabetic
patients with non-lab based risk level of greater than
10% should be considered high risk and managed
accordingly in areas where serum cholesterol cannot
be determined.
Variables for Non Lab based WHO Risk
Chart
• To use this chart, the following variables should be
available:
History:
– Age: specific numbers between 40 to 74 years. The risk
prediction doesn’t apply for age category out of the specified
range
– Smoking: current smoking
– Sex: Male OR Female
Physical Examination
– Blood Pressure: measured value of the systolic blood pressure
– BMI (Body Mass Index): Calculation of the BMI from weight and
height.
NO LABORATORY MEASUREMNET PARAMETER REQUIRED!
Figure 2: Steps in selecting appropriate Chart for WHO CV risk assessment
Unit 4:
INSTRUCTIONS FOR USING THE WHO
CVD RISK CHARTS
1. Laboratory- based Risk Chart
• These charts are to be used only for
individuals whose status regarding diabetes
and total cholesterol is available.
• Tests for diabetes and cholesterol can be
carried out at the time of assessment.
• If the information on diabetes and total
cholesterol is not available, then refer to the
instructions on use of non-laboratory-based
risk charts
Instructions for using laboratory
based WHO risk Chart
Step by Step Instructions for using laboratory
based WHO risk Chart
Laboratory based WHO risk Chart
Examples :
Table 3: Examples of Laboratory based Risk chart
Patient Demographic
data
Risk factor Profile 10-year risk of
cardiovascular event
(heart attack or
stroke)
Kemal 50 years,
Male
SBP=140 mmHg, TC=270mg/dl (7
mmol/l), non-smoker, no diabetes
Dereje 50 years,
Male
SBP=140 mmHg, TC=270mg/dl (7
mmol/l) non-smoker, diabetes
Kura 50 years,
Male
SBP=140 mmHg, TC=270mg/dl (7
mmol/l) smoker, diabetes
Mesfin 50 years,
Male
SBP=160 mmHg, TC=270 mg/dl (7
mmol/l) smoker, diabetes
NB: The given four patients do have the same age and sex, but risk factor variation will
result in significant change in the 10-year cardiovascular risk prediction. The risk
prediction score will ultimately help the clinicians to decide on life style intervention to
aggressive primary prevention therapy using statins.
2. Non-laboratory-based Who risk charts
• These charts are for the use in settings where
blood glucose and cholesterol cannot be
measured.
• They can also be used to identify people at
high risk who can be taken up for further
investigations.
• Table 2 and Figure 3 present the steps to apply
the non-laboratory WHO CVD risk charts.
Table 4: Instructions for using Non laboratory based WHO risk
Chart
Step by Step Instructions for using Non-
laboratory based WHO risk Chart
Non Laboratory based WHO risk Chart
Examples of Non laboratory based Risk Chart
Patient Demographic
data
Risk factor profile 10-year risk of
cardiovascularevent(heart
attack or stroke)
Rahel 50 years
Female
Nonsmoker, SBP=150 mmHg,
BMI=26Kg/m2
Wossen 60 years
Female
Nonsmoker, SBP=150 mmHg,
BMI=26Kg/m2
Tigist 60 years
Female
Nonsmoker, SBP=180 mmHg,
BMI=26Kg/m2
Tirsit 60 years Smoker, SBP=180 mmHg,
BMI=26Kg/m2
NB: Variations in risk factors affect the risk category
Unit 5:
APPLICATIONS OF WHO
RISK CHARTS
A. For Whom?
• As stated above the WHO risk chart applies for
patients who haven’t been diagnosed to have
cardiovascular diseases like stroke, heart
attack, peripheral arterial or aortic diseases.
• For patients with cardiovascular diseases,
management should include specific disease
management and more intense risk factor
management with life style interventions and
pharmacologic agents.
B. Specific Applications
1. Hypertension( See HTN treatment protocol for details)
– Target blood pressure should be less than 140/90mmHG.
– For patients with high WHO risk (> 10% with non-lab based and
>20% with lab based WHO risk), drug should be started to lower BP
below 130/80 on top of life style intervention
– For patients with BP of 140-159/90-99 mmHG and no end-organ
damage or cardiovascular diseases drug can be started after 3
months trial of life style interventions to keep BP <140/90mmHG
– For any WHO risk level and BP >160/100mmHG drug should be
started to lower BP below 140/90 on top of life style intervention
B. Specific Recommendation
2. Statin Treatment
• Indications
– Patients with high CVD risks (>20% with lab-based and >10
% with non-lab based WHO risk Charts).
– All patients with TC of 324mg/dl or serum LDL of > 190 if
lab is available.
– All diabetic patients older than 40 years should receive
statin regardless of WHO risk level or serum cholesterol
level
Dose: Atrovstatin 20mg/day, Simvastatin 40mg/day for
primary prevention of CV events.
• For patients with previous cardiovascular events double the above
doses.
B. Specific Recommentat..
3. Life style interventions
– All individuals should be encouraged to engage in
healthy life style (see specific topic for details) at any
risk level.
– If CVD risk is < 10% and no CVD risk factors, reassess
CVD risk after 5 years.
– Patients with any behavioral (unhealthy diet, smoking,
excess alcohol intake, sedentary life) and physiologic
risk factors (obese or patients with metabolic
syndrome) should be routinely evaluated for control
of these risk factors and have annual CV risk
assessment.
B. Specific Recommentat
4. For policy makers, Monitoring and
evaluation of CVD interventions
WHO risk can be used for
baseline cardiovascular risk assessment at
national, regional and facility level
 to assess the impacts of CV interventions at
national and subnational levels.
Management guidance for total CVD risk
Management of total CVD risk
Risk <10%  Counsel on diet, physical activity, smoking cessation and avoiding
harmful use of alcohol.
 If risk <5%, follow up in 12 months.
 If risk 5% to <10%, follow up every 3 months until targets are met, then 6–9
months thereafter.
Risk 10% to
<20%
 Counsel on diet, physical activity, smoking cessation and avoiding
harmful use of alcohol.
 Persistent BP ≥140/90 mmHg consider drugs (see below).
 Follow up every 3–6 months.
Risk >20%( or
>10% with Non
lab based WHO
risk)
 Counsel on diet, physical activity, smoking cessation and avoiding
harmful use of alcohol.
 Persistent BP ≥130/80, consider drugs (see below).
 Give a statin.
 Follow up every 3 months. If there is no reduction in cardiovascular risk after six
months of follow-up refer to next level.
Important
practical points
Management of hypertension and diabetes
 For management of hypertension refer National Hypertension Treatment
Protocol
 For management of diabetes mellitus type National Diabetes Treatment
Protocol
Consider drug treatment for following categories:
 All patients with established DM and CVD (coronary heart disease,
myocardial infarction, transient ischaemic attacks, cerebrovascular
disease or peripheral vascular disease), renal disease. If stable, should
continue the treatment already prescribed and be considered as having
risk >20%.
 People with albuminuria, retinopathy, left ventricular hypertrophy.
 All individuals with persistent raised BP ≥160/100 mmHg.
 Consider statin for high risk patients , diabetes, previous cardiovascular
disease and very high cholesterol levels( see above)
Follow-up visits:
 Ask about: new symptoms, adherence to advice on tobacco and alcohol
use, physical activity, healthy diet, medications etc.
 Assess (physical exam).
 Estimate cardiovascular risk.
 Refer if necessary.
 Counsel all and treat as shown in protocol.
• Case Studies on Using WHO Risk Charts:
Case Study 1
• A 65 year old female individual found to have
a weight of 86kg, height of 166cm, BP of
145/80 at one of remote health centers with
no facility for laboratory evaluation.
Questions
– Q1. What further information do you need to
calculate her future CV risk?
• On further inquiry she is found to be non-
smoker and had no previous cardiovascular
problems.
– Q2. Which chart will use to calculate her future
cardiovascular risk?
– Q3. What is her 10 year future CV risk?
– Q4. How do you define her risk level?
– Q5. How will you communicate about the risk level
with the patient?
Case Study 2
• Ato Yalew is a 43year old male teacher at
Bure high school . He was evaluated at Bure
hospital and was found to have a weight of
72kg, height of 174cm, BP of 160/100 . He is
smoker for greater than 10 years. His total
cholesterol was 267mg/dl and his fasting
blood glucose was 98mg/dl
• Q1
Case study 2….
• Q1. What risk factors does Ato Yalew have?
• Q2. Which chart will use to calculate his future
cardiovascular risk?
• Q3. What is his 10 year future CV risk?
• Q4. How do you define his risk level?
• Q5. How will you communicate about the risk
level with the patient?
Case Study 3
• Ato Abdi is a 53year old male farmer living in
one of rural kebles in West Harege Zone . On
examination at Woreda health center he had
a weight of 66kg, height of 168cm, BP of
130/170 . He usually chews chat and smokes
cigarettes . His total cholesterol and FBS
couldn’t be determined.
Case study 3..
• Q1. What risk factors does Ato Abdi have?
• Q2. Which chart will use to calculate his future
cardiovascular risk?
• Q3. What is his 10 year future CV risk?
• Q4. How do you define his risk level?
• Q5. How will you communicate about the risk
level with the patient?
Case Study 4
• W/o Amina is 65 years old woman who was
found to have a weight of 75kg, height of
160cm, BP of 180/100 at one of health
centers in Addis Ababa . She is known to be
diabetic on insulin and her total cholesterol
was 320mg/dl.
•
Case Study 4…
• Q1. What CV risk factors does W/o Amina
have?
• Q2. Which chart will use to calculate her
future cardiovascular risk?
• Q3. What is her 10 year future CV risk?
• Q4. How do you define her risk level?
• Q5. How will you communicate about the risk
level with the patient?
241
Learning Objectives
• Describe the characteristics of Group A Beta
Hemolytic Streptococci
• Describe the epidemiology of GABHS
tonsilopharyngitis
• Explain the difference between viral and GABHS
tonsilopharyngitis
• Outline the diagnostic modality of GABHS tonsilo-
pharyngitis
• Outline the management of GABHS tonsilopharyngitis
• Explain methods of prevention of tonsilopharyngitis
242
Introduction
• Rheumatic fever is an inflammatory disease involving the
joints, skin, heart and brain, which develops following an
untreated or partially treated group A b-haemolytic
streptococcal (GAS) infection of the throat (streptococcal
pharyngitis).
• Up to 30% of sore throats in children and young people are
caused by GAS, and 0.3% to 3% of young people with an
untreated GAS sore throat will develop RF.
• After recovery from the initial episode of RF, up to 60% to
65% of patients develop valvular heart disease and the risk of
RF recurrence following GAS infection rises to 50%.
• Identification and treatment of bacterial sore throat is an
important component of Rheuamtic Fever/Rheumatic Heart
Disease Prevention and Control Program
Tonsilopharyngitis
 Sore throat(Tonsilopharyngitis) is a symptom caused by
inflammation of pharynx, tonsils or other surrounding
structures
 Viral sorethroat is the predominate cause
 Group A beta hemolytic Streptococci is commonest
bacterial cause
20-40% in children
5-15% of sore throat clinic visits in adults
244
Group A Beta Hemolytic Streptococci (GABHS)
245
• Gram-positive, nonmotile,
non–spore-forming cocci
• 0.5-1.2µm in size. in pairs
or chains
• They are negative for
oxidase and catalase.
• Characterized by local
invasion and release of
extracellular toxins and
proteases
Group A Beta Hemolytic Streptococci …
– This organism may cause suppurative disease, such as
pharyngitis, impetigo, cellulitis, myositis, pneumonia, and
puerperal sepsis.
– It also may be associated with nonsuppurative disease, such
as rheumatic fever and Acute Poststreptococcal
Glomerulonephritis.
– Group A streptococci elaborate the cytolytic toxins
Streptolysins S and O.
– Of these, streptolysin O induces persistently high antibody
titers that provide a useful marker of group A streptococcal
infection and its nonsuppurative complications
– M protein fragments of certain serotypes of GABHS are similar
to heart muscle
– Antibodies produced against the bacteria Antigens are affect
the tissue and linked to development heart valve damage.
246
EPIDEMIOLOGY of GABHS
• Humans are exposed to GABHS in the environment
• Humans are the natural reservoir for GABHS
• Mostly spread through droplets of salivary or nasal
secretions
• Overcrowding , poverty, and close contact with
person with streptococcal sore throat are
considered risk factors for transmission
– The incubation period is 2 to 5 days
• Throat and skin are common sites of GABHS
infection
247
EPIDEMIOLOGY of GABHS…
– GABHS infections usually resolve without treatment
however if left uuntreated it can lead to acute
rheumatic fever in some people.
• Antibiotic treatment decreases severity of
symptoms and reduces the risk of transmission to
others after 24 hrs of treatment
• Treatment also decreases the risk of acute
rheumatic fever
• Studies show that ARF associated with GABHS
pharyngitis can be prevented if treatment is
commenced within 9 days of symptoms appearing.
248
Clinical Presentations of Sore Throat
4-1. GABHS pharyngitis
4-2. Viral Pharyngitis
249
4-1.GABHS PHARYNGITIS
 Sudden onset of sore throat
 Pain on swallowing and Fever above
380C
 Headache, nausea, vomiting and
abdominal pain
 Tonsilopharyngeal erythema
 Enlarged tonsils with exudate
 Tender and enlarged anterior cervical
lymph nodes (lymphadenitis)
250
4.2 VIRAL PHARYNGITIS
• Cough , runny nose conjunctivitis
• Hoarseness, coryza
• Anterior stomatitis, discrete intra-oral
ulcerative lesions
• Exanthema, ,diarrhea
• Absence of fever (strongly suggest)
251
Bacterial Vs Viral Pharyngitis
DIAGNOSIS OF BACTERIAL SORE
THROAT
 The diagnosis of streptococcal pharyngitis (GABHS)
can either be clinical only or using clinical criteria
supported by laboratory investigations.
 The gold standard diagnostic method is by using a
Clinical Prediction rule (CPR) supported by rapid
antigen test (RAT) and/or throat culture.
253
THROAT CULTURE
 Not available in all set ups
 Delay in getting results at least 48 hrs.
 Technical errors ( impact on the results)
 Cost of test is high
 Many people are asymptomatic carriers
(10% of school age children).
254
Rapid Antigen Detection Test for
GABHS
Not available
Not validated in Ethiopia
Expensive
255
ASO Titer:
NO role in Acute Tonsilopharyngitis
256
GABHS Diagnosis Clinical Decision Rules (CDR)
Cardinal Clinical features
Symptoms or Signs Points
History of high fever or
(objective record ≥ 38oC)
1
Absence of cough and
rhinorrhea
1
Tender anterior Cervical
adenopathy
1
Tonsillar swelling or exudates 1
Clinical Decision Rule
(CDR)
• ≥ 2 points, treat as
GAβHS pharyngitis
(with antibiotic) ,
• < 2 points, treat as
viral pharyngitis (no
antibiotic
257
Management of Tonsilo-pharyngitis
 Relief of acute symptoms
 Prevention of suppurative and non suppurative
complications
 Reduce communicability
 Pain and fever management (Paracetamol)
258
Antibiotics for GABHS Treatment
First Line:
Benzathine penicillin ( First Line )
Dose:
Wt. < 30kg:600,000 IU stat.
Wt. > 30 kg:1.2 million IU IM stat.
Use Safe BPG Injection Procedures!
Alternative
Amoxicillin
Dose :
Children < 7years: 50 mg/kg per day in three divided doses for
10 days.
Age>7Years: 500mg PO TID for 10 Days
259
Antibiotics for GABHS Treatment…
If Patient allergic to penicillin:
ERYTHROMYCIN
Dose
– Less than 7 years: 250 mg BD for 10 days
– More than 7 years: 500 mg BD for 10 days
260
Why Benzathine Penicillin?
• Single injection
• Better bactericidal effect than oral
• Oral treatment needs 10 whole days to be
effective
• Oral macrolides: clinical improvement but no
eradication of organism.
• Cost effective, evidence based.
• Parents and patients more satisfied.
Is it cost-effective to administer BPG
for all cases of suspected strep sore
throat?
• An overall protective effect for the use of penicillin against
acute rheumatic fever of 80% with an NNT of 60 children
per year to prevent 1 episode of rheumatic fever.
• Mild hypertension: have to treat 800 people per year to
prevent 1 episode of stroke
• The estimated cost of preventing one case of rheumatic
fever by a single monthly intramuscular injection of
penicillin is US$46
• Valve replacement surgery for 1 case of RHD is at least
US$15, 000
• Cardiac surgery only available in S Africa, Ghana and Egypt
Prevention and Health Education
Families should be educated about:
1.The symptoms of GAS pharyngitis.
2 The serious consequences of untreated pharyngitis
i.e. ARF and RHD and the need to consult medical
personnel as early as possible to avoid
complications.
3 The need to avoid pharyngitis by improving house
ventilation and hygiene and avoid crowding.
4. Importance of adherence to a 10 days course of
antibiotics in oral treatment.
Case study
W/O Almaz brought her five years old girl Helen to the
outpatient clinic with acute onset of fever, severe throat,
pain exacerbated by swallowing, headache and abdominal
pain. No runny nose, no cough.
Physical examination: Wt. 20 kg, her temperature was
38.30C axillary, the tonsils were symmetrically enlarged, red
with exudates. She had multiple enlarged painful anterior
neck lymphadenopathies. No other abnormal findings
detected.
264
Questions.
1. What is your clinical diagnosis of Helens’ illness?
2. What tests do you need to reach at a diagnosis?
3. What is the most likely causative organism of her
illness?
4. How would you like to treat Helen?
5. Which of the clinical presentation helps you to
decide about the treatment you are going to give?
6. What is the drug of choice (type, dose and route of
administration)?
7. What other additional Advice do you like to give to
W/O Almaz?
265
Key points
• Group A beta hemolytic streptococcus is one
of the commonest cause of bacterial tonsilo-
pharyngitis.
• Diagnosis should be suspected early and use
clinical decision rule.
• Drug of choice for GABHS is single injection of
Benzathine Penicillin G.
• Families should be educated about identifying
children with sore throat early and contacting
health care workers for 266
End of Unit 1
267
Welcome to
Rheumatic Fever and Rheumatic Heart
Disease Training
for Health Care Workers
Federal Ministry of Health &
College of Health Sciences, Addis Ababa
University
NATIONAL TRAINING ON
RHEUMATIC FEVER/RHEUMATIC
HEART DISEASE FOR HEALTH CARE
WORKERS IN ETHIOPIA
Course Goals, objectives
Goal
To develop critical mass of trained Health Care
Workers at all levels for scale up of RF/RHD
prevention and control services at all levels of
the health care system
Objectives
To have good knowledge and skills on:
• Diagnosis and management of bacterial tonsilo-
pharyngitis
• Diagnosis and management of acute rheumatic fever
• Safe administration of Benzathine penicillin
• Diagnosis and management of Rheumatic Heart
Disease (RHD).
• Monitoring and evaluation of RHD Program
ARF/RHD Training Package
• ARF/RHD Participants’ Manual
• ARF/RHD Facilitator Manual
• Power point presentations
• Algorithms and Treatment Protocols
• RHD Intake and Follow up form
• RHD Client Passport
• RHD Register
• Client education Materials
Training Approaches
• Mastery Learning
• Competency based
• Participatory
• Training/Learning Methods
–Illustrated lectures and group discussion
–Individual and group exercises
–Role plays
–Demonstrations using check lists
–Case studies
Introduction of participants and facilitators
–Name
–Current station
–Profession
–Service years
–Expectations(be specific)
Ground Rules
• Participation
• Time
• Energizer
• Mobile
• Discussions/side
• Recap
Information
• Rest room
• Administrative Issues
A healthy throat, a healthy heart for
us all!
277
Unit 2:
Acute Rheumatic Fever
• To know about the epidemiology of ARF
• To understand the pathogenesis of ARF
• To know about the clinical features of ARF
• To learn about the diagnosis of ARF
• To understand management of ARF
• To know about the prevention of ARF
• To discuss the principles of management of ARF
LEARNING OBJECTIVES
• ARF is a post infectious, non-suppurative sequel of
pharyngeal infection with Streptococcus pyogenes
• RHD is the only long-term sequel of ARF
• RHD manifests after several years of ARF with heart
failure or complications like stroke or infective
endcocarditis.
• ARF and RHD can easily be prevented by early
identification and treatment of streptococcal
pharyngeal infection.
• Currently, the 2015 AHA/ACC criteria are used to
diagnose ARF
Introduction
• Rheumatic heart disease currently affects over 33
million people worldwide.
• RHD is found all over the world, but most commonly
affects women, adolescents and children living in
conditions of poverty and overcrowding.
• RHD kills 275,000 people every year, even though it is a
preventable disease.
• A few rich countries (including the USA and UK) and
some LMIC Countries like Cuba have managed to reduce
their burden of RHD, but other countries continue to
struggle with the disease.
• RHD is a lifelong condition, which is often fatal if not
treated properly.
EPIDEMIOLOGY
RHD in Ethiopia
• Recent school and community based studies in
Ethiopia have shown the prevalence of RHD in 4-24
years age groups to be from 14-38/1000,which is
one highest in the world.
• Approximately 250, 000 people in the age group 5-
15 suffer from RHD in Ethiopia.
• More than 500,000 people of all age groups live
with RHD.
• Only few give history of Acute Rheumatic Fever
• RHD is the main cardiovascular diagnosis
accounting for 30-60% of all cardiac patients in
main hospitals of Ethiopia
• Patients usually come late with heart failure ,
stroke or during pregnancy with severe valvular
disease
• Mortality from RHD may reach 12.5% every year in
rural Ethiopia.
• It is also reported that 70% of RHD patients die before
the age of 26 years.
RHD in Ethiopia…
Risk Factors for Rheumatic Fever
• Socioeconomic status:
– Poverty
– Poorly made and overcrowded housing
– Lack of adequate health care
– Untreated GAS infections
• Sex
• Rheumatic fever occurs in equal numbers in males and
females, but the prognosis is worse for females than for males.
• Age
– Rheumatic fever principally affects children between 5-15
years of age with a median age of 10 years, although it also
occurs in adults (20% of cases).
• Risk factor for RHD
– Recurrent ARF
Risk factors for Rheumatic Fever
Determinants Effects Impact on ARF and RHD
burden
Socioeconomic &
environmental factors
1. Poverty
2. Poor nutrition
3. Overcrowding
4. Poor standard of living
1. Rapid spread of
GABHS
2. Difficulties accessing
health care
1. Higher incidence of acute strep
pharyngitis and complications
2. Higher incidence of ARF and
recurrent ARF
Health System Related Factors
1. Shortage of resources for
health care
2. Low level of knowledge of
disease among health care
providers
3. Low level of awareness of
disease in the community
1. Inadequate diagnosis
and treatment of strep
pharyngitis
2. Misdiagnosis or late
diagnosis of ARF
3. Inadequate secondary
prophylaxis delivery
1. Higher incidence of ARF and
recurrent ARF
2. Missed first ARF episode
3. Inadequate secondary prophylaxis
delivery
4. Higher rates of recurrent ARF with
more frequent and severe heart valve
involvement
5. Higher rates of repeated hospital
admissions and expensive heart
valve surgery
• Rheumatic fever is thought to result from an
inflammatory autoimmune response with antibodies
produced against streptococcal antigen induces
inflammation in host tissue having similar molecules
(ANTIGEN MIMICKERY THEORY)
• Only group A beta-hemolytic streptococcal infections
of the pharynx initiate or reactivate rheumatic fever.
• In 0.3-3% of streptococcal pharyngeal infection,
rheumatic fever develops several weeks after the sore
throat has resolved.
• Studies show the existence of genetic predisposition in
addition to bacterial factors.
Etiology and Pathogenesis
Etiology and Pathogenesis…
• After recovery from the initial episode of RF, up
to 60% to 65% of patients develop valvular heart
disease and the risk of RF recurrence following
GAS infection rises to 50%.
• Repeated GAS infections without appropriate
treatment (with benzathine penicillin G) leads to
RF recurrences and progressive valve damage-the
defining characteristic of RHD which can, in turn,
cause atrial fibrillation, heart failure, stroke and
endocarditis.
Pathogenesis of Acute Rheumatic Fever
Cascade of RF and RHD
Pathogenesis of Acute Rheumatic Fever …
Clinical Features
• Following sore throat with GABHS:
– Silent period of 2 - 6 weeks
– Sudden onset of fever, pallor, malaise, fatigue
• After which characteristic manifestations rheumatic fever
start to appear:
– Arthritis
– Carditis
– Erythema marginatum
– Subcutaneous nodules
– Sydenham’s chorea
• In one third of patients the streptococcal infection passes
unnoticed and 54 to 70% of recurrences of ARF were
caused by asymptomatic streptococcal infection.
Clinical Manifestations
1. Arthritis
• It occurs in about 75% of cases.
• Usually a polyarthritis involving big joints: knees,
ankles, elbows, wrists
• Asymmetrical
• Migratory (fleeting)
• Joints are hot, red, tender, swollen with limited
mobility
• It is unusual to involve the central joints as spines,
hips and the peripheral ones as the fingers and
toes. Infrequently it involves the
tempromandibular joint.
Arthritis…
• No residual deformity (licks)
• It is more common and more severe in
teenagers and young adults than in children
• Lasts 2-6 weeks
• Dramatic response to salicylates
2. Carditis
• Occurs in 40% of patients during the first attack
and almost 100% if ARF recurs.
• It may be the only major manifestations and
usually appears in the first week of the illness.
• Most serious manifestation
• May lead to death in acute phase or at later stage
• Any cardiac tissue may be affected
• Valvular lesion most common: mitral and aortic
• Seldom see isolated pericarditis or myocarditis
Pancarditis is the most serious and second most
common complication of rheumatic fever (50%).
In advanced cases, patients may complain of
dyspnea, mild-to-moderate chest discomfort,
pleuritic chest pain, edema, cough, or orthopnea
if they develop congestive heart failure and
pericarditis.
Upon physical examination, carditis is most
commonly detected by a new murmur and
tachycardia out of proportion to fever.
The murmurs of acute rheumatic fever are
typically due to valve insufficiency.
Carditis….
Carditis..
• Clinical signs:
High pulse rate
Murmurs : Mitral and aortic regurgitation most
common
 Pericarditis usually asymptomatic
 Occasionally causes chest pain, friction rubs or distant
heart sounds
 Cardiomegaly
 Rhythm disturbances (prolonged PR interval)
 Heart failure
Clinical Features of Carditis
3. Sydenham’s Chorea(10-20%)
• Due to basal ganglia involvement.
• May be associated with normal laboratory findings.
• Involuntary, sudden, semi-purposeful movements of
limbs face and tongue. Disappear during sleep.
• Hypotonia and hyporeflexia.
• Emotional labiality and instability.
• More in females.
• Latent period (2-6 months). No arthritis and ESR is
usually normal.
• Self-limiting.
Chorea..
4. Subcutaneous Nodule
– Small, painless, firm, free.
– Accumulated Aschoff nodules.
– Over bony prominences,
tendons .
– Often associated with severe
carditis.
– Can occur with other diseases
like rheumatoid arthritis
– They last for a week or two and
rarely more than a month, and
sometimes disappear within
several days.
5. Erythemia Marginatum (10%)
– Erythema with central pallor.
– More on trunk and proximal
limbs.
– It usually occurs in the covered
parts and may be manifested by
local application of heat.
– Nonpruritic, nonpainful.
– Often associated with acute
carditis.
– They disappear within hours and
may appear intermittently
within weeks to months
Clinical manifestations of ARF
Laboratory findings in ARF
1. Elevated acute phase reactants
1. Erythrocyte sedimentation rate(>30mm/hr)
2. Leukocytosis
3. C-reactive protein
2. Recent Evidence of Group A Streptococcal infection :
– Raised ASO titer (80% of cases)
– Anti DNAase B
– Antihyaluronidase
– Rapid Stretococcal antigen test.
– Positive throat culture for (GAS),
– Recent scarlet fever
3. Increased PR interval on EKG (first degree heart block )
Imaging
• Cardiomegaly and signs of Heart failure on
Chest x-ray
• 2D and Doppler Echocardiography
– To identify and assess severity of carditis
Diagnosis of ARF
• No specific diagnostic test for ARF
• Diagnosis is based on 2015 AHA/ACC with
constellation of major and minor
manifestations used as diagnostic criteria
• For diagnosis of ARF the evidence of recent
streptoccal infection should be demonstrated
in addition to the criteria.
Revised Jone’s Criteria for Diagnosis of ARF
(2015 ACC/AHA )
Evidence of preceding group A streptococcal infection (other than chorea):
 Raised ASO titer ,OR
 Positive throat culture for GABH,OR
 Positive Rapid antigen test, OR
 Clinical evidence of bacterial Tonsilo-pharyngitis
Diagnosis : Initial ARF 2 major or 1 major plus 2 minor manifestations PLUS evidence of
recent strep infection (other than chorea)
Recurrent ARF
2 major or 1 major and 2 minor or 3 minor PLUS evidence of
recent strep infection(other than chorea)
Criteria
A. Major B. Minor
 Arthritis (Monoarthritis or
polyarthritis or polyarthralgia)a
 Monoarthralgia
 Carditisb (Clinical and/or subclinical)  Fever (≥38°C)
 Chorea  ESR ≥30 mm/h and/or CRP ≥3 mg/dLc
 Erythema marginatum  Prolonged PR on ECG (for age) (unless carditis is a
major criterion
 Subcutaneous nodules
Diagnostic Classes of New ARF
Definite ARF: 2 major, or 1 major plus 2 minor
manifestations PLUS evidence of recent strep
infection (other than chorea)
Highly Probable ARF: If an ARF diagnosis is
considered highly probable (but not confirmed due
to lack of evidence for recent streptococcal infection)
Uncertain ARF: in patients from high-risk groups with
only one major manifestation of acute Rheumatic
fever or borderline echocardiographic findings .
Treatment for ARF
• Admission to hospital
–Admit all patients suspected to have ARF
• Confirmation of the diagnosis:
–Observation prior to anti-inflammatory
treatment: paracetamol may be given for
fever or joint pain
–Investigations: CBC,ESR,CXR,ECG,
Echocardiography
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Epidemiology, pathogenesis of asthma(1).pptx

  • 1.
  • 2. LEARNING OBJECTIVES By the end of this unit the participants will be able to – Discuss the definition and clinical characteristics of asthma – Review the signs and symptoms of asthma – Discuss current asthma epidemiology – Explain current asthma pathogenesis – Assess and diagnose asthma using clinical criteria – Demonstrate competence in the clinical assessment of suspected case of asthma including case history and clinical examination – Demonstrate correct use of a peak expiratory flow meter and interpret the results.
  • 3. DEFINITION OF ASTHMA: – 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. • GINA 2020 – Symptoms are associated with variable expiratory airflow, i.e. difficulty breathing air out of the lungs due to: • Bronchoconstriction (airway narrowing) • Airway wall thickening • Increased mucus
  • 4. Asthma Epidemiology o One of the most common disease worldwide. o Most common chronic disease in children. o Worldwide:  334 million people currently suffer from asthma,  Prevalence rates are increasing.  250,000 deaths each year  Over 80% of asthma deaths occur in low and middle-income countries • Asthma Global Report 2019
  • 5. Asthma Epidemiology – The prevalence of asthma in affluent countries  has risen over the last 30 years but  now appears to have stabilized,  with 10 - 12% of adults and 15% of children affected by the disease. – In developing countries where  the prevalence of asthma had been much lower,  there is a rising prevalence,  associated with increased urbanization.
  • 6. Asthma in Ethiopia o The prevalence of asthma is estimated between 1.5-3.0% of the population (3 million people) o 10 x prevalence of TB. o According to the latest WHO data ( 2018):  Asthma deaths in Ethiopia reached 4,485 or 0.73% of total deaths.  Age adjusted death rate 8.35/100,000 population  Ethiopia ranks #61 in the world in terms of asthma deaths.
  • 7. Asthma in Ethiopia – ISAAC Study :In Ethiopia, larger community-based prevalence studies done among school children in Addis Ababa, Jimma and Gondar  Prevalence of asthma was between 2 % and 4 %.  The 12-month prevalence of self-reported wheezing was found to be 10.7% and 16.2% in Addis Ababa and Gondar respectively. – Asthma prevalence was lower in rural compared to urban areas. – Use of ICS /Combination therapy in Ethiopia study;  4% in Jimma University Hospital  32% in Tikur Anbessa Hospital. – The Asthma Control rate was only 28.6% in patients from Jimma University Hospital.
  • 8. Definition of Severe Asthma o There is no universally accepted definition of severe asthma. o Severe asthma is not a single disease as evidenced by the variety of clinical presentations, physiologic characteristics, and outcomes. o 5-10% of all asthmatics may have severe disease. o Severe asthma is responsible for up to 50% of the total asthma related health care costs.
  • 13. Cause of Asthma – Heterogeneous disease with interplay between genetic and environmental factors – Several risk factors that predispose to asthma have been identified – These should be distinguished from triggers, which are environmental factors that worsen asthma in a patient with established asthma
  • 14. Risk factors and Triggers involved in Asthma
  • 15. Pathogenesis & Pathophysiology of Asthma – Airflow limitation in asthma is recurrent and caused by a variety of changes in the airway – These include: Bronchoconstriction, Airway edema, Airway hyperresponsiveness – Airway hyper-reactivity (AHR) – the tendency for airways to narrow excessively in response to triggers that have little or no effect in normal individuals – is integral to the diagnosis of asthma and appears to be related to airway inflammation as shown in the figures below.
  • 16. Current Paradigm of Asthma Immunology
  • 17. Pathogenesis of Asthma Genetic Predisposition Environmental Factors
  • 18.
  • 20. Asthma Diagnosis – History  Paroxysms of cough, wheezing, difficulty of breathing and chest tightness  History of allergic diseases( Rhinitis, eczema)  Family history of Asthma – Physical examination(Respiratory distress, Wheezing..) – Pulmonary Function test(PEAK flow /Spirometry – Positive allergy test – Increased IgE – CBC, CXR, Sputum examination for excluding infection and complication
  • 21. Diagnosis of asthma – symptoms Increased probability that symptoms are due to asthma if: Decreased probability that symptoms are due to asthma if:  More than one type of symptom (wheeze, shortness of breath, cough, chest tightness)  Symptoms often worse at night or in the early morning  Symptoms vary over time and in intensity  Symptoms are triggered by viral infections, exercise, allergen exposure, changes in weather, laughter, irritants such as car exhaust fumes, smoke, or strong smells  Isolated cough with no other respiratory symptoms  Chronic production of sputum  Shortness of breath associated with dizziness, light-headedness or peripheral tingling  Chest pain  Exercise-induced dyspnoea with noisy inspiration (stridor)
  • 22. Asthma Diagnosis-Physical Examination – Physical examination in people with asthma  Often normal  The most frequent finding is wheezing on auscultation, especially on forced expiration – Wheezing is also found in other conditions, for example:  Respiratory infections (Viral)  COPD  Upper airway dysfunction  Endobronchial obstruction  Inhaled foreign body – Wheezing may be absent during severe asthma exacerbations (‘silent chest’)
  • 23. Diagnosis of asthma in Ethiopia based on level of care Divided in to two levels:  Asthma diagnosis at Primary Health Care unit  Asthma Diagnosis at General Hospital and Above level
  • 24. Diagnosis of asthma at Primary Health Care Unit
  • 26. PEAK Expiratory Flow Meter in Asthma Diagnosis – USE OF PEAK EXPIRATORY FLOW METER IN ASTHMA  Peak expiratory flow (PEF) meters are handheld devices designed as personal monitoring tools.  Currently WHO recommend to use PEF for diagnosis of asthma in LMIC where there is no spirometry services  A peak flow meter measures how fast air can be blown out of the lungs.  NB: PEAK flow may under diagnose asthma
  • 27. USE OF PEAK EXPIRATORY FLOW METER IN ASTHMA Figure 1a: Example of hand held Peak flow meter Figure 1b: How to Measure PEF using a peak flow meter Figure 1c. Calculating percentage reversibility of PEFR
  • 28.
  • 29. USE OF PEAK EXPIRATORY FLOW METER IN ASTHMA – A change in PEF of at least 20%, is accepted as being consistent with asthma. – PEF values less than 200 L/min indicate severe airflow obstruction.  PEF can establish peak flow variability, quantify asthma severity, and provide both patient and clinician with objective measurements on which to base treatment decisions.  It is affordable means of support in the diagnosis of asthma in the primary health care level.  The standard however in the diagnosis of asthma is with the support of spirometry.
  • 30. Asthma Diagnosis at General Hospital and Above level – Features to make the diagnosis of Asthma as mentioned above – Evidence of variable expiratory airflow limitation – Document that variation in lung function is greater than in healthy people – The standard however in the diagnosis of asthma is with the support of spirometry
  • 31. Spirometry – Spirometry performed at least once documenting  Ratio of Forced Expiratory Volume in the first second (FEV1) to Forced Vital Capacity (FVC)(FEV1/FVC) is below 70% (below the limit of normal)  An increase of FEV1 by > 200ml and > 12% from the base line value after inhaling a bronchodilator  FEV1 increases by more than 12% and 200ml from baseline (in children, by >12% of the predicted value) after 4 weeks of anti- inflammatory treatment – In occasions where spirometry test is normal but the patient has the typical symptoms, bronchial challenge test can exclude the diagnosis of asthma.
  • 32. Spirometry – A fall in FEV1 from baseline of ≥20% with standard doses of methacholine challenge performed in a controlled setting demonstrates variability in expiratory airflow limitation which could not be evidenced by office spirometry test. – The other safer alternative is trial of treatment and asses the change in FEV1 post treatment. – Increase of FEV1 by 12% and 200 ml from baseline after 4 weeks of anti-inflammatory treatment, outside of recent respiratory illnesses, confirms significant variability.
  • 33. Spirometry Figure 2; Office Spirometry Machine
  • 34. Asthma diagnosis at General Hospital & above
  • 35. Case study 1 (30 min) • A 25 years old house wife presented with recurrent five months history of night time and morning productive cough of whitish sputum associated with low grade fever and running nose in the last three days. Discussion points: • What additional information would you like to get? • Possible differential diagnosis? • How do you make the diagnosis of this case?
  • 36. Summary: – Asthma is a major cause of illness and death in Ethiopia and the rest of the world. – Asthma causes symptoms of wheezing, coughing and shortness of breath. – There is usually a life long history of asthma, or at least a history from childhood. – Asthma is often associated with allergies or allergic conditions such as allergic rhinitis or eczema. – The symptoms of asthma are usually variable. The variation may be within the day, from day to day or depending on the seasons. – Asthma is a often clinical diagnosis in low & middle in come countries (LMIC). – In the absence of spirometry test peak flow meter can be used as diagnostic test for asthma in primary health care setup.
  • 37. Summary: – Asthma is a chronic disease causing inflammation of the airways with an unknown cause. – Asthma requires long term treatment to control the chronic inflammation in the airways. – If asthma inflammation is not controlled the airways become hypersensitive and to become narrowed. – The asthma patient can have exacerbations which cause wheezing, coughing, breathlessness and chest tightness. – Infections, allergens, irritants and exercise can all trigger asthma exacerbations.
  • 38. We would like to thank Dr Amsalu Bekele, Dr Rahel Argaw, Dr Hanan Yusuf and Dr Tewodros Haile for preparing this powerpoint
  • 39.
  • 40. MANAGEMENT OF ASTHMA IN ADULTS AND ADOLESCENTS ≥ 12 YEARS OF AGE
  • 41. Learning objectives – By the end of this unit, the learner should be able to:  Describes the goals of asthma management  Assess severity of asthma  State criteria for diagnosis of severe asthma  Describe means of minimizing or avoiding precipitating factors  List the main groups of asthma medications  Describe asthma management based on control  Describe the supportive care for acute severe asthma management  Identify patient who need referral to specialist.
  • 42. Goal of Asthma Management – Avoid troublesome symptoms during the day and night – Need little or no reliever medication – Have productive, physically active lives – Have normal or near-normal lung function – Avoid serious asthma flare-ups (also called exacerbations, or severe attacks).
  • 43. Goal of Asthma Management – Achieving these goals requires a partnership between patient and their health care providers  Ask the patient about their own goals regarding their asthma. Shared decision-making is associated with improved outcome  Good communication strategies are essential  Consider the health care system, medication availability, cultural and personal preferences and health literacy  Take every opportunity to assess patients, particularly when they are symptomatic or after a recent exacerbation
  • 44. Asthma control – Asthma control –Has two main domains  Assessment of symptom control over the last 4 weeks  Assessment of risk factors for poor outcomes
  • 45. Assessment of Asthma control (In the Past 4 weeks) 1. Symptom control assessment Level of asthma symptom control  In the past 4 weeks, he/she had: Well Partly controlled Uncontrolled  Daytime asthma symptoms for more than twice/week?  Yes No none 1-2 of these 3-4 of these  Any activity limitation due to asthma?  Yes No  Reliever needed* more than once a week?  Yes No  Any night waking or night coughing due to asthma?  Yes No 
  • 46. Asthma Control Inflammation Direct or Indirect Lung Function Utilization of Healthcare Resources Functional Status Missed Work and/or School Patient Self-Report of Control Daytime Symptoms Nighttime Awakenings Use of a “Quick Relief” Inhaler and/or Nebulizer How should control be measured in asthma? Adapted with permission from Chipps BE, Spahn JD. J Asthma. 2006;43:567-572.
  • 47. Assessment of risk factors for poor outcomes (In the past 12 months) 2. Assessment of risk factors for poor outcomes Risk factors for exacerbations  Uncontrolled asthma symptoms Additional risk factors, even if the patient has few symptoms  High SABA use (≥3 canisters/year)  Having ≥1 exacerbation in last 12 months  Incorrect inhaler technique and/or poor adherence  Smoking  Obesity, chronic rhinosinusitis, pregnancy, blood eosinophilia, low socioeconomic status, depression, anxiety Risk factors for fixed airflow limitation include  Lack of Inhaled Corticosteroid (ICS) treatment, smoking, occupational exposure, mucus hypersecretion, preterm birth, low birth weight. Risk factors for medication side effects include  Frequent Oral corticosteroid (OCS) use, high dose and /or potent ICS, some drugs that decrease steroid metabolism, poor inhaler technique
  • 48. Principles of asthma management 1. Asthma management of patients not on treatment or for first time presenters – For patients presenting with acute symptoms, follow the algorithm for management of asthma exacerbation – For patients with indolent but variable symptoms once the diagnosis is confirmed, assess for any risk for poor outcome – Patients with any risk factor for poor outcome are eligible to start higher dose of controller therapy and based on response/control of asthma, treatment
  • 49. Principles of asthma management cont… 2. Management of asthma among patients on pharmacologic treatment – Assess for asthma control in each visit and determine asthma severity based on the level of step needed to control the symptoms • Mild asthma – Control achieved with step 1 or 2 medications • Moderate asthma – Step 3 management is required to control asthma • Severe asthma- Steps higher than 3 are needed for control – Reassess for risk factor for poor outcome
  • 50. Asthma management for Adults and Adolescents 12 years and above at PHC in Ethiopia Step 1. Low dose inhaled Beclometasone 100µg taken whenever Inhaled Salbutamol (SABA) is needed. Step 2a. Standing dose of daily Beclometasone inhaler 100µg (1 puff) BID plus Salbutamol puff when needed. Step 2b. Standing dose of daily Beclometasone inhaler 200µg (2 puffs ) BID plus Salbutamol puff when needed. If total daily dose of Beclometasone is more than
  • 51. During initial presentation • Start in step 1 – Symptoms less than twice per month • Start with Step 2 – Symptoms twice a month or more, but less than daily
  • 52. Asthma management for Adults and Adolescents above 12 years at General hospital & above in Ethiopia Steps 1 and 2 – Refer management for PHC Step 3. Standing dose of Low dose Budesonide - Formoterol combination (160/4.5µg) one puff BID OR Standing Medium dose of Beclomethasone 400µg (4 Puffs of 100µg) BID alone OR Low dose Beclomethasone 200µg (2 puffs) BID + Monteleukast 10mg po daily OR Low dose Beclomethasone 200µg (2 puffs) BID +Theophylline 10mg/kg
  • 53. Asthma management at General hospital & above in Ethiopia Step 4. Medium dose Budesonide- Formoterol combination (160/4.5µg) two puffs BID OR High dose Beclomethasone 600µg puffs BID (200µg of beclomethasone 3 puffs BID) + Monteleukast or Theophylline Step 5. High dose Budesonide-Formoterol combination (160/4.5µg) three puffs BID OR
  • 54. During initial presentation • Start with Step 3 if : – Symptoms most days, or waking with asthma once a week or more • Start with step 4 if : – Symptoms most days, or waking with asthma once a week or more, and low lung function
  • 55. Reliever Therapy • The preferred reliever therapy for those on standing dose of Budesonide- Formoterol is the use of the same combination of low dose ICS- formoterol (SMART) as-needed based. • Maximum Total Daily dose of Formoterol should not exceed 72μg. • Alternative reliever is Salbutamol puff as needed
  • 56. Asthma control – Follow the continuous control-based asthma management cycle: –Assess symptom control + risk factors –Adjust treatment (pharmacological and non- pharmacological) –Review the response: symptoms, exacerbations, side effect
  • 57. Reviewing Response and Adjusting treatment  Stepping up asthma treatment;  Sustained step-up, for at least 2-3 months if asthma poorly controlled;  Short-term step-up, for 1-2 weeks, e.g. with viral infection or allergen;  Day-to-day adjustment;  For patients prescribed low-dose ICS/formoterol maintenance and reliever regimen
  • 58.  Stepping down asthma treatment;  Consider step-down after good control maintained for 3 months.  Find each patient’s minimum effective dose that controls both symptoms and exacerbations without the development of adverse effects.  Stopping ICS often leads to potentially dangerous worsening of asthma.
  • 59.
  • 60. Asthma medication and common side effects – SABAs- Short acting beta agonists bronchodilators  Should be the main therapy only during acute exacerbations but  NOT recommended as a stand-alone therapy except in pediatric age group – LABAs- Long acting beta agonists  Provide bronchodilation for up to 12 hours after a single dose.  Salmeterol and formoterol are the LABAs available for asthma in combination with ICS.  Formoterol has similar duration of action with salmeterol but bronchodilation with formoterol is significant within minutes of inhalation, maximal within 2 hours
  • 61. Cont… – Inhaled Corticosteroids (ICS)  Preferred, first-line controller agents for all patients especially for those at risk for poor outcome  Most patients with asthma don’t need high dose, at a group level, most of the benefit is obtained at low dose.  Have few side effects at standard treatment doses.  Local side effects include oral candidiasis, dysphonia, reflex cough and bronchospasm.  High dose ICS and long-term use of oral steroids predisposes to systemic side effects which includes adrenal suppression, osteoporosis, skin thinning, easy bruising, diabetes, hypertension, infections, glaucoma
  • 62. Theophylline  Provides mild bronchodilation in asthmatic patients. Has also weak anti-inflammatory and immunomodulatory properties  Theophylline use needs to be monitored closely owing to  The medication’s narrow therapeutic-toxic range,  Individual differences in metabolism, and  The effects of many factors on drug absorption and metabolism.  At therapeutic doses, potential adverse effects include  Insomnia, aggravation of dyspepsia ,GERD, and urination difficulties in men with prostatic hyperplasia.  Dose-related toxicities include :
  • 63. Leukotriene antagonist(LTRA) – Leukotriene receptor antagonists (LTRA) are less effective than ICS particularly for exacerbations.; – Used as add on for  Patients who experience intolerable side-effects from ICS; or  For patients with concomitant allergic rhinitis. – Before prescribing montelukast (adult dose 10 mg once daily), health professionals should counsel
  • 64. Inhaled corticosteroids (ICS) and Combinations for Adults and adolescents (≥12 years) Inhaled corticosteroid Total daily dose (mcg) Low Medium High Beclomethasone dipropionate (HFA) 200–500 500–1000 >1000 Fluticasone/salmeterol (DPI) 100/50 250/50 500/50 Budesonide (DPI) 200-400 400-800 >800 Mometasonefuroate (HFA-pMDI) 200-400  400 NB: DPI-Dry Powder inhaler, MDI -Metered dose inhaler CFC-Chloroflourocarbon HFA-Hydroflouroalkane *When Budesonide/formoterol is prescribed as maintenance and reliever therapy, the maximum recommended dose of formoterol in a single day is 72 mcg.
  • 65. Non-Pharmacological Strategies and Interventions for asthma management – Reduce indoor air pollution by cooking outside or using smokeless cooking stoves – Avoid allergens that the patient is sensitive to – Avoidance of tobacco smoke exposure – Occupational asthma – Encourage Physical activity – Avoid medications that may worsen asthma – Remediation of dampness or mold in homes
  • 66. Patients with poor asthma control should be assesses for the following – Reasons for poor adherence and misunderstanding the difference between relievers and controllers – Poor inhaler technique – Exposure to trigger factors at home and work – Presence of gastro-esophageal acid reflux disease (GERD) – Rhinitis and sinusitis – Use of medications that may aggravate asthma such as aspirin, non-steroidal anti-inflammatory drugs and ß blockers – Other medical conditions mimicking asthma symptoms (e.g. cardiac disease).
  • 67. Case study 2 (30 min) • A 30 years old man came with history of cough for 1 month. The cough is Productive of whitish sputum and phlegm in the morning, it is worse at night, day and better during the day. He feels shortness of breath during the day when he goes upstairs. His mother is asthmatic. He is a banker and used to have sneezing and running nose whenever he counts money. He has no night Sweating, weight loss, or fever no chest pain, no pedal Edema, or Orthopnea. Physical findings show no distress but has wheezing in the chest bilaterally. • What is the most likely diagnosis? Differentials? • How do you classify the severity of patient? • How do you manage this patient?
  • 68. Summary – Asthma is a chronic inflammatory disorder of the airway, persistent asthma is most effectively controlled with daily long-term control medication directed toward suppression of airway inflammation. – A stepwise approach to pharmacologic therapy is recommended to gain and maintain control of asthma in both the impairment and risk domains. – Asthma treatment should contain appropriate controller medicines with as needed reliever.
  • 69. • We would like to thank – Dr. Amsalu Bekele, Dr Hanan Yusuf, Dr Tewodros Haile and Dr Rahel Argaw for preparing this powerpoint
  • 70.
  • 71. Definition • 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, i.e. they represent a change from the patient's usual status that is sufficient to require a change in treatment.
  • 72. • Definition based on combination of symptom, clinical findings and lung function is more objective in assessing severity. • A minority of patients perceive airflow limitation poorly and can experience a significant decline in lung function change in symptoms. This especially affects patients males with a history of near fatal asthma.
  • 73. Assessment of risk The prevention of exacerbations is the most important aim for patients with asthma and healthcare professionals. In order to achieve this aim, it is important to plan the re-assessment of asthma patients and treatment adjustments because of the immediate risks (i.e. acute respiratory failure, death) and future risks (recurrence of exacerbations, decline in lung function, and side-effects of treatments)
  • 74. • Factors which are associated with exacerbation 1) the level of asthma control, 2) asthma severity based on ERS/ATS definition, 3) lung function, 4) the presence of comorbidities, 5) the psychosocial status (to assess the ability to seek help in case of clinical worsening), 6) previous history of near fatal attacks and 7) response to treatment. • Such factors seem important in guiding treatment decisions and, importantly, decisions regarding hospitalizations.
  • 75. Triggers of exacerbation • Indoor allergens – House dust mites in bedding, coach roach eggs carpet, stuffed furniture, pollution and pet dander • Outdoor allergen – Pollen, molds • Tobacco smoke • Chemical irritants in workplace • Cold air and physical exercise • Certain medications, such as aspirin, NSAID
  • 76. Classification of asthma severity & management • Mild • Moderate • Severe • Very severe
  • 77. DEGREE OF SEVERITY SYMPTOMS AND SIGNS INITIAL PEF (OR FEV1) CLINICAL COURSE Mild Dyspnea only with activity (assess tachypnea in young children) PEF ≥ 70 percent of predicted or personal best Usually treated at home Prompt relief with inhaled short-acting beta2 agonist Possible short course of oral systemic corticosteroids Moderate Dyspnea interferes with or limits usual activity O2 saturation 90-95% PEF 50-69 percent of predicted or personal best Usually requires office or emergency department visit Relief from frequent inhaled short-acting beta2 agonist Oral systemic corticosteroids; some symptoms last for one to two days after treatment begins
  • 78. Self management of exacerbation • Severe exacerbations are potentially life threatening and their treatment requires careful assessment and monitoring by health care professionals. • A careful written asthma action plan helps patients to recognize and respond appropriately to worsening of symptoms. • The criteria for initiating an increase in controller medication will vary from patient to patient.
  • 80. ICS-Formoterol • For patients with mild asthma prescribed as-needed combination low dose ICS-formoterol, increasing the as-needed doses of ICS-formoterol when asthma worsens reduces the risk of severe exacerbations requiring OCS by 2/3rd compared to SABA-only treatment. However the benefit is achieved when initiated at the early stage of worsening asthma.
  • 81. ICS • For patients with maintenance-only ICS containing treatment should generally be increased if asthma symptoms are interfering with normal activities, or PEF has fallen by >20% for more than 2 days. Possible options – Temporarily doubling ICS dose (delay of 5-7 days may contribute to failure) – Age >16 years quadrupling ICS dose can reduce use of OCS.
  • 82. OCS Short course of 40 mg prednisolone for 5 days with instructions can be tried if: – Fail to respond to an increase in reliever and controller medication for 2-3 days – Deteriorate rapidly or who have a PEF or FEV1< 60% of their personal best or predicted value. – Have a history of sudden severe exacerbations.
  • 83. Follow up after outpatient management • Ideally before ceasing oral corticosteroids if prescribed. • Maintenance controller treatment can generally be resumed at previous levels 2-4 weeks after exacerbation, unless the history suggests that the exacerbation occurred on a background of long-term poorly controlled asthma. • In this situation use this opportunity to train inhaler technique, check adherence and provide additional asthma education. • After checking technique and adherence a step up in
  • 84.
  • 85. First Line Therapy at PHC 1. Prednisolone 30-40 mg per day for five days for adults initiated within one hour of presentation AND 2. Salbutamol four- six puffs by metered dose inhaler and by spacer every 20 minutes for one hour 3. Oxygen supplementation if saturation is below 90%.
  • 86. Second Line treatment at General Hospital and above • Increase frequency of dosing via metered dose inhaler and spacer or give salbutamol by continuous nebulization at 5-10 mg per hour. • Add nebulized ipratropium, if available • Continue steroid therapy • IV magnesium sulfate (2g infused over 20 minutes) • IV theophylline or Aminophylline
  • 87. Review • Patient’s response after discharge (within a week) • Patient’s understanding of the cause of their asthma • Modifiable risk factors for asthma • Understanding of correct uses of medications • Adult and adolescent patients with more than 1-2 exacerbations per year despite more than Step 3 therapy should be referred to a specialist.
  • 88. Part II Asthma education
  • 89. Goals of asthma education • An explanation of the nature of asthma and its inflammatory basis • A description of the different classes of drugs and their purpose in treatment (i.e. as-needed “relievers” and regular “controllers”) • Advice on prevention strategies (allergen, irritant, and tobacco smoke avoidance)
  • 90. • How to recognize worsening asthma and how and when to implement their action plan • In some patients, particularly those requiring stabilization or patients who have had a recent exacerbation or deterioration, the use of a PEF meter and chart. • The correct choice and use of inhalers and the opportunity to practice under supervision
  • 91. INHALER USE FOR ASTHMA MANAGEMENT • An inhaler is a medical device used for delivering medication into the body via the lungs. It is mainly used in the treatment of asthma and chronic obstructive pulmonary disease. The two most common forms are: – Metered-dose inhaler – Dry powder inhalers (Accuhalers and turbuhalers) • Some of the types of inhalers include: Autohalers (Breath Activated aerosol devices), Nebulizers mists and nasal inhalers
  • 92. • Most patients (up to 80%) cannot use their inhaler correctly. This contributes to poor symptom control and exacerbations. To ensure effective inhaler use. • Choose the most appropriate device for the patient before prescribing, check in haler technique at every opportunity, correct using physical demonstrations, paying attention to incorrect steps and confirm that you have checklists.
  • 93. Metered-dose inhaler (MDIs) • The medicine is in a small canister, inside a plastic case. When the inhaler is pressed, a measured dose of medicine comes through the mouthpiece. • MDIs require good technique and coordination by pressing down on the inhaler and breathing in at the same time. • Because using the inhaler correctly can be difficult, spacer devices are recommended for use with MDIs. The spacer is attached to the MDI to make it easier to use the inhaler and get more medicine into the lungs
  • 94. A. How to use Metered Dose Inhaler • Remove the cap and check the mouthpiece is clean and free of objects. • Shake the inhaler four or five times • Holding the inhaler upright with your thumb on the base, breathe out as far as comfortable • Place the mouthpiece in your mouth; closing your lips around it to form a good seal - do not bite • Start to breathe in slowly; press down firmly on the top of the canister to release a dose; while continuing to breathe in slowly and deeply
  • 95. • Removing the inhaler from your mouth; hold your breath for about 10 seconds, or as long as is comfortable. • Breathe out gently away from your inhaler mouthpiece • For a second dose, wait approximately 30 seconds before repeating steps 2-7 • Replace the cap
  • 96. Dry Powder Inhaler (DPI) • Dry powder inhalers are handheld devices that deliver medication to the lungs and airways as you inhale through it. • Examples of dry powder inhalers include: Turbuhaler; Accuhaler; Handihaler; Ellipta inhaler and Breezhaler. The common forms available in Ethiopia are Turbuhaler (eg.Symbicort) and Accuhaler (eg.Seritide)
  • 97. B. How to use Accuhaler® (Dry powder inhaler- DPI) • Check dose counter. • Open cover. (Use thumb grip) • Hold the casing of the Accuhaler® in one hand while sliding the thumb grip away until a click is heard • Holding your Accuhaler® with the mouthpiece towards you slide the lever away from you until a click is heard. This makes the dose available for inhalation and moves the dose counter on.
  • 98. • Holding the inhaler horizontally, breathe out as far as comfortable • Place the mouthpiece in your mouth; closing your lips around it to form a good seal - do not bite • Breathe in as strongly and deeply as possible • Removing the inhaler from your mouth; hold your breath for about 10 seconds, or as long as is comfortable • Breathe out gently away from your inhaler mouthpiece • To close the Accuhaler®, slide the thumb grip back towards you as far as it will go until it clicks.
  • 99. Turbuhaler (DPI) • Since the turbuhaler is a breath-activated device, to use the turbuhaler properly, you must be able to breathe in deeply. Adults and children 7 years of age and older should be able to use the turbuhaler.
  • 100. C. How to use Turbuhaler (DPIs ) 1. Open: unscrew and remove the cap. Hold the turbuhaler upright. 2. Load the dose: twist the base anticlockwise and then back in the other direction until you hear a click. Your turbuhaler is now loaded with one dose of medicine 3. Breathe out: breathe out, away from the turbuhaler. Do not blow directly into the turbuhaler. 4. Inhale your dose: place the mouth piece in your mouth and form a seal with your lips. Breathe in deeply. Remove the turbuhaler and hold your breath for up to 10 seconds.
  • 101. 5. Close: replace the cap and twist until it is on properly. 6. Cleaning and storing your turbuhaler: wipe the mouthpiece with a clean dry tissue. Do not wash the mouthpiece or allow it to get wet when cleaning. Keep the cap on when not in use. The device may clog if exhaled or dribbled into or if stored in an area of high humidity with the cap off or unsealed.
  • 102. Common problems when using a turbuhaler • To get the most benefit, it is important to use the correct technique. Here are a few common problems: • Not holding your turbuhaler upright (vertical) while loading the dose. • Covering the air inlets with your lips. • Breathing in through your nose instead of your mouth. • Shaking the inhaler to see how much is left. • Storing your turbuhaler in a damp place with the cap off.
  • 103. • How to use Spacers • If patient unable to use an inhaler correctly, add a spacer to increase drug delivery to the lungs, especially if using inhaled corticosteroids. This may also reduce the risk of oral candida. • Clean the spacer before first use and every second week: remove the canister and wash spacer with soapy water. Allow it to drip dry. Avoid rinsing with water after each use. • Spacers are not commonly available in Ethiopia so a plastic water bottle. See figure below. • To modify a 500ml plastic bottle for use as an effective spacer
  • 104. How to use a bottle spacer Use a modified 500ml plastic bottle in a similar way to a conventional spacer
  • 105.
  • 106. Case study 3 (30 min) • The above patient returns back after 2 weeks with Shortness of breath, fever and cough productive of yellowish sputum appears to be in distress with difficulty of speaking, his RR was 30, pulse was 100/mt and BP-130/80mmhg and T-37.5, He has no wheezing and difficult to hear the breath sounds, heart beatare normal and no murmur, no gallop, no pedal edema. He appears weak and occasionally confused. • What is the diagnosis? • What are the abnormal findings in this patient? • What do these abnormal findings imply? • Classify the severity of asthma? • What are the steps of management?
  • 107. • We would like to thank Dr Hanan Yusuf, Dr Tewodros Haile, Dr Amsalu Bekele and Dr Rahel Argaw for preparing this powerpoint
  • 108. Diagnosis and management of asthma in children under the age of five years
  • 109. Learning objective • Identifying asthma in children • Prenatal risk factors of asthma • Algorithm in identifying asthma in under five years of age child at PHC and General Hospital • Steps Asthma Management • Assessing asthma control in preschool children • Preparing locally made spacer out of plastic bottles bottle 109
  • 110. What is asthma in preschool children ? • Wheezing or coughing that occurs with exercise, laughing or crying, and symptoms in the absence of apparent respiratory infection • History of other allergic disease (eczema or allergic rhinitis), allergen sensitization or asthma in first- degree relatives • Clinical improvement during 2–3 months of controller treatment, and worsening after cessation 110
  • 111. Prenatal Risk factors for Asthma 111 • Family history of atopic disease • Maternal smoking and asthma • Environmental pollution (especially tobacco smoke and indoor biomass exposure), • Nutrition • Maternal stress • Use of antibiotics • Birth by caesarean section
  • 113. Impact of asthma • Uncontrolled asthma is associated with – missed school days – repeated hospitalization – risk of airway remodeling – general poor quality of life in the affected children 113
  • 114. 114
  • 115. 115
  • 118. Low, medium and high ICS doses: children 6- 11 years GINA 2020, Box 3-6B DPI: dry powder inhaler; HFA: hydrofluoroalkane propellant; pMDI: pressurized metered dose inhaler (non-CFC); * see product information This is NOT a table of equivalence. These are suggested total daily doses for the ‘low’, ‘medium’ and ‘high’ dose treatment options with different ICS. 118
  • 119. Low, medium and high ICS doses: children 5 years and younger GINA 2020, Box 3-6B This is NOT a table of equivalence. These are suggested total daily doses for the ‘low’ dose treatment options with different ICS. 119 BDP: beclometasone dipropionate; DPI: dry powder inhaler; HFA: hydrofluoroalkane propellant; pMDI: pressurized metered dose inhaler (non-CFC)
  • 120. Assessing asthma control in preschool children 120
  • 121. …Cont Watch patients inhaler technique, check adherence . Remove potential risk factors : Assess and manage risk factors Refer to specialist for confirmation of asthma If asthma is confirmed escalate the steps of treatment 121
  • 122. Inhalation technique for preschool children • Use spacers with face mask, in all children less than five years of age • Locally prepared plastic bottle based spacers can be used. • Clean the spacers with detergents without rinsing it at least every 2 weeks. • Tight seal should be created between mask and face during inhalation and cleaning face • Mouth rinse after steroid administration should be practiced regularly 122
  • 123. Constructing locally made spacers 1. Wash the bottle with soap and water and air dry for a minimum of 12 hours to reduce electrostatic charge on the interior plastic. 2. Make a wire mould similar in size and shape to the mouthpiece of the MDI. 3. Heat the mould and hold in position on the outside of the base of the plastic bottle until the plastic begins to melt (~10 seconds). Rotate the mould 180% and reapply to the bottle until the mould melts through to make a hole. 4. While the bottle is still warm, insert the MDI into the hole to ensure a tight fit between the MDI and bottle spacer. Prime initially with 10 puffs of the medicine to reduce electrostatic charge on the walls 123
  • 124. Summary • Asthma in under five children is recognized using symptoms rather than lung function tests. • Genetics, environmental , perinatal risk factors are identified . • Inhaled corticosteroids are the backbone of asthma management in under five years of age • Locally made spacer is effective in delivering inhaled drugs for asthma symptom control . 124
  • 125. • We would like to thank – Dr. Rahel Argaw, Dr Hanan Yusuf, Dr Tewodros Haile and Dr Amsalu Bekele for preparing this powerpoint
  • 126.
  • 127. LEARNING OBJECTIVES: The participant will be able to: • Describe the epidemiology, risk factors and pathogenesis of COPD • Describe the diagnostic approach in COPD • Define COPD screening tools • Explain strategies for prevention of COPD • Manage COPD
  • 128. Definition A common, preventable and treatable disease characterized by -Persistent respiratory symptoms and -Airflow limitation that is due to >Airway and/or alveolar abnormalities >Usually caused by significant exposure to noxious particles or gases
  • 129. Outline  Definition, Epidemiology, risk factors & pathogenesis  Clinical manifestations  Diagnosis and initial assessment  Preventive strategies  Management of stable COPD
  • 130. Definition • Chronic bronchitis Clinically defined condition with chronic cough and phlegm Small airways disease A condition in which small bronchioles are narrowed • Emphysema Anatomically defined condition Characterized by destruction and enlargement of the lung alveoli
  • 131. COPD
  • 132. Epidemiology • NCDIs -Major public health problem in Ethiopia accounting for an estimated -52% of the total annual mortality -46% of total national disease burden (DALY’s lost) in 2016 • Based on Global Burden of Diseases Study 2016 CRDs contribute to -2.5% of the deaths due to NCDs
  • 133. Epidemiology Third leading cause of death in the world  Estimated 384 million cases of COPD globally with estimated prevalence of 12% More than 3 million people died of COPD in 2016 accounting for 6% of all deaths globally Burden is projected to increase because of continued exposure to COPD risk factors and aging of the population Prevalence of COPD is higher in smokers and ex-smokers compared to non-smokers Higher in ≥ 40year group compared to those < 40 years of age Higher in men than in women The prevalence of COPD is not precisely known even though hospital based studies show it is probably fairly common in Ethiopia
  • 135. Epidemiology STEPS Survey indicated -Prevalence of current smokers to be 4.2% of adults GATS -29.3% (6.5 million) were exposed to environmental tobacco smoke (ETS) in their workplace in the past 30 days -Overall, 12.6% (8.4 million) of adults were exposed to ETS at home -60.4% in bars and nightclub -31.1% in restaurant -19.7% in government buildings -11.4% in public transportation -7.0% in health-care facilities
  • 136. Epidemiology Shisha use Indoor air pollution due to biomass fuel use Industrialization and urbanization -exposure to particulate matter are rising Whereas, Availability of services for CRDs is very low at 45% in Health facilities Among those facilities mean readiness was only 55% based on SARA 2016 report
  • 138. PATHOGENESIS AND PATHOPHYSIOLOGY OF COPD • The chronic air flow limitation caused by a mixture of small air ways diseases (e.g. Obstructive bronchiolitis) and parenchymal destruction(emphysema), the relative contributions of which of which vary from person to person • COPD is characterized by: – Airflow limitation and gas trapping – Gas exchange abnormalities – Mucus hypersecretion – Pulmonary hypertension
  • 139.
  • 140. Noxious particles and gases Lung inflammation Host factors COPD pathology Proteinases Oxidative stress Anti-proteinases Anti-oxidants Repair mechanisms
  • 142. Note: This is a simplified diagram of FEV1 progression over time. In reality, there is tremendous heterogeneity in the rate of decline in FEV1 owing to the complex interactions of genes with environmental exposures and risk factors over an individual’s lifetime [adapted from Lange et al. NEJM 2015;373:111-22].
  • 143.
  • 144. Clinical manifestations Symptoms of COPD – Cough(usually the first symptoms) – Sputum production – Chronic and progressive dyspnea – Wheezing and chest tightness – Others – including fatigue, weight loss, anorexia, syncope, rib fractures, ankle swelling, depression, anxiety Physical examination in COPD – The respiratory examination is the most important examination when assessing a COPD patient – Even in quite severe disease there may be no physical findings in a COPD patients – Chest auscultation may demonstrate bilateral wheeze or crackles
  • 146. Pathways to diagnosis of COPD at primary health care
  • 147. Pathways to diagnosis of COPD at General hospital & above
  • 148. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 149. CLINICAL SCREENING OF COPD • Spirometry is required to make the diagnosis of COPD • Clinical criteria can be used to determine probability of COPD in the absence of spirometry • The COPD Population Screener™ (COPD-PS™) Easy-to-use Validated tool designed to identify patients at risk for COPD
  • 150. About the score: Score 5-10 — High risk of COPD Score 0-4 — Low risk of COPD Confirmation of COPD diagnosis requires spirometry.
  • 151. Management of COPD • An effective COPD management plan includes four components: 1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD 4. Manage exacerbations
  • 152. Initial assessment  The goals of COPD assessment are to determine -Level of airflow limitation -Impact of disease on the patient’s health status -Risk of future events (such as exacerbations, hospital admissions, or death) in order to guide therapy  Concomitant chronic diseases occur frequently in COPD patients  Cardiovascular disease  Skeletal muscle dysfunction  Metabolic syndrome  Osteoporosis  Depression  Anxiety  Lung cancer
  • 153. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 154.
  • 155. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 156. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 157.
  • 158. Pharmacologic treatment of COPD in Ethiopia
  • 159. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 160. © 2019 Global Initiative for Chronic Obstructive Lung Disease
  • 161. © 2019 Global Initiative for Chronic Obstructive Lung Disease
  • 162. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 163. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 164. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 165. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 166. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 167. COPD PREVENTIVE STRATEGIES • The following are strategies to prevent COPD: – Reduce indoor air pollution • Smokeless cooking stoves • Cooking in a well-ventilated room • Cooking meals outside the house • – Smoking cessation-counseling • Smoking cessation has the greatest capacity to influence the natural history of COPD • If effective resources and time are dedicated to smoking cessation, long-term quit success rates of up to 25% can be achieved
  • 168. Case study 4 (30 min ) • A 45yearold woman from rural village has noticed a persistent, occasionally productive cough for the past 6 months. The cough is worse whenever she spends the day at her home while cooking where is exposed to the smoke of the wood fire. She finally decides to visit the health center. Her husband and she never smoked cigarettes. • The cough has been present for almost a year. She has no fever or chills. She does admit to more shortness of breath when she walks for long distance over the past six months. • Physical examination was normal findings. • Discussion points: • What further questions do you want to ask? • What differential diagnoses do you consider? • At this point, what further investigations do you think would be appropriate? • What would be the best option to improve her symptoms and slow progression?
  • 169. Summary – COPD is characterized by chronic cough, dyspnea, wheezing and sputum production – Caused by exposure to inhaled pollutants, almost always smoke from either domestic fires or tobacco smoking – Rhonchi, decreased intensity of breathe sounds, and prolonged expiration on physical examination – Airflow limitation on pulmonary function testing that is not fully reversible and is most often progressive – Occurs later in life, usually older than 35 years old – Prevention involves decreasing exposure to tobacco and avoiding indoor air pollution
  • 170. • We would like to thank – Dr. Tewodros Haile, Dr. Aschalew Worku, Dr Amsalu Bekele, Dr Hanan Yusuf and Dr Rahel Argaw for preparing this powerpoint
  • 172. Outline • Definition & causes • Differential diagnosis • Classification of severity • Indications for hospitalizations • Management of severe exacerbations • Indications for MICU admission, NIV & IMV • Discharge criteria and recommendations for follow up
  • 173. Definition • An exacerbation of COPD is a sustained worsening of the patient's condition, from the stable state and beyond normal day-to-day variations that is acute in onset and may warrant additional treatment in a patient with underlying COPD. • Exacerbations are infrequent in early COPD and are largely a feature of moderate-to-severe disease.
  • 174. COPD exacerbation • Negatively affects a patient’s quality of life • Accelerates the rate of decline of lung function • Associated with significant mortality, particularly in those requiring hospitalizations
  • 175. Main Causes of COPD Exacerbations • Bacterial and viral infections • pollution events • cold weather • interruption of regular treatment
  • 176. © 2020 Global Initiative for Chronic Obstructive Lung Disease
  • 177. Classification of severity of COPD exacerbations • Mild: treated with antibiotics but no systemic corticosteroid. Absence of respiratory failure. • Moderate: treated with parenteral corticosteroids with or without an antibiotic. Absence of respiratory failure. • Severe: Type 1 respiratory failure with hypoxaemia but no carbon dioxide retention or acidosis. • Very severe & Life-threatening: Type 2 respiratory failure, decompensated with acidosis and carbon dioxide retention. © 2019 Global Initiative for Chronic Obstructive Lung Disease
  • 178. Potential indications for hospitalization assessment*
  • 179. Management of severe but not life threatening exacerbations*
  • 180. What are the indications to add antibiotics • Three cardinal symptoms-increase in dyspnea, sputum volume and sputum purulence • Signs of pneumonia • Mechanical ventilation
  • 181. Key points for the management of exacerbations
  • 182. Indications for medical intensive care unit admission*
  • 183. Indications for Noninvasive mechanical ventilation (NIV)
  • 184. Indications for Invasive mechanical ventilation
  • 187. Case study 4 • A 45 year old woman from rural area has noticed a mild, occasionally productive cough for the past 3-4 months. The cough is worse whenever she spends the day at her home while cooking where is exposed to the smoke of the wood fire. • She finally decides to visit you at the health center. Her husband and she never smoked cigarette. • The cough has been present for almost a year. She has no fever or chills. She does admit to more shortness of breath when she walks for long distance over the past six months. • Physical examination was normal findings. • Discussion points – 1- What further questions do you want to ask ? – 2- What differential diagnoses do you consider? – 3-At this point, what further investigations do you think would be appropriate? – 4-What would be the best option to improve her symptoms and slow progression?
  • 188. Answers 1- What further questions do you want to ask ? -characteristic of cough intermittent or persistent? -cough with phlegm or productive? -nigh sweating, fever or weight loss? 2- What differential diagnoses do you consider? Tuberculosis Bronchial asthma Bronchiectasis Lung cancer COPD 3-At this point, what further investigations do you think would be appropriate? Chest x ray, Sputum AFB, ESR, CBC Lung function studies: flow meter and spirometer and response to salbutamol 4-What would be the best option to improve her symptoms and slow progression? • Reduce exposure to Smoking (outdoor cooking) • Behavioral change communication • Nutrition and regular treatment of chest infection etc… • Bronchodilator treatment • Exercise to improve exercise tolerance and quality of life • Home oxygen treatment and morphine depending on the advance of disease
  • 189. We would like to thank • Dr. Tewodros Haile, Dr Hanan Yusuf, Dr Amsalu Bekele and Dr Rahel Argaw for preparing this powerpoint
  • 190. Cardiovascular Risk Assessment for Health Professionals In Ethiopia March 2021
  • 191. Unit 1: INTRODUCTION • CVDs : – are number one cause of death globally – 17.9 million people deaths from CVDs in 2016, ( 31% of all global deaths). – 80% occur in low- and middle-income countries, often in people less than 60 years of age. – CVDs are rising alarmingly in Ethiopia on top of already existing CVDs like Rheumatic heart diseases, cardiomyopathy and cor-pulmonale.
  • 192. Introduc.. • CVDs are preceded by longtime exposure to single or combined risk factors which can be modifiable or non- modifiable. • Continuing exposure to these risk factors leads to further progression of cardiovascular diseases which include one or more of the following: – Coronary artery disease (CAD) manifested by fatal or nonfatal myocardial infarction (MI), angina pectoris, and/or heart failure – Cerebrovascular disease manifested by fatal or nonfatal stroke and transient ischemic attack – Peripheral artery disease manifested by intermittent claudication and critical limb ischemia – Aortic atherosclerosis and thoracic or abdominal aortic aneurysm
  • 193. Introduc.. • Early identification, control and avoidance of the modifiable risk factors can significantly reduce or retard the progression of cardiovascular diseases . • Control of the risk factors before development of CVDs is the most cost effective and applicable intervention especially for low income countries likes Ethiopia. • Several attempts were made globally and nationally for the control of these risk factors for reducing development of cardiovascular diseases.
  • 194. Introduc… Single versus Multiple Risk factors approach Previous guidelines did not take into consideration some important facts: • that multiple risk factors are responsible for cardiovascular disease, • that risk factors and determinants of heart attacks and strokes are very similar, and, therefore, prevention approaches are similar. The new guidelines integrate the management of multiple risk factors e.g. raised blood pressure, raised cholesterol, and raised blood sugar and tobacco use.
  • 195. Introduction.. • Multiple risk factor-interventions targeting individuals with high baseline cardiovascular risk are cost effective especially in low income countries like ours. • Though the presence of one risk factor may increase the chance of having future CV event, this chance of developing CVDs is variably influenced by the presence or absence of other risk factors. • Therefore treatment decision of the single risk factor is better made on the analysis of the combined effect of the total risk factor than the sole magnitude of the single risk factor.
  • 196. Unit 2.CARDIOVASCULAR RISK ESTIMATION Current components of management of individual CV risk factors for prevention of atherosclerosis and CVD include : – CV risk assessment. – Treatment of those at high risk for disease. – Management adjusted to patient’s total risk of CHD or CVD; the higher the risk, the greater the intensity of management. – Employment of a range of interventions to address risk factors for CVD
  • 197. CV Risk Estimation.. • No single absolute test or score used to predict the future development of CVDs. • A general estimate of the relative risk for CVD can be approximated by counting the number of traditional risk factors present in a patient • The increased risk of CVD resulting from multiple risk factors is frequently greater than simply additive. • Hence we need a more precise estimation of the absolute risk for a first CVD event desirable when making treatment recommendations for a specific individual.
  • 198. CV risk Estimation… • The total risk approach relies on risk prediction scores derived from large epidemiologic cohort studies involving diverse groups of individuals with risk factors but with no CVDs at baseline. • Score are developed after long years of follow up • These prediction scores have been developed and validated primarily in high-income countries and subsequently adapted to other populations after re-calibration • The World Health Organization (WHO) and the International Society of Hypertension (ISH) recently developed a set of CV risk prediction charts for use in all regions of the world
  • 199. CV Risk Estimation.. • The first WHO risk prediction chart was developed in 2007 and recent update was made in 2019. • The world was divided into 21 GBD regions and Ethiopia is represented by the Eastern Sub-saharan African Region. • It was suggested by the WHO working group of CV risk prediction chart that each country should adapt the risk chart to its national context. • It is with this basis that the national CV working group developed this risk charts to be used in Ethiopia.
  • 200. Case Study • Case study 1 – A 40 year old smoker was evaluated at health center and had a BP of 130/85 and has no history or physical findings of previous stroke, heart failure, MI or diabetes mellitus. • The second case was a 50 years nonsmoker with BP of 120/80 with no history or findings of stroke, heart failure, and diabetes mellitus but was diagnosed to have myocardial infarction 5 years ago.
  • 201. Case study.. • Q. 1.List the cardiovascular risk factors in these patients. • 2. How do compare future cardiovascular risk of these two patients? Which one has higher risk and why? • 3. For which patient WHO risk prediction chart is applicable?
  • 202. Unit 3: WHO CV RISK CHARTS:
  • 203. 1. Definitions of terms: • CV risk: in the WHO risk assessment CV risk refers to the chance of having fatal or nonfatal heart attack or stroke in the next 10 years with the current risk profile of the patient. • CV risk factors are any biologic or environmental conditions known to increase the inherent risk/chance of having CV event. They are classified into modifiable and non- modifiable risk factors.( See Table below)
  • 205. Defini.. • Cardiovascular disease (CVD): is manifested cardiovascular event (stroke, heart attack, peripheral arterial or aortic disease). • Risk chart: is collection of tables of risk estimates with different types and levels of risk factors. • Primary Prevention: This is control of risk factors before cardiovascular disease develops. • Secondary Prevention: Prevention of further occurrence or progression of previous cardiovascular disease.
  • 206. 2. Types of WHO risk charts • WHO risk charts were developed for estimation of the chance of future cardiovascular event in those individuals who never had cardiovascular diseases. • It does not apply for patients who have already developed cardiovascular diseases. • There are two types of WHO risk charts based on availability of laboratory facility to measure blood glucose and cholesterol levels
  • 207. Laboratory-based WHO CVD risk charts • These are CVD risk charts that include measurements of total cholesterol and information on diabetes mellitus . • The laboratory-based CVD risk charts should be used for treatment decisions. • This is the indicated risk chart in a setting where laboratory facilities and human and financial resources are accessible. • These charts will facilitate health providers to initiate an intervention and treatment regimen, and to implement an appropriate follow-up plan based on the patient’s total risk status.
  • 208. Parameters needed for Lab Based WHO Risk Chart • The variables needed for using this chart are as follows: History: • Age: specific numbers between 40 to 74 years. The risk prediction doesn’t apply for age category out of the specified range • Smoking: current smoking • Sex: Male OR Female • Diabetes: Yes OR No. If history of diabetes is not known OR there is no blood sugar determination facility; then risk assessment should be done using the other risk prediction chart (non-laboratory based charts) Physical Examination • Blood Pressure: measured value of the systolic blood pressure
  • 209. Laboratory parameters for Lab Based WHO Risk Chart 1. Blood sugar: to diagnose diabetes 2. Total cholesterol: Measured valves of total cholesterol. – In most of the Ethiopian Laboratories, total cholesterol is in mg/dl units; but the risk prediction score applies values in mmol/l units. – The cholesterol value in mg/dl should be multiplied by 0.02586 before applying the value for risk prediction.
  • 210. B.Non-laboratory-based WHO risk charts • Many low-resource settings have limited testing facilities or limited financial and physical capacity for biochemical measurements (e.g. blood sugar determination and cholesterol assays). • WHO CVD risk (non-laboratory-based) charts can be used to predict total CVD risk without information on total cholesterol and diabetes. • In most primary health care facilities of Ethiopia, laboratory facilities exist to diagnose diabetes either with fasting or random blood glucose levels.
  • 211. Non Lab.. • If the patient is not diabetic, the non- laboratory based WHO risk chart correlates well with laboratory based risk chart when a 10 % cut of point is used as high risk. • The non-laboratory-based WHO CVD risk charts are aimed at stratification in low-resource communities and office settings and can be used for decisions regarding referral. • Patients diagnosed to have diabetes and non-diabetic patients with non-lab based risk level of greater than 10% should be considered high risk and managed accordingly in areas where serum cholesterol cannot be determined.
  • 212. Variables for Non Lab based WHO Risk Chart • To use this chart, the following variables should be available: History: – Age: specific numbers between 40 to 74 years. The risk prediction doesn’t apply for age category out of the specified range – Smoking: current smoking – Sex: Male OR Female Physical Examination – Blood Pressure: measured value of the systolic blood pressure – BMI (Body Mass Index): Calculation of the BMI from weight and height. NO LABORATORY MEASUREMNET PARAMETER REQUIRED!
  • 213. Figure 2: Steps in selecting appropriate Chart for WHO CV risk assessment
  • 214. Unit 4: INSTRUCTIONS FOR USING THE WHO CVD RISK CHARTS
  • 215. 1. Laboratory- based Risk Chart • These charts are to be used only for individuals whose status regarding diabetes and total cholesterol is available. • Tests for diabetes and cholesterol can be carried out at the time of assessment. • If the information on diabetes and total cholesterol is not available, then refer to the instructions on use of non-laboratory-based risk charts
  • 216. Instructions for using laboratory based WHO risk Chart
  • 217. Step by Step Instructions for using laboratory based WHO risk Chart
  • 218. Laboratory based WHO risk Chart
  • 219. Examples : Table 3: Examples of Laboratory based Risk chart Patient Demographic data Risk factor Profile 10-year risk of cardiovascular event (heart attack or stroke) Kemal 50 years, Male SBP=140 mmHg, TC=270mg/dl (7 mmol/l), non-smoker, no diabetes Dereje 50 years, Male SBP=140 mmHg, TC=270mg/dl (7 mmol/l) non-smoker, diabetes Kura 50 years, Male SBP=140 mmHg, TC=270mg/dl (7 mmol/l) smoker, diabetes Mesfin 50 years, Male SBP=160 mmHg, TC=270 mg/dl (7 mmol/l) smoker, diabetes NB: The given four patients do have the same age and sex, but risk factor variation will result in significant change in the 10-year cardiovascular risk prediction. The risk prediction score will ultimately help the clinicians to decide on life style intervention to aggressive primary prevention therapy using statins.
  • 220. 2. Non-laboratory-based Who risk charts • These charts are for the use in settings where blood glucose and cholesterol cannot be measured. • They can also be used to identify people at high risk who can be taken up for further investigations. • Table 2 and Figure 3 present the steps to apply the non-laboratory WHO CVD risk charts.
  • 221. Table 4: Instructions for using Non laboratory based WHO risk Chart
  • 222. Step by Step Instructions for using Non- laboratory based WHO risk Chart
  • 223. Non Laboratory based WHO risk Chart
  • 224. Examples of Non laboratory based Risk Chart Patient Demographic data Risk factor profile 10-year risk of cardiovascularevent(heart attack or stroke) Rahel 50 years Female Nonsmoker, SBP=150 mmHg, BMI=26Kg/m2 Wossen 60 years Female Nonsmoker, SBP=150 mmHg, BMI=26Kg/m2 Tigist 60 years Female Nonsmoker, SBP=180 mmHg, BMI=26Kg/m2 Tirsit 60 years Smoker, SBP=180 mmHg, BMI=26Kg/m2 NB: Variations in risk factors affect the risk category
  • 225. Unit 5: APPLICATIONS OF WHO RISK CHARTS
  • 226. A. For Whom? • As stated above the WHO risk chart applies for patients who haven’t been diagnosed to have cardiovascular diseases like stroke, heart attack, peripheral arterial or aortic diseases. • For patients with cardiovascular diseases, management should include specific disease management and more intense risk factor management with life style interventions and pharmacologic agents.
  • 227. B. Specific Applications 1. Hypertension( See HTN treatment protocol for details) – Target blood pressure should be less than 140/90mmHG. – For patients with high WHO risk (> 10% with non-lab based and >20% with lab based WHO risk), drug should be started to lower BP below 130/80 on top of life style intervention – For patients with BP of 140-159/90-99 mmHG and no end-organ damage or cardiovascular diseases drug can be started after 3 months trial of life style interventions to keep BP <140/90mmHG – For any WHO risk level and BP >160/100mmHG drug should be started to lower BP below 140/90 on top of life style intervention
  • 228. B. Specific Recommendation 2. Statin Treatment • Indications – Patients with high CVD risks (>20% with lab-based and >10 % with non-lab based WHO risk Charts). – All patients with TC of 324mg/dl or serum LDL of > 190 if lab is available. – All diabetic patients older than 40 years should receive statin regardless of WHO risk level or serum cholesterol level Dose: Atrovstatin 20mg/day, Simvastatin 40mg/day for primary prevention of CV events. • For patients with previous cardiovascular events double the above doses.
  • 229. B. Specific Recommentat.. 3. Life style interventions – All individuals should be encouraged to engage in healthy life style (see specific topic for details) at any risk level. – If CVD risk is < 10% and no CVD risk factors, reassess CVD risk after 5 years. – Patients with any behavioral (unhealthy diet, smoking, excess alcohol intake, sedentary life) and physiologic risk factors (obese or patients with metabolic syndrome) should be routinely evaluated for control of these risk factors and have annual CV risk assessment.
  • 230. B. Specific Recommentat 4. For policy makers, Monitoring and evaluation of CVD interventions WHO risk can be used for baseline cardiovascular risk assessment at national, regional and facility level  to assess the impacts of CV interventions at national and subnational levels.
  • 231. Management guidance for total CVD risk Management of total CVD risk Risk <10%  Counsel on diet, physical activity, smoking cessation and avoiding harmful use of alcohol.  If risk <5%, follow up in 12 months.  If risk 5% to <10%, follow up every 3 months until targets are met, then 6–9 months thereafter. Risk 10% to <20%  Counsel on diet, physical activity, smoking cessation and avoiding harmful use of alcohol.  Persistent BP ≥140/90 mmHg consider drugs (see below).  Follow up every 3–6 months. Risk >20%( or >10% with Non lab based WHO risk)  Counsel on diet, physical activity, smoking cessation and avoiding harmful use of alcohol.  Persistent BP ≥130/80, consider drugs (see below).  Give a statin.  Follow up every 3 months. If there is no reduction in cardiovascular risk after six months of follow-up refer to next level. Important practical points Management of hypertension and diabetes  For management of hypertension refer National Hypertension Treatment Protocol  For management of diabetes mellitus type National Diabetes Treatment Protocol Consider drug treatment for following categories:  All patients with established DM and CVD (coronary heart disease, myocardial infarction, transient ischaemic attacks, cerebrovascular disease or peripheral vascular disease), renal disease. If stable, should continue the treatment already prescribed and be considered as having risk >20%.  People with albuminuria, retinopathy, left ventricular hypertrophy.  All individuals with persistent raised BP ≥160/100 mmHg.  Consider statin for high risk patients , diabetes, previous cardiovascular disease and very high cholesterol levels( see above) Follow-up visits:  Ask about: new symptoms, adherence to advice on tobacco and alcohol use, physical activity, healthy diet, medications etc.  Assess (physical exam).  Estimate cardiovascular risk.  Refer if necessary.  Counsel all and treat as shown in protocol.
  • 232. • Case Studies on Using WHO Risk Charts:
  • 233. Case Study 1 • A 65 year old female individual found to have a weight of 86kg, height of 166cm, BP of 145/80 at one of remote health centers with no facility for laboratory evaluation.
  • 234. Questions – Q1. What further information do you need to calculate her future CV risk? • On further inquiry she is found to be non- smoker and had no previous cardiovascular problems. – Q2. Which chart will use to calculate her future cardiovascular risk? – Q3. What is her 10 year future CV risk? – Q4. How do you define her risk level? – Q5. How will you communicate about the risk level with the patient?
  • 235. Case Study 2 • Ato Yalew is a 43year old male teacher at Bure high school . He was evaluated at Bure hospital and was found to have a weight of 72kg, height of 174cm, BP of 160/100 . He is smoker for greater than 10 years. His total cholesterol was 267mg/dl and his fasting blood glucose was 98mg/dl • Q1
  • 236. Case study 2…. • Q1. What risk factors does Ato Yalew have? • Q2. Which chart will use to calculate his future cardiovascular risk? • Q3. What is his 10 year future CV risk? • Q4. How do you define his risk level? • Q5. How will you communicate about the risk level with the patient?
  • 237. Case Study 3 • Ato Abdi is a 53year old male farmer living in one of rural kebles in West Harege Zone . On examination at Woreda health center he had a weight of 66kg, height of 168cm, BP of 130/170 . He usually chews chat and smokes cigarettes . His total cholesterol and FBS couldn’t be determined.
  • 238. Case study 3.. • Q1. What risk factors does Ato Abdi have? • Q2. Which chart will use to calculate his future cardiovascular risk? • Q3. What is his 10 year future CV risk? • Q4. How do you define his risk level? • Q5. How will you communicate about the risk level with the patient?
  • 239. Case Study 4 • W/o Amina is 65 years old woman who was found to have a weight of 75kg, height of 160cm, BP of 180/100 at one of health centers in Addis Ababa . She is known to be diabetic on insulin and her total cholesterol was 320mg/dl. •
  • 240. Case Study 4… • Q1. What CV risk factors does W/o Amina have? • Q2. Which chart will use to calculate her future cardiovascular risk? • Q3. What is her 10 year future CV risk? • Q4. How do you define her risk level? • Q5. How will you communicate about the risk level with the patient?
  • 241. 241
  • 242. Learning Objectives • Describe the characteristics of Group A Beta Hemolytic Streptococci • Describe the epidemiology of GABHS tonsilopharyngitis • Explain the difference between viral and GABHS tonsilopharyngitis • Outline the diagnostic modality of GABHS tonsilo- pharyngitis • Outline the management of GABHS tonsilopharyngitis • Explain methods of prevention of tonsilopharyngitis 242
  • 243. Introduction • Rheumatic fever is an inflammatory disease involving the joints, skin, heart and brain, which develops following an untreated or partially treated group A b-haemolytic streptococcal (GAS) infection of the throat (streptococcal pharyngitis). • Up to 30% of sore throats in children and young people are caused by GAS, and 0.3% to 3% of young people with an untreated GAS sore throat will develop RF. • After recovery from the initial episode of RF, up to 60% to 65% of patients develop valvular heart disease and the risk of RF recurrence following GAS infection rises to 50%. • Identification and treatment of bacterial sore throat is an important component of Rheuamtic Fever/Rheumatic Heart Disease Prevention and Control Program
  • 244. Tonsilopharyngitis  Sore throat(Tonsilopharyngitis) is a symptom caused by inflammation of pharynx, tonsils or other surrounding structures  Viral sorethroat is the predominate cause  Group A beta hemolytic Streptococci is commonest bacterial cause 20-40% in children 5-15% of sore throat clinic visits in adults 244
  • 245. Group A Beta Hemolytic Streptococci (GABHS) 245 • Gram-positive, nonmotile, non–spore-forming cocci • 0.5-1.2µm in size. in pairs or chains • They are negative for oxidase and catalase. • Characterized by local invasion and release of extracellular toxins and proteases
  • 246. Group A Beta Hemolytic Streptococci … – This organism may cause suppurative disease, such as pharyngitis, impetigo, cellulitis, myositis, pneumonia, and puerperal sepsis. – It also may be associated with nonsuppurative disease, such as rheumatic fever and Acute Poststreptococcal Glomerulonephritis. – Group A streptococci elaborate the cytolytic toxins Streptolysins S and O. – Of these, streptolysin O induces persistently high antibody titers that provide a useful marker of group A streptococcal infection and its nonsuppurative complications – M protein fragments of certain serotypes of GABHS are similar to heart muscle – Antibodies produced against the bacteria Antigens are affect the tissue and linked to development heart valve damage. 246
  • 247. EPIDEMIOLOGY of GABHS • Humans are exposed to GABHS in the environment • Humans are the natural reservoir for GABHS • Mostly spread through droplets of salivary or nasal secretions • Overcrowding , poverty, and close contact with person with streptococcal sore throat are considered risk factors for transmission – The incubation period is 2 to 5 days • Throat and skin are common sites of GABHS infection 247
  • 248. EPIDEMIOLOGY of GABHS… – GABHS infections usually resolve without treatment however if left uuntreated it can lead to acute rheumatic fever in some people. • Antibiotic treatment decreases severity of symptoms and reduces the risk of transmission to others after 24 hrs of treatment • Treatment also decreases the risk of acute rheumatic fever • Studies show that ARF associated with GABHS pharyngitis can be prevented if treatment is commenced within 9 days of symptoms appearing. 248
  • 249. Clinical Presentations of Sore Throat 4-1. GABHS pharyngitis 4-2. Viral Pharyngitis 249
  • 250. 4-1.GABHS PHARYNGITIS  Sudden onset of sore throat  Pain on swallowing and Fever above 380C  Headache, nausea, vomiting and abdominal pain  Tonsilopharyngeal erythema  Enlarged tonsils with exudate  Tender and enlarged anterior cervical lymph nodes (lymphadenitis) 250
  • 251. 4.2 VIRAL PHARYNGITIS • Cough , runny nose conjunctivitis • Hoarseness, coryza • Anterior stomatitis, discrete intra-oral ulcerative lesions • Exanthema, ,diarrhea • Absence of fever (strongly suggest) 251
  • 252. Bacterial Vs Viral Pharyngitis
  • 253. DIAGNOSIS OF BACTERIAL SORE THROAT  The diagnosis of streptococcal pharyngitis (GABHS) can either be clinical only or using clinical criteria supported by laboratory investigations.  The gold standard diagnostic method is by using a Clinical Prediction rule (CPR) supported by rapid antigen test (RAT) and/or throat culture. 253
  • 254. THROAT CULTURE  Not available in all set ups  Delay in getting results at least 48 hrs.  Technical errors ( impact on the results)  Cost of test is high  Many people are asymptomatic carriers (10% of school age children). 254
  • 255. Rapid Antigen Detection Test for GABHS Not available Not validated in Ethiopia Expensive 255
  • 256. ASO Titer: NO role in Acute Tonsilopharyngitis 256
  • 257. GABHS Diagnosis Clinical Decision Rules (CDR) Cardinal Clinical features Symptoms or Signs Points History of high fever or (objective record ≥ 38oC) 1 Absence of cough and rhinorrhea 1 Tender anterior Cervical adenopathy 1 Tonsillar swelling or exudates 1 Clinical Decision Rule (CDR) • ≥ 2 points, treat as GAβHS pharyngitis (with antibiotic) , • < 2 points, treat as viral pharyngitis (no antibiotic 257
  • 258. Management of Tonsilo-pharyngitis  Relief of acute symptoms  Prevention of suppurative and non suppurative complications  Reduce communicability  Pain and fever management (Paracetamol) 258
  • 259. Antibiotics for GABHS Treatment First Line: Benzathine penicillin ( First Line ) Dose: Wt. < 30kg:600,000 IU stat. Wt. > 30 kg:1.2 million IU IM stat. Use Safe BPG Injection Procedures! Alternative Amoxicillin Dose : Children < 7years: 50 mg/kg per day in three divided doses for 10 days. Age>7Years: 500mg PO TID for 10 Days 259
  • 260. Antibiotics for GABHS Treatment… If Patient allergic to penicillin: ERYTHROMYCIN Dose – Less than 7 years: 250 mg BD for 10 days – More than 7 years: 500 mg BD for 10 days 260
  • 261. Why Benzathine Penicillin? • Single injection • Better bactericidal effect than oral • Oral treatment needs 10 whole days to be effective • Oral macrolides: clinical improvement but no eradication of organism. • Cost effective, evidence based. • Parents and patients more satisfied.
  • 262. Is it cost-effective to administer BPG for all cases of suspected strep sore throat? • An overall protective effect for the use of penicillin against acute rheumatic fever of 80% with an NNT of 60 children per year to prevent 1 episode of rheumatic fever. • Mild hypertension: have to treat 800 people per year to prevent 1 episode of stroke • The estimated cost of preventing one case of rheumatic fever by a single monthly intramuscular injection of penicillin is US$46 • Valve replacement surgery for 1 case of RHD is at least US$15, 000 • Cardiac surgery only available in S Africa, Ghana and Egypt
  • 263. Prevention and Health Education Families should be educated about: 1.The symptoms of GAS pharyngitis. 2 The serious consequences of untreated pharyngitis i.e. ARF and RHD and the need to consult medical personnel as early as possible to avoid complications. 3 The need to avoid pharyngitis by improving house ventilation and hygiene and avoid crowding. 4. Importance of adherence to a 10 days course of antibiotics in oral treatment.
  • 264. Case study W/O Almaz brought her five years old girl Helen to the outpatient clinic with acute onset of fever, severe throat, pain exacerbated by swallowing, headache and abdominal pain. No runny nose, no cough. Physical examination: Wt. 20 kg, her temperature was 38.30C axillary, the tonsils were symmetrically enlarged, red with exudates. She had multiple enlarged painful anterior neck lymphadenopathies. No other abnormal findings detected. 264
  • 265. Questions. 1. What is your clinical diagnosis of Helens’ illness? 2. What tests do you need to reach at a diagnosis? 3. What is the most likely causative organism of her illness? 4. How would you like to treat Helen? 5. Which of the clinical presentation helps you to decide about the treatment you are going to give? 6. What is the drug of choice (type, dose and route of administration)? 7. What other additional Advice do you like to give to W/O Almaz? 265
  • 266. Key points • Group A beta hemolytic streptococcus is one of the commonest cause of bacterial tonsilo- pharyngitis. • Diagnosis should be suspected early and use clinical decision rule. • Drug of choice for GABHS is single injection of Benzathine Penicillin G. • Families should be educated about identifying children with sore throat early and contacting health care workers for 266
  • 267. End of Unit 1 267
  • 268. Welcome to Rheumatic Fever and Rheumatic Heart Disease Training for Health Care Workers Federal Ministry of Health & College of Health Sciences, Addis Ababa University
  • 269. NATIONAL TRAINING ON RHEUMATIC FEVER/RHEUMATIC HEART DISEASE FOR HEALTH CARE WORKERS IN ETHIOPIA Course Goals, objectives
  • 270. Goal To develop critical mass of trained Health Care Workers at all levels for scale up of RF/RHD prevention and control services at all levels of the health care system
  • 271. Objectives To have good knowledge and skills on: • Diagnosis and management of bacterial tonsilo- pharyngitis • Diagnosis and management of acute rheumatic fever • Safe administration of Benzathine penicillin • Diagnosis and management of Rheumatic Heart Disease (RHD). • Monitoring and evaluation of RHD Program
  • 272. ARF/RHD Training Package • ARF/RHD Participants’ Manual • ARF/RHD Facilitator Manual • Power point presentations • Algorithms and Treatment Protocols • RHD Intake and Follow up form • RHD Client Passport • RHD Register • Client education Materials
  • 273. Training Approaches • Mastery Learning • Competency based • Participatory • Training/Learning Methods –Illustrated lectures and group discussion –Individual and group exercises –Role plays –Demonstrations using check lists –Case studies
  • 274. Introduction of participants and facilitators –Name –Current station –Profession –Service years –Expectations(be specific)
  • 275. Ground Rules • Participation • Time • Energizer • Mobile • Discussions/side • Recap
  • 276. Information • Rest room • Administrative Issues
  • 277. A healthy throat, a healthy heart for us all! 277
  • 279. • To know about the epidemiology of ARF • To understand the pathogenesis of ARF • To know about the clinical features of ARF • To learn about the diagnosis of ARF • To understand management of ARF • To know about the prevention of ARF • To discuss the principles of management of ARF LEARNING OBJECTIVES
  • 280. • ARF is a post infectious, non-suppurative sequel of pharyngeal infection with Streptococcus pyogenes • RHD is the only long-term sequel of ARF • RHD manifests after several years of ARF with heart failure or complications like stroke or infective endcocarditis. • ARF and RHD can easily be prevented by early identification and treatment of streptococcal pharyngeal infection. • Currently, the 2015 AHA/ACC criteria are used to diagnose ARF Introduction
  • 281. • Rheumatic heart disease currently affects over 33 million people worldwide. • RHD is found all over the world, but most commonly affects women, adolescents and children living in conditions of poverty and overcrowding. • RHD kills 275,000 people every year, even though it is a preventable disease. • A few rich countries (including the USA and UK) and some LMIC Countries like Cuba have managed to reduce their burden of RHD, but other countries continue to struggle with the disease. • RHD is a lifelong condition, which is often fatal if not treated properly. EPIDEMIOLOGY
  • 282. RHD in Ethiopia • Recent school and community based studies in Ethiopia have shown the prevalence of RHD in 4-24 years age groups to be from 14-38/1000,which is one highest in the world. • Approximately 250, 000 people in the age group 5- 15 suffer from RHD in Ethiopia. • More than 500,000 people of all age groups live with RHD. • Only few give history of Acute Rheumatic Fever
  • 283. • RHD is the main cardiovascular diagnosis accounting for 30-60% of all cardiac patients in main hospitals of Ethiopia • Patients usually come late with heart failure , stroke or during pregnancy with severe valvular disease • Mortality from RHD may reach 12.5% every year in rural Ethiopia. • It is also reported that 70% of RHD patients die before the age of 26 years. RHD in Ethiopia…
  • 284. Risk Factors for Rheumatic Fever • Socioeconomic status: – Poverty – Poorly made and overcrowded housing – Lack of adequate health care – Untreated GAS infections • Sex • Rheumatic fever occurs in equal numbers in males and females, but the prognosis is worse for females than for males. • Age – Rheumatic fever principally affects children between 5-15 years of age with a median age of 10 years, although it also occurs in adults (20% of cases). • Risk factor for RHD – Recurrent ARF
  • 285. Risk factors for Rheumatic Fever Determinants Effects Impact on ARF and RHD burden Socioeconomic & environmental factors 1. Poverty 2. Poor nutrition 3. Overcrowding 4. Poor standard of living 1. Rapid spread of GABHS 2. Difficulties accessing health care 1. Higher incidence of acute strep pharyngitis and complications 2. Higher incidence of ARF and recurrent ARF Health System Related Factors 1. Shortage of resources for health care 2. Low level of knowledge of disease among health care providers 3. Low level of awareness of disease in the community 1. Inadequate diagnosis and treatment of strep pharyngitis 2. Misdiagnosis or late diagnosis of ARF 3. Inadequate secondary prophylaxis delivery 1. Higher incidence of ARF and recurrent ARF 2. Missed first ARF episode 3. Inadequate secondary prophylaxis delivery 4. Higher rates of recurrent ARF with more frequent and severe heart valve involvement 5. Higher rates of repeated hospital admissions and expensive heart valve surgery
  • 286. • Rheumatic fever is thought to result from an inflammatory autoimmune response with antibodies produced against streptococcal antigen induces inflammation in host tissue having similar molecules (ANTIGEN MIMICKERY THEORY) • Only group A beta-hemolytic streptococcal infections of the pharynx initiate or reactivate rheumatic fever. • In 0.3-3% of streptococcal pharyngeal infection, rheumatic fever develops several weeks after the sore throat has resolved. • Studies show the existence of genetic predisposition in addition to bacterial factors. Etiology and Pathogenesis
  • 287. Etiology and Pathogenesis… • After recovery from the initial episode of RF, up to 60% to 65% of patients develop valvular heart disease and the risk of RF recurrence following GAS infection rises to 50%. • Repeated GAS infections without appropriate treatment (with benzathine penicillin G) leads to RF recurrences and progressive valve damage-the defining characteristic of RHD which can, in turn, cause atrial fibrillation, heart failure, stroke and endocarditis.
  • 288. Pathogenesis of Acute Rheumatic Fever
  • 289. Cascade of RF and RHD
  • 290. Pathogenesis of Acute Rheumatic Fever …
  • 291. Clinical Features • Following sore throat with GABHS: – Silent period of 2 - 6 weeks – Sudden onset of fever, pallor, malaise, fatigue • After which characteristic manifestations rheumatic fever start to appear: – Arthritis – Carditis – Erythema marginatum – Subcutaneous nodules – Sydenham’s chorea • In one third of patients the streptococcal infection passes unnoticed and 54 to 70% of recurrences of ARF were caused by asymptomatic streptococcal infection.
  • 293. 1. Arthritis • It occurs in about 75% of cases. • Usually a polyarthritis involving big joints: knees, ankles, elbows, wrists • Asymmetrical • Migratory (fleeting) • Joints are hot, red, tender, swollen with limited mobility • It is unusual to involve the central joints as spines, hips and the peripheral ones as the fingers and toes. Infrequently it involves the tempromandibular joint.
  • 294. Arthritis… • No residual deformity (licks) • It is more common and more severe in teenagers and young adults than in children • Lasts 2-6 weeks • Dramatic response to salicylates
  • 295. 2. Carditis • Occurs in 40% of patients during the first attack and almost 100% if ARF recurs. • It may be the only major manifestations and usually appears in the first week of the illness. • Most serious manifestation • May lead to death in acute phase or at later stage • Any cardiac tissue may be affected • Valvular lesion most common: mitral and aortic • Seldom see isolated pericarditis or myocarditis
  • 296. Pancarditis is the most serious and second most common complication of rheumatic fever (50%). In advanced cases, patients may complain of dyspnea, mild-to-moderate chest discomfort, pleuritic chest pain, edema, cough, or orthopnea if they develop congestive heart failure and pericarditis. Upon physical examination, carditis is most commonly detected by a new murmur and tachycardia out of proportion to fever. The murmurs of acute rheumatic fever are typically due to valve insufficiency. Carditis….
  • 297. Carditis.. • Clinical signs: High pulse rate Murmurs : Mitral and aortic regurgitation most common  Pericarditis usually asymptomatic  Occasionally causes chest pain, friction rubs or distant heart sounds  Cardiomegaly  Rhythm disturbances (prolonged PR interval)  Heart failure
  • 298. Clinical Features of Carditis
  • 299. 3. Sydenham’s Chorea(10-20%) • Due to basal ganglia involvement. • May be associated with normal laboratory findings. • Involuntary, sudden, semi-purposeful movements of limbs face and tongue. Disappear during sleep. • Hypotonia and hyporeflexia. • Emotional labiality and instability. • More in females. • Latent period (2-6 months). No arthritis and ESR is usually normal. • Self-limiting.
  • 301. 4. Subcutaneous Nodule – Small, painless, firm, free. – Accumulated Aschoff nodules. – Over bony prominences, tendons . – Often associated with severe carditis. – Can occur with other diseases like rheumatoid arthritis – They last for a week or two and rarely more than a month, and sometimes disappear within several days.
  • 302. 5. Erythemia Marginatum (10%) – Erythema with central pallor. – More on trunk and proximal limbs. – It usually occurs in the covered parts and may be manifested by local application of heat. – Nonpruritic, nonpainful. – Often associated with acute carditis. – They disappear within hours and may appear intermittently within weeks to months
  • 304. Laboratory findings in ARF 1. Elevated acute phase reactants 1. Erythrocyte sedimentation rate(>30mm/hr) 2. Leukocytosis 3. C-reactive protein 2. Recent Evidence of Group A Streptococcal infection : – Raised ASO titer (80% of cases) – Anti DNAase B – Antihyaluronidase – Rapid Stretococcal antigen test. – Positive throat culture for (GAS), – Recent scarlet fever 3. Increased PR interval on EKG (first degree heart block )
  • 305. Imaging • Cardiomegaly and signs of Heart failure on Chest x-ray • 2D and Doppler Echocardiography – To identify and assess severity of carditis
  • 306. Diagnosis of ARF • No specific diagnostic test for ARF • Diagnosis is based on 2015 AHA/ACC with constellation of major and minor manifestations used as diagnostic criteria • For diagnosis of ARF the evidence of recent streptoccal infection should be demonstrated in addition to the criteria.
  • 307. Revised Jone’s Criteria for Diagnosis of ARF (2015 ACC/AHA ) Evidence of preceding group A streptococcal infection (other than chorea):  Raised ASO titer ,OR  Positive throat culture for GABH,OR  Positive Rapid antigen test, OR  Clinical evidence of bacterial Tonsilo-pharyngitis Diagnosis : Initial ARF 2 major or 1 major plus 2 minor manifestations PLUS evidence of recent strep infection (other than chorea) Recurrent ARF 2 major or 1 major and 2 minor or 3 minor PLUS evidence of recent strep infection(other than chorea) Criteria A. Major B. Minor  Arthritis (Monoarthritis or polyarthritis or polyarthralgia)a  Monoarthralgia  Carditisb (Clinical and/or subclinical)  Fever (≥38°C)  Chorea  ESR ≥30 mm/h and/or CRP ≥3 mg/dLc  Erythema marginatum  Prolonged PR on ECG (for age) (unless carditis is a major criterion  Subcutaneous nodules
  • 308. Diagnostic Classes of New ARF Definite ARF: 2 major, or 1 major plus 2 minor manifestations PLUS evidence of recent strep infection (other than chorea) Highly Probable ARF: If an ARF diagnosis is considered highly probable (but not confirmed due to lack of evidence for recent streptococcal infection) Uncertain ARF: in patients from high-risk groups with only one major manifestation of acute Rheumatic fever or borderline echocardiographic findings .
  • 309. Treatment for ARF • Admission to hospital –Admit all patients suspected to have ARF • Confirmation of the diagnosis: –Observation prior to anti-inflammatory treatment: paracetamol may be given for fever or joint pain –Investigations: CBC,ESR,CXR,ECG, Echocardiography