one airway disease

Asthma &Allergic Rhinitis=

Allergic rhinobronchitis =

United Airway Disease =

One Airway Disease =

Linked Airway Disease

Gamal Rabie Agmy, MD, FCCP Professor of chest Diseases, Assiut university

Definition of allergic rhinitis

“Rhinitis is defined as an inflammation of the lining of the nose and is characterised by nasal symptoms including anterior or posterior rhinorrhoea, sneezing, nasal blockage and/or itching of the nose…It is often associated with ocular symptoms.”

Definition of asthma

“Asthma is a common and chronic inflammatory condition of the airways that is complex and characterized by variable and

recurring symptoms, airflow obstruction, bronchial

hyperresponsiveness, and an underlying inflammation” 2

1 Guidelines for the Diagnosis and Management of Asthma Expert Panel Report 3 . 2007

2. National Asthma Education and Prevention Program Expert Panel Report 3:Guidelines for the Diagnosis and Management of Asthma. 2007

SAR, seasonal allergic rhinitis

PAR, perennial allergic rhinitis

Asthma is a 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.

Definition of asthma

NEW!

GINA 2014

Link between Asthma and

Rhinitis

Allergic rhinitis (AR) and asthma affect

the upper and lower respiratory tracts,

respectively.

Both are characterized by inflammation

of the respiratory mucosa and involve

similar inflammatory cells and

mediators.

Link between Asthma and

Rhinitis

Upper and lower airways form a continuous

respiratory tract

Many inflammatory changes of allergic

rhinitis are similar to those of allergic

asthma

The anatomical and immunological link

between the lung and nose means that

inflammation in one organ influences

symptoms in the other

Epidemiologic Links between Allergic Rhinitis and Asthma

Many Patients with Asthma Have

Allergic Rhinitis

Up to 88%

of all asthmatic patients have allergic rhinitis

BMJ 2002; 324 doi: http://dx.doi.org/10.1136/bmj.324.7334.403 (Published 16 February 2002) Cite this as: BMJ 2002;324:403

8


Many Patients with Asthma Have

Allergic Rhinitis

Adapted f rom Bousquet J et al J Allergy Clin Immunol 2001;108(suppl 5):S147–S334; Sibbald B, Rink E Thorax 1991;46:895–901; Leynaert B

et al J Allergy Clin Immunol 1999;104:301–304; Brydon MJ Asthma J 1996:29–32.

Up to 80%

of all asthmatic patients have allergic rhinitis

All asthmatic patients

Coexistence of Asthma and

Rhinitis

88%

50%

Percentage of Patients with Co-existing Conditions

0%

20%

40%

60%

80%

100%

Asthma patients Rhinitis patients

% p

atients

88% 50%

BMJ 2002; 324 doi: http://dx.doi.org/10.1136/bmj.324.7334.403 (Published 16 February 2002) Cite this as: BMJ 2002;324:403

Allergic Rhinitis


Allergic Rhinitis and Asthma Have Similar

Prevalence Patterns

Study of worldwide prevalence of atopic diseases in 463,801 children 13–14 years of

age. Children self-reported symptoms over 12 months using questionnaires.

UK

Australia

Canada

Brazil

USA

South Africa

Germany

France

Argentina

Algeria

China

Russia

0 5 10 15 20 25 30 35 40

% prevalence

UK

Australia

Canada

Brazil

USA

South Africa

Germany

France

Argentina

Algeria

China

Russia

0 5 10 15 20 25 30 35 40

% prevalence

Asthma

Adapted from the International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee Lancet 1998;351:1225–1232.

Adapted from National Institutes of Health Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention: A Pocket Guide for Physicians and Nurses. Publication No. 95-3659B. Bethesda, MD: National Institutes of Health, 1998; Bousquet J et al J Allergy Clin Immunol 2001;108(suppl 5):S148–S149.

One Airway, One Disease

Both Asthma and Allergic Rhinitis Are Inflammatory Conditions

Asthma is fundamentally a disease of inflammation

Inflammation of the lower airways causes

bronchoconstriction and airway hyperresponsiveness,

resulting in asthma symptoms

Allergic rhinitis is an IgE-mediated inflammatory disorder

Inflammation of the nasal membranes in response to

allergen exposure results in nasal symptoms

IgE=immunoglobulin E


Both Asthma and Allergic Rhinitis Are Inflammatory

Conditions

In AR, one distinction is heavy

vascularization of the nasal passages,

which may lead to severe nasal

obstruction.

In asthma, the presence of smooth

muscle from the trachea to the

bronchioles can result in characteristic

bronchoconstriction

Robert A. Nathan, MD. Management of Patients with Allergic Rhinitis and Asthma: Literature Review.2009

14


Allergic Rhinitis and Asthma Share Common

Inflammatory Cells and Mediators

Adapted f rom Casale TB et al Clin Rev Allergy Immunol 2001;21:27–49; Kay AB N Engl J Med 2001;344:30–37.

Early-phase

response

Late-phase

response T cells

Inflammatory

mediators

Allergen

Cytokines

Preformed Mediators Cysteinyl leukotrienes

Prostaglandins

Platelet-activating factor

Eosinophils

Membrane-bound

IgE

Mast

cell

Promotes eosinophil and other cell migration and infiltration

Nasal mucosa

Allergic inflammatory response

• Nasal inflammation

• Nasal obstruction • Difficulty breathing • Tinnitus

Late-Phase Inflammatory Response

(4–24 hours)

Histaminic response

• Sneezing

• Itchy, watery eyes

• Rhinorrhoea

• Nasal congestion

Histamine binds to H1 receptors

Early-Phase Inflammatory Response

(minutes-1 hour)

Allergic Rhinitis

Leukotriene C4

Prostaglandin D2

Tryptase

HISTAMINE

CYTOKINES

IL-1

IL-3

IL-4

IL-5

IL-6

IL-13

TNF-

CHEMOKINES

IL-8

Eotaxin

RANTES

ADHESION MOLECULES

P-selectin

ICAM

Allergen

Allergic Rhinitis and Asthma Share a Similar Inflammatory

Process and Occur in the Mucosa

Eos=eosinophils; neut=neutrophils; MC=mast cells; Ly=lymphocytes; MP=macrophages

Adapted from Bousquet J et al J Allergy Clin Immunol 2001;108(suppl 5):S148–S149.

Eosinophil infiltration

Allergic rhinitis Asthma

Nasal mucosa Bronchial mucosa

Asthma Inflammation

The underline cause of Asthma is the

inflammation…

Does the ICS based therapy is enough?

Clinical Links between Allergic Rhinitis and Asthma

Many Patients with Asthma Have Nasal Inflammation

Eosinophil counts in the nasal mucosa

Study of whether nasal mucosal inflammation exists in asthma regardless of the presence of allergic rhinitis in atopic

subjects 20 to 66 years of age

Bars represent median values.

Adapted from Gaga M et al Clin Exp Allergy 2000;20:663–669.

18

16

14

12

10

8

6

4

2

0

Eosinophils/ field of nasal biopsy

Rhinitis No rhinitis Control

(n=9) (n=8) (n=10)

p<0.001 p<0.001

Asthmatic

Clinical Links between Allergic Rhinitis and Asthma

Inflammatory Changes in the Nasal and

Bronchial Mucosa Are Correlated

Study of whether nasal mucosal inflammation exists in asthma regardless of the presence of allergic

rhinitis in atopic subjects 20 to 66 years of age

Adapted from Gaga M et al Clin Exp Allergy 2000;20:663–669.

40

35

30

25

20

15

10

5

0

Asthmatic nasal mucosa eosinophils

0

r=0.851, p<0.001

Asthmatic bronchial mucosa eosinophils

5 10 15 20 25 30

(n=17)


Symptoms Correlate with the Early- and Late-Phase

Responses in Allergic Rhinitis and Asthma

FEV1=forced expiratory volume in one second Adapted from Varner AE, Lemanske RF Jr. In: Asthma and Rhinitis. 2nd ed. Oxford: Blackwell Science, 2000:1172–1185; Togias A J Allergy Clin Immunol 2000;105(6 pt 2):S599–S604.

(Asthma)

Score for nasal

symptoms Sneezing Nasal pruritus Congestion Rhinorrhea

Time post-challenge (hours)

1 Antigen

challenge

3–4 8–12 24

Immediate (early) phase Late phase

FEV1

(% change)

Time (hours)

0

50

100

1 10 24 0 2 3 4 5 6 7 8 9

Upper Airways

Lower Airways

(Allergic rhinitis)

22

Congestion and Inflammation: Adverse Clinical Impact in Upper Respiratory Disease

Allergic rhinitis

Nasal polyps

Sleep disturbance, including sleep-disordered breathing

Rhinosinusitis (acute and chronic)

Asthma with AR

Congestion

Inflammation

Common cold

23

Burden of Allergic Rhinitis in

US and Europe: 2005

0

10

20

30

40

50

60

70

US Europe France Germany Italy Spain UK

Prevalence

Diagnosed

Drug-treated

Source: Decision Resources Report.

Pati

en

ts (

Mil

lio

ns)

24

Congestion and Other Symptoms of Allergic Rhinitis Impair Learning in

Pediatric Patients

40

44

48

52

56

60

Mean Composite Learning Scores

in Children 10-12 Years of Age At 2 Weeks

Vuurman et al. Ann Allergy. 1993;71:121.

Children with

Allergic Rhinitis

(n=12)

Mean

co

mp

osit

e learn

ing

Sco

re a

t 2

weeks (%

)

Healthy

Children (n=13)

P=0.007

25

Prevalence of Allergic Rhinitis worldwide

• AR is estimated to affect over 500 million people worldwide1

– Prevalence is increasing in most countries of the world, particularly

in areas with low or medium levels of prevalence

– Prevalence may be plateauing or even decreasing in the highest

prevalence areas

• What about EGYPT?

AR = allergic rhinitis; 1. Bousquet J et al. Allergy. 2008;63(suppl 86):8–160; 2. Bauchau V et al. Eur Respir J. 2004;24:758–764; 3. Executive summary: adult. Allergies in America: a landmark survey of nasal

allergy sufferers. http://www.mmcpub.com/scsaia/AdultSummary.pdf. ccessed February 2011; 4. Ait-Khaled N et al. Allergy. 2009;64:123–148.

Allergies In the Middle East AIME survey, 2011

Impact of allergic rhinitis on lung

function

Both AR and asthma have airflow limitation as the main functional consequence

The forced expiratory volume in 1 second (FEV1), a measurement of exhaled volume during the first second of a forced expiratory maneuver, may be impaired in approximately 5% of patients with AR who report only nasal symptoms.

How Allergic rhinitis affects

asthma Allergic rhinitis may promote or exacerbate

asthma through several physiologic mechanisms that link the disorders.

These include :

1- The vagal (rhinobronchial) reflex, which causes nasal stimulation to induce bronchoconstriction.

2- Systemic release of mediators and cytokines.

3- Postnasal drip and resulting irritation.

4- The need for oral respiration caused by nasal obstruction, which causes dry, cold air to penetrate into the bronchi and promote bronchial hyperreactivity

Mechanisms of pathologic relationships between upper and lower airways

Fig. Copyright © 2010 Southern Me1.20Reproduced with permission from Meltzer EO.Allergy Asthma

Proc2005;26:336-340.

dical Association. Published by Lippincott Williams & Wilkins. 29

Other Proposed pathophysiologic mechanisms of

asthma exacerbated by sinusitis

Spread of inflammatory mediators and

chemotactic factors to lower airways triggers

sinobronchial reflex mechanism.

Stimulation of autonomic nervous system

causes acute bronchial hyperresponsiveness.

Other Proposed pathophysiologic mechanisms of

asthma exacerbated by sinusitis

Reversible partial beta-adrenergic blockade is enhanced.

Depressed nitric oxide concentration promotes acute bronchial hyperresponsiveness.


Allergic Rhinitis Is a Risk Factor for Asthma

Allergic rhinitis increased the risk of asthma about threefold 1

23-year follow-up of first-year college students undergoing allergy testing; data based on 738 individuals

(69% male) with average age of 40 years

1. Celine Bergeron and Qutayba Hamid. Relationship between Asthma and Rhinitis: Epidemiologic, Pathophysiologic, and Therapeutic

Aspects Allergy Asthma Clinical Immunol.2005

Adapted f rom Settipane RJ et al Allergy Proc 1994;15:21–25.

12

10

8

6

4

2

0

% of patients who developed asthma

10.5

Allergic rhinitis at baseline (n=162)

3.6

No allergic rhinitis at baseline (n=528)

p<0.002

Post Hoc Resource Use Analysis of IMPACT

Allergic Rhinitis Increased the Risk of Asthma Attacks

Post hoc analysis of medical resource use/asthma attacks in asthmatic patients with and without concomitant allergic rhinitis over

52 weeks

Adapted from Bousquet J et al Clin Exp Allergy 2005;35:723–727.

25

20

15

10

0

% of patients

21.3

Patients with asthma + allergic rhinitis (n=893)

17.1

Patients with asthma (n=597)

p=0.046

Allergic Rhinitis Worsens Asthma

Allergic Rhinitis Doubled the Risk of ER Visits in Patients

with Asthma

Post hoc analysis of medical resource use/asthma attacks in asthmatic patients with and without concomitant allergic rhinitis over

52 weeks

ER=emergency room

Adapted from Bousquet J et al Clin Exp Allergy 2005;35:723–727.

% of patients


Patients with asthma (n=597)

4.0

3.5

3.0

2.5

2.0

1.5

1.0

0.5

0

p=0.029

1.7

3.6

Retrospective Cohort Study of UK Mediplus Database

Allergic Rhinitis Increased the Number of Prescriptions for Rescue Therapy (SABA) in Patients with Asthma

Analysis of health-care resource use in adults 16 to 55 years of age with asthma and allergic rhinitis in general practice in the UK

SABA=short-acting beta2-agonists

Adapted from Price D et al Clin Exp Allergy 2005;35:282–287.


Patients with asthma (n=22,692)

3.3

3.2

3.1

3.0

2.9

2.8

2.7

2.6

2.5

2.4

0

Annual prescriptions per patient

3.2

2.7

p<0.0001

Treating Rhinitis May Help

Asthma

The key to successful therapy for rhinitis

and asthma is the prevention or

suppression of inflammation

Treatment of rhinitis has been shown to be

beneficial to the lower airways

Treating inflammation in the upper airways

indirectly improves asthma symptoms and

decreases bronchial hyperreactivity

Classification of allergic rhinitis

Intermittent symptoms

<4 days per week

Or <4 consecutive weeks

Mild

All of the following

Normal sleep

Normal daily activities, sport,

leisure

Normal work and school

No troublesome symptoms

Persistent symptoms

>4 days per week

And >4 consecutive weeks

Moderate/Severe

One or more items

Abnormal sleep

Impairment of daily activities,

sport, leisure

Problems caused at work

or school

Troublesome symptoms

Reference: 1. ARIA 2007

© Global Initiative for Asthma

GINA assessment of symptom control

A. Symptom control

In the past 4 weeks, has the patient had: Well-

controlled

Partly

controlled

Uncontrolled

• Daytime asthma symptoms more

than twice a week? Yes No

None of

these

1-2 of

these

3-4 of

these

• Any night waking due to asthma? Yes No

• Reliever needed for symptoms*

more than twice a week? Yes No

• Any activity limitation due to asthma? Yes No

B. Risk factors for poor asthma outcomes

• Assess risk factors at diagnosis and periodically

• Measure FEV1 at start of treatment, after 3 to 6 months of treatment to record the patient’s

personal best, then periodically for ongoing risk assessment

ASSESS PATIENT’S RISKS FOR:

• Exacerbations

• Fixed airflow limitation

• Medication side-effects

GINA 2015 Box 2-2B (1/4)

Level of asthma symptom control

ARIA Guidelines:

Recommendations for

Management of Allergic

Rhinitis

2012

© Global Initiative for Asthma

Step 1 – as-needed inhaled short-acting beta2-agonist (SABA)

GINA 2015, Box 3-5, Step 1 (4/8)

PREFERRED

CONTROLLER

CHOICE

Other controller

options

RELIEVER

STEP 1 STEP 2 STEP 3

STEP 4

STEP 5

Low dose ICS

Consider low dose ICS

Leukotriene receptor antagonists (LTRA) Low dose theophylline*

Med/high dose ICS Low dose ICS+LTRA

(or + theoph*)

As-needed short-acting beta2-agonist (SABA) As-needed SABA or low dose ICS/formoterol**

Low dose

ICS/LABA*

Med/high

ICS/LABA

Refer for add-on

treatment e.g.

anti-IgE

*For children 6-11 years, theophylline is not recommended, and preferred Step 3 is medium dose ICS

**For patients prescribed BDP/formoterol or BUD/formoterol maintenance and reliever therapy # Tiotropium by soft-mist inhaler is indicated as add-on treatment for patients with a history of

exacerbations; it is not indicated in children <18 years.

Add tiotropium# High dose ICS + LTRA

(or + theoph*)

Add tiotropium# Add low dose OCS


ARIA and IPAG Guidelines Recommend

a Combined Approach to Managing Asthma and Allergic Rhinitis

Patients with allergic rhinitis should be

evaluated for asthma

Patients with asthma should be evaluated for

allergic rhinitis

A strategy should combine the treatment of

upper and lower airways in terms of efficacy

and tolerability

ARIA=Allergic Rhinitis and its Impact on Asthma; IPAG=International Primary Care Airways Groups

Adapted from Bousquet J et al J Allergy Clin Immunol 2001;108(suppl 5):S147–S334; International

Primary Care Airways Group, Los Angeles, California, USA, MCR Vision, 2005.

Shared Epidemiological Findings of Allergic Rhinitis and Asthma

Summary

Several epidemiological findings suggests the link between

asthma and allergic rhinitis as well as the worsening effect of

allergic rhinitis on asthma:

AR coexists in the majority of asthma patients

Asthma patients with concomitant AR experience more

asthma attacks and use more resources to control their

asthma than patients with asthma alone.

Asthma patients with concomitant AR experience worse

quality of life (physical functioning) than patients with AR alone

during the pollen season.

TH2-associated asthma

Aspirin exacerbated airway disease (AERD)

Case 1

A 45-year-old man complains of nasal blockage and loss

of smell and taste. He is an asthmatic who has been well

controlled on ICS and LABA therapy. His past history is

significant for chronic rhinosinusitis and one previous hospital admission for asthma with intubation and

mechanical ventilation.

He was told following that admission that he was allergic

to Aspirin, which he had taken for a back pain. On physical examination his lungs are clear of wheeze.

The findings on nasal examination are seen

in this Figure

A. Leukotriene receptor antagonist.

B. A 3-week course of prednisone.

C. Inhaled topical nasal corticosteroid.

D. Allergen immunotherapy to relevant antigens.

E. Aspirin desensitization program.

The most appropriate treatment at this time is:

The patient under discussion has asthma and nasal

polyposis. The aim of therapy for nasal polyps is to restore

nasal patency, and this may return lost taste and smell and

restore sinus drainage.

Topical corticosteroids have been the drugs of choice for

many years as they have been shown to reduce the size of

small polyps and prevent or delay the recurrence of nasal

polyps after surgery. Oral corticosteroids are also very

effective for nasal polyps and in severe cases are preferred

for 3 weeks followed by prolonged topical therapy.

Oral and not topical corticosteroids are usually effective for

anosmia and therefore are preferred in this patient, making

option B correct and C incorrect. When corticosteroids are

not effective, surgery is unavoidable.

Having both asthma and nasal polyposis places a patient up

to a 40% risk of having or developing aspirin sensitivity,

otherwise known as aspirin intolerant asthma (AIA).

Nasal polyps are smooth gelatinous semitranslucent

structures that seem to be outgrowths of the nasal mucosa.

Most polyps arise from the ethmoid sinus and histologically

are a mass of edema fluid with an abundance of eosinophils

and other inflammatory cells such as mast cells,

lymphocytes, and neutrophils. Nasal polyposis is an non-

IgE mediated inflammatory condition and is often

associated with nonallergic rhinitis, aspirin sensitivity, and

nonallergic asthma.

Atopy is no more prevalent in patients with nasal polyps

than in the general population; therefore, option D would not

be an appropriate step in this patient.

Most patients with AIA have a long history of

perennial rhinitis, which begins in the third decade,

often after a viral illness. Over months to years

nasal polyps develop followed by the appearance

of moderately severe to severe asthma and aspirin

sensitivity.

After ingestion of aspirin or a nonsteroidal

antiinflammatory drug (NSAID), an acute asthma

exacerbation occurs, often accompanied by

rhinorrhea, periorbital edema, conjunctival

congestion, and occasionally flushing of the face.

Evidence suggests that by inhibiting the

cyclooxygenase (COX) pathway, aspirin and

NSAIDS divert arachadonic metabolism to the

lipoxygenase pathway which is involved in the

pathogenesis of this syndrome. Leukotriene

pathway modifiers such as the receptor

antagonists have shown to be effective

Leukotriene pathway pathway which is involved in the

pathogenesis of this syndrome. Leukotriene pathway

modifiers such as the receptor antagonists have shown to

be effective for asthma but not nasal polyps; therefore,

option A is not correct

Aspirin desensitization is done by giving small increasing

oral doses of aspirin over 2 to 3 days and then a daily dose

after a refractory period is reached. The asthma is improved

and the nasal inflammatory disease responds the best. This

procedure is ideal in those patients who have just had

surgical polypectomy, as it has been shown to delay the

recurrence of polyps for an average of 6 years.

It would not improve nasal patentcy in this patient;

therefore, option E is not correct. The addition of

nedocromil sodium is incorrect because there is no need to

“step up” her asthma therapy at this time.

oMr Samir a lifelong heavy smoker and asthmatic, the seventy year old Mr Samir is wheezing most days and always is short of breath. He is on regular combivent, beclomethasone 200mcg bd and intermittant salbutamol.

Case 2

oThe most likely diagnosis is Uncontrolled

Asthma.

but The COPD element should not be neglected in this patient with a high smoking index (old age and heavy smoker). It definitely has a share in his symptoms and airflow limitation.

What is the likely diagnosis?

A 46 year old man comes to your clinic for management of

his asthma. He takes high-dose inhaled corticosteroids

and a long-acting beta agonist, along with a leukotriene

inhibitor. His adherence and technique are perfect.

He still has symptoms of cough, wheezing, and chest

tightness that bother him most days and nights each

week. He is using albuterol daily. The symptoms persist

when he goes on vacation out of state.

Sputum culture is negative. IgE level is 3,600 ng/mL. His

primary doctor obtained imaging and a chest CT, which

are shown.

Case 3

What should be the next step? A. Schedule spirometry for next week to

guide step-up therapy.

B. Start omalizumab injections every 2

weeks.

C. Sweat chloride testing.

D. Skin testing for reactivity to Aspergillus

fumigatus.

E. HIV test.

Allergic bronchopulmonary aspergillosis (ABPA) is an

ongoing hypersensitivity reaction in response to

bronchial colonization by Aspergillus, and is a common

cause of poorly controlled asthma. Cystic fibrosis

patients are also often affected. Bronchial obstruction

by mucus and chronic inflammation can lead to

bronchiectasis and lung fibrosis with irreversible loss

of lung function.

Clinical features: Cough productive of sputum, frequent

"bronchitis"; often with dyspnea and wheezing.

Diagnosis:

By constellation of symptoms and objective

findings. "Classic" ABPA would include the

following:

Asthma history Immediate reactivity on skin prick with Aspergillus

antigens

Precipitating serum antibodies to A. fumigatus Serum total IgE concentration >1,000 ng/mL

Peripheral blood eosinophilia >500/mm3 Lung opacities on chest x-ray or chest HRCT

Central bronchiectasis present on chest CT

Elevated specific serum IgE and IgG to A. fumigatus

A skin test is the best first test, as it

is considered 100% sensitive (i.e., a

negative test rules out the condition).

A serum IgE < 1,000 or negative

precipitating antibodies also rule out

ABPA with high confidence.

Case 4

Your internal medicine colleague asks you about

a patient she is about to discharge home after a

hospitalization for asthma exacerbation. The

patient, takes a beta-blocker for coronary artery

disease and hypertension. Your colleague is

considering stopping the beta-blocker to avoid

any contribution to future asthma exacerbations,

but wants your opinion first.

What do you recommend?

A. Stop the beta blocker.

B. Continue the beta blocker.

C. Stop the beta blocker; order a stress test.

D. Continue the beta blocker; order an

echocardiogram.

Case 5

o Yusuf is 4 years old. He has had a persistant cough for

weeks that wakes him at night. “Every cold goes to his

chest” This is the fifth consultation for cough in the last

year. Only once has a wheeze been documented. His

father is known asthmatic.

1- What is the likely diagnosis? 2- What treatment would you give?

Self-fulfilling: Infant Wheezing

Phenotypes

• Never (51%)

• Transient (20%) – Wheeze 0-3, not at age 6

• Persistent (14%) – Wheeze 0-3 still present

age 6

• Late onset (15%) – Wheeze after age 3

Diagnosing Asthma in Young

Children – Asthma Predictive

Index

• > 4 episodes/yr of wheezing lasting more than 1 day affecting sleep in a child with one MAJOR or two MINOR criteria

• Major criteria

– Parent with asthma

– Physician diagnosed

atopic dermatitis

• Minor criteria

– Physician diagnosed

allergic rhinitis

– Eosinophilia (>4%)

– Wheezing apart from

colds

1Adapted from Castro-Rodriquez JA, et al. AJRCCM 2000; 162: 1403

Modified Asthma Predictive Index (API)

Cough-variant asthma

Cough-variant asthma presents as dry

cough at night. It worsens with exercise

(EIA) and nonspecific triggers (cold air).

Cough-variant asthma responds to asthma

therapy with ICS.

Cough-variant asthma is diagnosed with

pulmonary function testing (PFTs) with

response to bronchodilator. The most

common cause of chronic cough in children

is cough-variant asthma.

1- What is the likely diagnosis?

The likely diagnosis is Bronchial Asthma (childhood asthma): - Family history. - Symtoms (cough mainly at night, every cold goes to the chest). - Signs: chest wheeze.

Treatment

Severe asthma - differential diagnosis and management

Case 7 oA 30-year-old G2P1 pregnant woman at 15 weeks gestation presents to an outpatient clinic with worsening dyspnea over the preceding two weeks. Her past medical history is significant for asthma diagnosed in childhood, seasonal allergies, and gastroesophageal reflux disease (GERD) during her previous pregnancy. She notes that her asthma symptoms had been well-controlled on inhaled Budesonide/formoterol (160mcg/4.5mcg), Salbutamol MDI as needed, and a nasal steroid spray prior to pregnancy. However, she discontinued all of her medications when she learned that she was pregnant for fear that they might harm her baby.

oAt today’s visit she feels that she is unable to take a deep breath. She also describes one to two episodes of wheezing daily and night time cough two to three times per week. Warm air, dust, and exposure to cats seem to exacerbate her symptoms. oOn physical exam, the patient is in no acute distress. The lungs are clear to auscultation bilaterally.

1- Is the patient controlled?

2- Is asthma medications safe in pregnancy?

3- Treatment needed?

1- Is the patient controlled?

NO…… Breathlessness. Frequent nocturnal symptoms

(cough and wheezes).

2- Is asthma medications safe in pregnancy?

Yes, There is little evidence suggesting that medications used to treat asthma may harm the fetus. AND also Pregnant patients with asthma should be advised that the greater risk for their babies lies in poorly controlled asthma and most modern asthma medications are safe.

For this reason, using medications to obtain optimal asthma control is justified.

3- Treatment needed?

Asthma control was already achieved on this treatment: o Inhaled Budesonide/formoterol (160mcg/4.5mcg). o Salbutamol MDI as needed. o Nasal steroid spray. o It may be repeated with reassurance about the safety of the medications and regular follow up to assess asthma control.

Case 8

A 48-year-old postmenopausal woman has a 15-year

history of asthma. Her asthma is triggered by aspirin,

cigarette smoke, and upper respiratory tract infections. Six

months ago, after an upper respiratory tract infection, she

had an asthma exacerbation with peak expiratory flow rate

(PEFR) values of 45% of her personal best, with

continuous asthma symptoms, which were treated with a

10-day course of oral corticosteroids. Her PEFR improved

to 80% of her personal best and she was able to taper

and discontinue oral corticosteroids without a decrease in

her PEFR values or worsening of her asthma symptoms.

Now, 6 months later, she feels at her baseline with

minimal asthma symptoms when she exercises. She

denies nocturnal asthma symptoms.

Case 8

On physical examination, she is free of wheeze, even with

forced inspiratory and expiratory efforts. Her spirometry

shows an FEV1 level that is 90% of predicted. Her current

medical regimen for treatment of asthma includes the

following: salmeterol by metered-dose inhaler (MDI), 2

puffs bid; fluticasone propionate by MDI, 250 μg, 2 puffs

bid; montelukast, 10 mg qhs; and salbutamol by MDI, 2

puffs prn, rescue for shortness of breath.

The best treatment recommendation for her currently is to:

A. Continue her current medical regimen.

B. Discontinue montelukast.

C. Discontinue salmeterol.

D. Decrease fluticasone propionate dose to 125 μg, 2

puffs bid.

E. Add nedocromil sodium by MDI, 2 puffs qid

All of the following statements concerning the

natural history of asthma are true EXCEPT:

A. The age-related decline in FEV1 is greater for

asthmatic than non-asthmatic adults.

B. Most adult asthmatics do not experience complete

asthma remission.

C. Regular use of inhaled corticosteroids is associated

with reduced asthma mortality.

D. Delayed introduction of inhaled corticosteroids

reduces the likelihood that FEV1 will normalize with

therapy.

E. The risk of a fatal asthma episode is greatest for

asthmatics with severe disease and fixed airflow

obstruction.

Case 9

The greatest risk of a fatal outcome in asthma appears to be in those

patients who demonstrate the highest degrees of airway

hyperresponsiveness and FEV1 lability, rather than in those with severe but

fixed airflow obstruction. In one study, the relative risk of death from asthma

was seven times higher for patients who demonstrated a 50% or greater

increase in FEV1 in response to bronchodilator, compared to those whose

FEV1 improved by less than 25%. While this observation might seem

somewhat contrary to expectations, it emphasizes that the most important

result of poor asthma control is the persistence of excessive airway lability,

with its attendant risk of asthma exacerbation. Persisting FEV1 lability is

most common among smokers and those with persistent atopic asthma.

Other documented risk factors for asthma mortality include age > 40 years,

smoking, and blood eosinophilia. Middle-aged and older adults with asthma

rarely achieve complete remission. The remission rate in adults is also

substantially lower than in children (10% to 15% vs over 50%). In a 25-year

study of adult asthma, remission, which was defined as becoming

asymptomatic with normal FEV1 and normal airway responsiveness, was

noted in only 20 of 190 subjects (10.5%).

In this study, remission was associated with milder asthma and younger age at

first diagnosis, together with male gender and less initial airway

hyperresponsiveness. Control of asthma symptoms, FEV1, and airway

hyperresponsiveness also appears to be influenced by the timing of the

introduction of inhaled corticosteroids (ICS). Several trials have shown that

FEV1 is much less likely to normalize if the institution of ICS is delayed

following the initial diagnosis of asthma. Similar to the situation in COPD,

several longitudinal studies have demonstrated a more rapid age-related

decline in FEV1 in adult asthmatics compared to the nonasthmatic population,

and this is further compounded by smoking. There are few long-term studies of

the effects of treatment on the natural history of asthma. However, a recent

study of asthmatics aged 5 to 44 years has clearly demonstrated a dose-

dependent reduction in asthma mortality with increasing use of ICS, in that the

death rate from asthma was reduced by approximately 50% with the use of 6 or

more canisters of ICS during a 12-month period, compared to patients who

used smaller amounts of ICS

Radiographic Signs of Pneumomediastinum

Subcutaneous emphysema

Thymic sail sign

Pneumoprecardium

Ring around the artery sign

Tubular artery sign

Double bronchial wall sign

Continuous diaphragm sign

Extrapleural sign

Air in the pulmonary ligament

http://radiopaedia.org/images/576804

http://radiographics.rsnajnls.org/cgi/content/full/24/1/e17/F27A


http://radiographics.rsnajnls.org/cgi/content/full/24/1/e17/F27B


http://radiographics.rsnajnls.org/cgi/content/full/24/1/e17/F26C



one airway disease

Health & Medicine