2. History
Asthma : derived from the Greek aazein, meaning "sharp
breath." The word first appears in Homer's Iliad.
In 450 BC. Hippocrates: more likely to occur in tailors, anglers,
and metalworkers.
Six centuries later, Galen: caused by partial or complete
bronchial obstruction.
1190 AD, Moses Maimonides: wrote a treatise on asthma,
describing its prevention, diagnosis, and treatment
17th century, Bernardino Ramazzini: connection between
asthma and organic dust.
1901: The use of bronchodilators started.
1960s: inflammatory component of asthma was recognized and
anti-inflammatory medications were added to the regimens.
4. ASTHMA
Chronic inflammatory condition of the
airways characterized by;
- airflow limitation (reversible with
treatment)
- airway hyper-responsiveness to a wide
range stimuli
- inflammation of the bronchi
In chronic asthma, inflammation maybe
accompanied by irreversible airflow
limitation
Symptoms are cough, wheeze, chest
tightness, and shortness of breath which
often worse at night
5. Simple Definition
A reversible chronic inflammatory airway disease
which is characterized by bronchial hyper-
responsiveness of the airways to various stimuli,
leading to widespread bronchoconstriction, airflow
limitation and inflammation of the bronchi causing
symptoms of cough, wheeze, chest tightness and
dyspnoea.
6. Epidemiology
Common disease with
unacceptably high
morbidity and mortality
Commonly
underdiagnosed and
undertreated
Only 36.1% of adult
asthmatics ever had
their peak flow
measured
Higher prevalence in
rural (4.5%) than in
urban areas (4%),lower
educational status(5.6%)
and lower income
Majority of
patients(87.3%) had mild
asthma; 9.9% had
moderate asthma and
2.7% had severe asthma
Among severe
asthmatics, only 19.4%
were on inhaled
corticosteroids
87%
10% 3%
Asthmatic patient
Mild Moderate Severe
8. EPIDEMIOLOGY
The prevalence of asthma has increased 61% over
the last two decades.
Asthma is the leading chronic illness among
children.
Asthma results in 10 million lost school days and 3
million lost work days.
Deaths from asthma have increased by 31% since
1980.
9. Classification
Extrinsic – implying a definite external cause
more frequently in atopic inviduals
(atopic – individual which tends to develop hypersensitivity by
contact with allergens)
often starts in childhood - accompanied by eczema
Intrinsic/cryptogenic – no causative agent can be identified
starts in middle age
10. Types of Asthma
According to the severity:
helpful for treatment and
management.
Very mild
Mild
Moderate
Moderately
Severe
Severe
11. Types of Asthma
According to pathophysiology
Allergic asthma
Intrinsic (Non-Allergic)
Exercise-induced
Occupational (allergic)
Steroid-resistant
ABPA (allergic)
12. Pathogenesis
Complex, not fully understood
numbers of cells, mediators, nerves, and
vascular leakage -activated by expose to
allergens or several mechanism
Inflammation
Eosinophils, T-lymphocytes, macrophages and
mast cell
Remodeling
Deposition of repair collagens and matrix proteins-
damage
Loss of ciliated columnar cells- metaplasia –
increase no of secreting goblet cells
13. Pathologic features of asthma
i. Inflammatory cell infiltration of the airways
ii. Increased thickness of the bronchial smooth muscle
iii. Partial or full loss of the respiratory epithelium
iv. Subepithelial fibrosis
v. Hypertrophy and hyperplasia of the submucosal glands and
goblet cells
vi. Partial or full occlusion of the airway lumen by mucous plugs
vii. Enlarged mucous glands and blood vessels
14. Pathophysiology
Smooth muscle contraction
Thickening of airway –cellular infiltration and inflammation
Excessive secrection of mucus
Genetic factor
Cytokine gene complex (chromosome 5)-IL-4
gene cluster control IL-3, IL-4 , IL-5 and IL-13
Environment factor
Childhood expose irritants or childhood infection
15. Pathophysiology
Extrinsic asthma: Atopic/allergic,
occupational, allergic
bronchopulmoary aspergillosis.
Atopic or allergic
Dust, pollens, animal dander, food etc.
Family history of atopy.
↑ serum IgE.
Skin test with Ag wheal, flare (
Classical IgE mediated response)
Exposure of pre-sensitised mast cells to
the Ag stimulates chemical mediators
from these cells. Type 1 hypersensitivity.
16. 1.Early phase
Inhaled Antigen
Sensitised mast cells on the mucosal surface
mediator release.
Histamine bronchoconstriction, increased vascular
permeability.
prostaglandin D 2 bronchoconstriction,
vasodilatation.
Leucotriene C4,D4, E4 Increased vascular
permeability, mucus secretion and
bronchoconstriction.
Direct subepithelial parasympathetic stimulation
bronchoconstriction.
17. 2.Late phase
starts 4 to 8 hours later
Mast cell release additional cytokine
Influx of leukocytes(neutrophil,eosinophil)
Eosinophils are particularly important- exert a variety of effect
22. Aetiology and triggers
Complex and multiple environmental and genetic
determinant
a) Genetic factors
b) Allergen exposure house dust mite, household pets, grass
pollen
c) Atmospheric polution sulphur dioxide, ozone, ciggerate
smoke, perfume
d) Dietary deficiency of antioxidants vit E and selenium may
protect asthma in children(freshfruits and vegetables)
23. Aetiology and triggers
e) Occupational sensitizers
isocyanates(from industrial coating, spray painting)
colophony perfumes(electronic industries)
e) Drugs
NSAIDS
B-blocker(B1 adrenergic blocker drug such as atenolol is avoided to
treat HPT and angina in asthmatic pt
f) Cold air
g) Exercise exercise-induced wheeze is driven by histamin
and leukotrienes which are release from mast cells when
epithelial lining fluid of the bronchi become hyperosmolar
owing to drying and cooling during exercise
h) Emotion
24.
25.
26.
27.
28. History
Presenting symptoms:
Cough ± sputum
- time: become worse at night
- duration: chronic / acute
- associated with wheezing
- fever? URTI
Wheeze
- max during expiration and accompanied by prolonged
expiration
29. Cough History
1.Ask specifically about the symptoms:
-Cough?how is the cough?
more severe at night or on day?
associated symptoms like dyspnea &
wheezing?
how long is the cough?
Recurrent?Any previous similar episode?
Aggravated factor?like cough become severe
after exercise?or the cough is initiated after
exercise?
30. Cough History
2.If the cough is associated with dyspnea and
wheezingis it relieved by bronchodilator?
3.Ask for any precipatating factors
-whether the symptoms(cough,dyspnea,wheezing)
started after exposure to weather changes, dust,
exercise, infection or drugs?
4.Is there any pets,carpet or feather pillow in home?(easily
trapped dust and the dust or animal
fur will cause exacerbation of asthma)
31. Dyspnoea History
Dyspnoea
- onset: after exercise? cold? dust?
animal fur? emotion?
- severity and pattern: varies from day to
day or from hour to hour
- no chest pain
32. History
Clinical features
Recurrent episodes of wheezing,chest tightness,breathlessness
and cough
Precipitants- cold,allergen,pollutant,viral urti
Exercise tolerance
Disturbed sleep
Other atopic disease
Home-Pet?Carpet?
Occupation
33. History
Clinical features
Display diurnal pattern,symptoms
and PEF worse in the morning
Mild intermittent asthma-
asymptomatic between
exacerbation
Persistent asthma-chronic wheeze
and breathlessness
34. History
5.Any history of atopy(eczema,hay fever) or allergic
rhinitis?
6.Any family history of asthma?Any childhood asthmatics?
7.Whether he is a smoker or any family members is a smoker?
8.What is his occupation? Exposure to chemicals?
35. History
Past medical history:
Experienced asthma attack before
Taking any medications: NSAIDs / β-blocker / aspirin (non
atopic asthma)
Family history:
Has family history of asthma
36. History
Social history:
Occupation: expose to fumes/organic/chemical dust
House: near to factory? Pets? Dust? Carpet? Feather pillow?
Smoking in any family members
37. known asthmatic
When he was diagnosed with asthma?
How the asthma was diagnosed?
Who diagnosed it?
Whether he is on prophylaxis?
What type of prophylaxis?
How he get the drugs and how many dosage of the
drugs?
Whether he know how to deliver the drugs properly?
How is his compliance to drugs?
38. Physical examination
General inspection:
- tachypnoeic, sign of respiratory distress, effort of breathing,
cyanosis (life-threatening)
Inspection:
- fingers: tar staining
- pulse rate: tachycardia and pulsus paradoxus, bradycardia (life-
threatening)
- used of accessory muscles or recession
- wheezing
39. Chest
Inspection:
- shape: hyperinflated in severe
asthma
- movement of chest/silent chest
(life-threatening)
- chest deformity:
- recession:
Palpation:
- chest expension may be reduce
(hyperinflated)/ normal
- apex beat: may be displaced
-vocal fremitus: decrease
Percussion:
- may be
hyperresonance /
normal
Auscultation:
- breath sound:
vesicular
- ronchi in expiratory
phase, may be both in
severe asthma
- prolonged expiratory
phase
-vocal resonance
decrease / normal
40.
41. Clinical features
Sign
• Tachypnoea,audible wheeze,hyperinflated
chest,hyperresonant percussion note,diminished air
entry,widespread polyphonic wheze
• Severe attack – inability to complete sentences, pulse
>110bpm, RP>25/min, PEF 33-50%
• Life-threatening attack- silent
chest,cyanosis,bradycardia,exhaustion, PEF <
33%,confusion
• Pulsus paradoxus (exaggeration of the normal variation in
the pulse volume with respiration, becoming weaker with
inspiration and stronger with expiration )
42. Correlation
+ The symptoms of asthma consist of a triad of dyspnea,
cough, and wheezing.
+ At the onset of an attack, patients experience a sense of
constriction in the chest, often with a nonproductive
cough.
+ Respiration becomes audibly harsh; wheezing in both
phases of respiration becomes prominent; expiration
becomes prolonged; and patients frequently have
tachypnea, tachycardia, and mild systolic hypertension.
+ The lungs rapidly become overinflated.
+ If the attack is severe or prolonged, there may be a loss of
adventitial breath sounds, and wheezing becomes very
high pitched.
+ The accessory muscles become visibly active, and a
paradoxical pulse often develops.
44. Diagnosing asthma
Reversible and variable airflow limitation-as
measured by a peak expiratory flow (PEF)
meter in any of the following ways:
PEF increases more than 15% and 200mls
15 to 20 mins after inhaling a short acting
beta2 agonist, or
PEF varies more than 20% from morning
measurement upon arising to measurement
12 hours later in patients who are taking a
bronchodilator, or
PEF decreases more than 15% after 6 mins
of running or exercise
47. Non-specific investigation
Non-specific:
- full blood count and differential count: increase
number of eosinophils number
- arterial blood gases
- sputum test: number of eosinophils
- chest X-ray: hyperinflated
48. Specific investigation
Specific:
- respiratory function test:
1. peak expiratory flow
2. spirometry
- exercise tests
-histamine/methacholine bronchial provocation test
- trial of corticosteroids
49. Reversibility Test
+ This test is done to see whether the obstruction can
be relieved by the use of a short-acting
bronchodilator eg salbutamol
+ An improvement of 15% or more (as measured on
the peak flow meter) is diagnostic of asthma.
+ However, in severe chronic disease or patient who
has treated with long-acting bronchodilators, little
reversibility will be demonstrated.
50. Reversibility test
Forced expiratory manoeuvres
before 20 minutes after
inhalation of a beta-2-
adrenoceptor agonist. Note the
increase in FEV1 from 1.0 to 2.5
litres.
51. Peak expiratory flow rate
Simple and cheap
Subject take full inspiration then blow out forcefully
into peak flow meter.
Best used to monitor progression of the asthma and
its treatment.
To access possible occupational asthma
PEFR value varies with sex, age and height.
52. Peak Expiratory Flow Rate (PEFR)
The maximum rate of air breathed out as hard as
possible through a measuring device called a peak
flow meter, (after a full breath taken in).
Reading is measured in litres/minute (l/min).
Take 3 readings and choose the best
Reading < 80% - presense of obstruction, but not
diagnostic of asthma
53. Require to take a series of reading
- on waking up
- prior taking bronchodilator
- after taking bronchodilator (before sleep)
54. PEF measurements
1. During periods of well-being: provides measurement
of the patients best PEF value which will provide the
target for the doctor and the patient to aim
for.Twice daily measurements before any inhaled
bronchodilator tx will determine the diurnal variability
of airway calibre.Good control of asthma means PEF
variability is maintained at less than 10%.
2. During symptomatic episodes: During an attack of
asthma PEF fairly accurately measures the degree of
bronchospasm.A PEF of less than 50% of normal or
best suggests a very severe attack and a PEF of less
than 30% suggests a life-threatening attack
60. Spirometry Test
+ It is the single best diagnostic test for patients with airflow
limitation.
+ A Spirometry Test
+ - measures the volume of air blown out against time
+ - gives more specific information about lung function.
+ A value is calculated for the amount of air blown out in one
second - “Forced Expiratory Volume” or FEV1).
+ This is divided by the total amount of air blown out until all air is
expired - Forced Vital Capacity or FVC).
+ FEV1/FVC expressed as a percentage value
61. + Reading is affected by age, gender and height
+ Male Spirometry reading range
Mild reduction: 2.5 litres or more
Moderate reduction :1.5 to 2.49 litres
Severe reduction :Less than 1.5 litre
+ Female Spirometry reading range
Mild reduction :2.0 litres or more
Moderate reduction: 1.0 to 1.99 litres
Severe reduction: Less than 1.0 litre
+ In asthma, the readings will be reduced, returning to normal
between episodes
62. TLC
VC
RV
IC
FRC
IRV
ERV
RV
TV
TLC : total lung capacity
VC : vital capacity
RV : reserve volume
IC : inspirational capacity
FRC : functional residual capacity
IRV : inspirational reserve volume
TV : tidal volume
ERV : expiratory reserve volume
Normal:75-80%
Obstructive airway
disease: reduced ratio
Restrictive lung disease:
ratio normal or increase
(enhanced elastic recoil).
63. Exercise Test
+ Done especially in children
+ Peak flow reading measured before hand
+ Ask patient to run for 6 min, to increase HR > 160 beats/min
+ Cannot run – use cold air challenge, isocapnoiec (CO2)
hyperventilation, aerosol challenge with hypertonic solution
+ After exercise – take readings at intervals of 5, 10 and 15
minutes.
+ Diagnosed asthma - fall in peak flow of 15% or more, after
exercise.
66. Chest X-ray
Showed lung hyperinflation.
Not diagnostic of asthma
Useful to rule out other causes eg.
Pneumothorax
-----------------------------------------------
Hyperinflation and increased
bronchovascular markings
67. Allergies & Atophy
Allergen Provocation Test
In suspected occupational
asthma and food-allergy
related asthma
Skin-Prick Test
To identify allergens
A drop of allergen is placed
on skin , site is marked and
pricked with needle,
measured any weals
70. Severity assessment for acute setting of AEBA
Mild Moderate Severe
Breathless Walking Talking At rest
Can lie down Prefer sitting Hunched forward
Talk in Sentences Phrases Words
Alertness May be Usually agitated Agitated
Central cyanosis Absent Absent Present
Use of accessory
muscle
Absent Moderate Marked
Sternal retraction Absent Moderate Marked
Wheeze on
auscultation
Moderate, often end
expiratory
Loud Loud Silent Chest
Pulsus paradoxus Not palpable May be palpable Often palpable
Initial PEF More than 80% 60 – 80% Less than 60%
Oximetry on
presentation
More than 95% 91 – 95% Less than 90%
74. Management of Chronic Asthma
Aims of management
• to recognize asthma
• to abolish symptoms
• to restore normal or best possible long term airway
function
• to reduce morbidity and prevent mortality
75. Approach of chronic asthma
Education of patient and family
Avoidance of precipitating factors
Use of the lowest effective dose of convenient
medications minimizing short and long term side
effects.
Assessment of severity and response to treatment.
76. 1) Education of patient and family
i. Nature of asthma
ii. Preventive
measures/avoidance of
triggers
iii. Drugs used and their side-
effects
iv. Proper use of inhaled
drugs
v. Proper use of peak flow
meter
vii. Knowledge of the
difference between
relieving and preventive
medications
vii. Recognition of features
of worsening asthma
increase in
bronchodilator
requirement
development of
nocturnal symptoms
reducing peak flow
rates).
viii. Self management plan
for selected, motivated
patients or parents.
ix. The danger of non
prescribed self
medication including
certain traditional
medicines.
77. 2) Avoidance of precipitating
factors
The following factors may
precipitate asthmatic attacks:
• Beta blockers
contraindicated in all
asthmatics
• Aspirin and nonsteroidal anti-
inflammatory drugs if known
to precipitate asthma, these
drugs should be avoided.
• Allergens e.g. house dust
mites, domestic pets, pollen
should be avoided whenever
possible.
• Occupation should be
considered as a possible
precipitating factor.
• Smoking active or passive.
• Day to day triggers such
as exercise and cold air. It is
preferable to adjust
treatment if avoidance
imposes inappropriate
restrictions on lifestyle.
• Atmospheric pollution.
• Food if known to trigger
asthma, should be avoided.
78. 3) Medication
2 major groups of drugs:
Bronchodilator drugs
•to relieve
bronchospasm and
improve symptoms.
Anti inflammatory
drugs
•to treat the airway
inflammation and
bronchial
hyperresponsiveness,
the underlying cause
of asthma, i.e. to
prevent attacks.
79. Drug Delivery
The inhaled route is preferred for beta2-
agonists and steroids as it produces the same
benefit with fewer side effects
Inhaled medications exert their effects at lower
doses
pMDI is suitable for most patients as long as the
inhalation technique is correct
Alternative methods include spacer
devices,dry powder inhalers and breath-
actuated pMDI
Nebulised route is preferred in the
management of acute attacks
80. 3 main groups of bronchodilators [β2
agonists]
Inhaled β2agonist
•Salbutamol
(Ventolin,
Respolin)
•terbutaline
(Bricanyl)
•fenoterol
(Berotec)
•salmeterol
(Serevent) - long
acting
Oral long acting β2
agonist:
•salbutamol
(Volmax)
•terbutaline
(Bricanyl durules)
•bambuterol
(Bambec)
Oral short acting β2
agonist:
•salbutamol
•terbutaline etc.
82. Approach To Drug Therapy
- "Stepwise Approach"
[step 1]
Start at the step most appropriate to severity, moving up if needed
or down if control is good for > 3 months. Rescued courses of
prednisolone may be needed
STEP 1
MILD EPISODIC ASTHMA
• Infrequent symptoms
• No nocturnal symptoms
• PEF 80-100% predicted
Treatment:
inhaled beta2 agonist "as needed" for
symptom relief. If needed more than once a
day, advance to Step 2
83. Approach To Drug Therapy -
"Stepwise Approach" [step 2]
STEP 2
MODERATE ASTHMA
• Frequent symptoms
• Nocturnal symptoms present
• PEF 60-80% predicted
Treatment
• inhaled steroids, e.g. beclomethasone
or budesonide 200-800 mcg/day
• inhaled sodium cromoglycate plus
• inhaled beta2 agonist "as needed"
84. Approach To Drug Therapy -
"Stepwise Approach" [step 3]
STEP 3
SEVERE CHRONIC ASTHMA
• Persistent symptoms
• Frequent nocturnal symptoms
• PEF 60% predicted or less
Treatment:
• inhaled beclomethasone or budesonide 800-2000
mcg/day plus
• inhaled beta2 agonist as needed plus, if necessary
• oral beta2 agonist preferably long acting, or
• inhaled long acting beta2 agonist, or
• inhaled ipratropium bromide 40 mcg 3-4 times a day,
or
• oral theophylline (sustained release), or
85. Approach To Drug Therapy -
"Stepwise Approach" [step 4]
STEP 4
VERY SEVERE ASTHMA
• Persistent symptoms not controlled by step 3
medications
Treatment:
• as in step 3, plus oral steroids (the lowest dose possible)
STEP DOWN
• Patients should be reviewed regularly.
• When the patient’s condition has been stable for 3-6
months, drug therapy may be stepped down
gradually.
• The monitoring of symptoms and peak flow rate should
be continued during drug reduction.
86.
87. Management of acute severe asthma
•RR >50/min
•PEFR <50%
•Pulse >140 beats/min
•breathlessness
•10 puffs Bronchodilator
and Metered Dose Inhaler
•High flow 02, bronchoD
•MDI, nebulizer(1-2h)
•Oral prednisolone (3-5d)
•Monitore PEFR/O2
•B2 agonist / 02 if required
•PEFR <33%
•Tiredness
•Cyanosis
•Decrease respiratory
effort
•Silent chest
•iv aminophylline
•Iv hydrocortisone
•Salbutamol
•Ipratropium bromide
•Adequate hydration
•antibiotic
•ICU
•Artificial ventilation•Wean iv
•Β2 Agonist
•Oxygen if required
•Oral prednisolone
•Monitor PEFR
•Patient’s education
•Review maintenance
medication
•Review inhaler
technique
•Follow up
•PEFR monitor
DISCHARGE PLAN
response
Give
treatment
improve
88. Management Of Acute Asthma
Aims Of Management
i. To prevent death
ii. To relieve respiratory distress
iii. To restore the patient’s lung function
to the best possible level as soon as
possible.
iv. To prevent early relapse
89. 1. Assess severe attack
Severe attack:
a) Unable to complete sentences
b) RR>25/min
c) PR>110 bpm
d) PEF< 50% of predicted or best
Life-threatening attack:
a) PEF<33% of predicted or best
b) Silent chest, cyanosis, feeble respiratory effort
c) Bradycardia/ hypotension
d) Exhaustion, confusion, or coma
e) ABG : normal/high PaCO2>5kPa (36mmHg)
PaO2< 8kPa (60mmHg)
low pH, e.g. <7.35
90. 2. Start treatment immediately
• Sit patient up & give high dose
O2 in 100% via non-rebreathing
bag
• Salbutamol 5mg (or terbutaline
10mg) + ipratropium bromide
0.5 mg nebulized with O2
• Hydrocortisone 100mg
IV/prednisolone 30 mg PO
(both if very ill)
• CXR to exclude pneumothorax If life threatening features (above)
present:
• Inform ITU, and seniors
• Add MgSO4 1.2-2g IV over 20 min
• Give Salbutamol nebulizers every 15
min, or 10mg continuously per hour
91. Further management
If improving
• 40-60% O2
• Prednisolone 30-60mg/24h PO
• Nebulized salbutamol every 4 h
• Monitor peak flow and O2 saturations
If not improving after 15-30min
• Continue 100% O2 and steroids
• Hydrocortisone 100mg IV or prednisolone 30mg
PO if not already given
• Give Salbutamol nebulizers every 15 min, or 10
mg continuously per hour
• Continue ipratropium 0.5 mg every 4-6h
92. Post-attempt….
If patient still not improving
• Discuss with seniors and ITU.
• Repeat salbutamol nebulizers
every 15 mins
• MgSO4 1.2-2g IV over 20 min,
unless already given.
• Consider aminophylline, if not
already on a theophylline.
Alternatively, give salbutamol IVI.
Monitoring the effects of
treatment
• Repeat PEF 15-30min after
initiating treatment
• Pulse oximeter monitoring:
maintain SaO2 >92 %.
• Check blood gases within
2h if:initial PaO2 was
normal/ raised or initial
PaO2 <8 kPa (60mmHg)
or patient deteriorating
• Record PEF pre- and post-
β-agonist in hospital at
least 4 times.
93. Once patient improving…
Once patient is improving
• Wean down and stop aminophylline over 12-24
h.
• Reduced nebulized salbutamol and switch to
inhaled β-agonist.
• Initiate inhaled steroids and stop oral steroids if
possible
• Continue to monitor PEF. Look for deterioration
on reduced treatment and beware early
morning dips in PEF
• Look for the cause of the acute exacerbation
and admission
99. Follow-Up and Monitoring
Include review of symptoms and
measurement of lung function
o PEF monitoring at every visit along
with review of symptoms helps in
evaluating the patient’s response to
therapy and adjusting tx.PEF
consistently >80% of the patient’s
personal best suggests good
control.
o Regular visits (at 1 to 6 month
interval as appropriate) is essential
even after control of asthma is
established
100. Asthma Management Plan
When PEF >80%: continue current
dose of inhaled corticosteroids
When PEF 60-80%:double the dose
of inhaled corticosteroids
When PEF 40- 60%:start rescue
course prednisolone
When PEF persists below 60%
despite rescue course prednisolone
with worsening symptoms,advised
to come to EMERGENCY DEPT
immediately
101. Management of asthma in
pregnancy
In general during pregnancy,asthma
becomes worse in a third of women,is
stable in another third and improves in
the remaining third.
Women should be reassured that their
asthma medication carries less risk to
the foetus than a severe asthma
attack
Inadequately treated asthma can
cause maternal and foetal
hypoxaemia,which leads to
complications during pregnancy and
poorer birth outcomes
102. Management: Pregnancy in
asthmatics
Treatment should be aggressive,with
the aim of eliminating symptoms and
restoring and maintaining normal lung
function
Beta2 agonists: No evidence of a
teratogenic risk with the commonly
used inhaled beta2 agonists
Ipratropium bromide: appears to be
safe for use during pregnancy
Salmeterol/formoterol: not been tested
extensively in pregnant women
103. Management: Pregnancy in
asthmatics
Theophyllines: may aggravate the nausea and
GERD and can caause transient neonatal
tachycardia and irritabilityTeratogenicity has
been shown in animals.
Sodium cromoglycate: no adverse foetal effects
Inhaled corticosteroids: mainstay of tx in
persistent asthma,good safety profile in
pregnancy
Oral corticosteroids: necessary for severe
asthma in pregnancy but usually only for short
periods.Increased risk of cleft palate in animals
given huge doses of oral steroids
Anti-leukotrienes: no data available
104. Labour and Breastfeeding
Women with very severe asthma
may be advised to have an
elective caesarean section at a
time when their asthma control is
good
Breastfeeding should be continued
in women with asthma
In general,asthma medications are
safe during pregnancy and
lactation and the benefits outweigh
any potential risks to the foetus and
baby
105. Allergic Rhinitis and Asthma
80% of patients with asthma have
allergic rhinitis
When allergic rhinitis is undetected
or untreated,patients have frequent
exacerbations not responding to
conventional treatment
Nasal inhalation of corticosteroids
are mainstay of treatment with or
without oral antihistamine
106. Status Asthmaticus
Acute exacerbation of asthma that does
not respond to standard treatment of
bronchodilators and corticosteroids.
Symptoms include chest tightness, rapidly
progressive dyspnoea, dry cough and
wheezing
The lung failure means that oxygen can
no longer be provided, carbon dioxide
can no longer eliminated.
Hence, leading to acidosis.
107. It is not just asthma
CASE PRESENTATION / UMMC
108. MIBMH
10.5 years old boy, known case of mild intermittent
asthma presented to HSB with:
Fever, cough and runny nose ----- 1 wk.
Hemoptysis and loss of appetite ---- 5d
No night sweating .
Seen by GP and managed with oral antibiotic and
symptomatic treatment but the patient did not
improve.
109. Review of symptoms
The patient is unable to lie flat for the past 2 weeks
due to feeling of breathlessness.
110. In HSB
respiratory distress upon admission
CXR:
mediastinal mass on right perihilar region
multiple cannon ball lesions in both lung fields, so
CT thorax, abdomen and pelvis done
Huge anterior mediastinal mass encasing great vessels with lung
metastasis and lymphadenopathy.
Referred to UMMC for possibility of malignancy.
111. Past history
Asthma
since age of 7 years
not on regular follow-up or treatment/prophylaxis
mild infrequent diurnal symptoms
no interference with general activity or school attendance.
acute exacerbation: twice a year and precipitated mainly
by coldness.
No hospital admission
112. Perinatal history: uneventful.
Developmental history: attends school, average
level, very shy.
Immunization: full schedule.
Allergy: allergic to dust.
Family and social history:
No ill family member.
No H/O contact with T.B
113. O/E
Looks lethargic, dyspneic RR 32/min with recessions,
HR 120/min, SpO2 96% on face mask O2 5l/min, temp
36.4C
No lymphadenopathy.
Lungs: -reduced breath sounds on right medial and
lower zones with crepitations on the right side
CVS: S1 + S2 , no murmur.
Abdomen: soft, liver 2cm firm.
114. Genitalia: pubic hair stage 3, penile length 7.5cm,
testes 2 ml each.
Breast tissue: gynaecomastia.
123. diagnosis
Mediastinal germ cell tumor with bilateral lung
metastasis and pseudoprecocious puberty.
Klinefelter syndrome.
124. Management and progress
Respiratory support, required BiPAP .
Required neb Salbutamol 4 hourly.
Had spikes of fever, covered with Erythromycin and
Ceftriaxone.
After 4 days in PICU transferred to P6.
Started chemotherapy(UKCCSG).
Had NNF covered with piptazocin then imipenem
and later on Ampho-B.
127. Klinefelter syndrome
In 1942 Klinefelter et al published a paper on 9 men
with large breasts, minimal sexual and body hair, small
testes and inability to produce sperms.
It is the most common syndrome assoc with male
hypogonadism and infertility.
Classically 47XXY, but many variants like 48 XXXY,
48XXYY,49XXXXY,49XXXYY,50XXXXYY.
It is due to meiotic non-disjunction. mosaic patients
may be fertile .
128. Features
Hypogonadism (small testes and azoospermia-hyalinzation
and fibrosis of seminiferous tubules).
Gynaecomestia in late puberty (30-50%) due to increase
estradiol/testosterone ratio.
Psychosocial problems.
Elevated urinary gonadotrophins.
Mental retardation is affected by number of X chromosomes
(decreased IQ 15 points for each X chromosome) [most males
with 47XXY have normal intellegence, 70% have minor
developmental and learning disability]
129. Other features:
Pes cavus, genu valgus, fifth finger clinodactily.
Taurodontism (prominent molar teeth): 40% in
Klinefelter, 1% in general population.
Radio-ulnar synostosis---- 49XXXXY.
132. Mortality
40% of conceptions with Klinefelter survive fetal
period.
Mortality is not significantly higher in healthy
individuals.
133. Prevalence: in USA 1:500-1000
Race: no race difference.
Age: it goes undetected in most affected males
until adulthood. the common indication for
karyotyping is hypogonadism and infertility.
134. investigations
Mid-puberty: increase FSH and LH, decrease
testosterone.
Increase estradiol/testosterone ratio-----gynaecomastia
80%.
Cortisol should be checked (47% have low cortisol).
Decrease osteocalcin---- bone resorption.
Coagulation profile because of increased risk of DVT
and pulm embolism.
Karyotyping:47 XXY 80-90 % - 10% mosaic.
136. Primary mediastinal germ cell
tumors
Comprise only 1-3% of germ cell tumors.
Overall teratoma is the most common variant,
seminoma is the most common malignant variant.
Malignant variants are uncommon and more in males.
Benign variants are equally disributed among males
and females.
Testicular examination, U/S and CT are mandatory to
rule out testicular primary cancer.
137. Serum markers
Alpha-fetoprotein: indicates malignant non-
seminomatous type.
BhCG: suggests trophoblastic component.
Malignant non-seminomatous and
mixed GCTs carry worse prognosis
than other GCTs.
138. Association of M- GCTs with
Klinefelter syndrome
Klinefelter syndrome is present in 20% of patients
with M-GCT.
The incidence of M-GCT is 50 fold increased
in patients with Klinefelter syndrome.
M-GCT mask the usual clinical signs of Klinefelter
syndrome by inducing puberty by BhCG.
139. Comparison of GCT between KS
and general population
Klinefelter syndrome:
All contain non-seminominatous
elements
Present at younger age (mean
17 years)
Precocious puberty is seen more
often.
Almost exclusively extragonadal.
General population:
Pure seminoma is the most
common malignant variant.
Older age at presentation (mean
29 years)
Precocious puberty is less often.
Only 2-5% extragonadal.