Asthma

Asthma in general
practice

Dr. Avinash Bhondwe

Definition of asthma

• Asthma is a chronic inflamm. disorder of
the airways.
• Chronically inflamed airways are hyper
responsive;
• They become obstructed and airflow is
limited (by broncho-constriction, mucus
plugs,and increased inflammation)
• When airways are exposed to various
risk factors.

Definition of Asthma
• Chronic lung disease characterized by:
– Airway narrowing that is reversible (± completely)
either spontaneously or with treatment
– Airway inflammation
– Airway hyper-responsiveness to a variety of stimuli.

• Episodic dyspnea with associated wheezing

• Heterogeneous group with:
– Shortness of breath
– Wheezing
– Cough

Asthma pathophysiology
• Components:

• Airway inflammation with wall thickening and
increased vascular permeability
• Mucus hypersecretion
• Bronchial smooth muscle contraction

On exposure to allergen
• Stimulus causes cascade of inflammatory cell
migration and activation, with numerous
cytokines and other mediators involved.
• Major players:
• Mast cells
• Eosinophils
• T cells

The pathophysiology of asthma.

I can write better than
anybody who can write faster,
and I can write faster than
anybody who can write
better. - A. J. Liebling

Differential diagnosis of
asthma in adults
Some of symptoms of asthma are shared with diseases of other systems

Numerous relatively common lung diseases

Need to differentiate from infections and restrictive lung
disorders, and between local and generalised obstruction

Differential diagnoses include:
• COPD • interstitial lung disease
• cardiac disease • pulmonary emboli
• laryngeal, tracheal or lung tumour • aspiration
• bronchiectasis • vocal cord dysfunction
• foreign body • hyperventilation

Diagnosis and natural history. Thorax 2003; 58 (Suppl I): i1-i92

Indications for referral of
adults with suspected asthma
• Diagnosis unclear or in doubt
• Unexpected clinical findings e.g. crackles, clubbing, cyanosis,
heart failure
• Spirometry or PEF measurements do not fit the clinical picture
• Suspected occupational asthma
• Persistent shortness of breath (not episodic, or without
associated wheeze)
• Unilateral or fixed wheeze
• Stridor
• Persistent chest pain or atypical features
• Weight loss
• Persistent cough and/or sputum production
• Non-resolving pneumonia

Diagnosis of asthma in
adults: practice points

 Record presence of wheeze in patient’s notes

Try to confirm diagnosis with objective tests before
 long-term therapy is started

 Question diagnosis if little response to treatment

 Perform chest X-rays in patients with atypical symptoms


NAEPP Guidelines
• National Asthma Education and Prevention
Program (NAEPP)

• Classification of chronic asthma:
–Mild intermittent asthma
–Mild persistent asthma (>2 days/wk,
>2 nights/mo)
–Moderate persistent asthma
–Severe persistent asthma

• Inhaled corticosteroids (ICS) are “preferred
treatment” for all patients with persistent asthma

ED and Hospital Management:
Goals

1. Correct significant hypoxemia

2. Rapidly reverse airflow obstruction

3. Decrease likelihood of recurrence

Initial Treatment

Mild-to-Moderate Exacerbation (PEF > 50%)

• Oxygen to achieve O2 sat > 90%

• Inhaled  2-agonist by MDI or neb, up to 3 in
1st hr

• Oral corticosteroid if no immediate response
or if patient recently took oral corticosteroid

Initial Treatment (continued)

Severe Exacerbation (PEF < 50%)
• Oxygen to achieve O2 sat > 90%

• Inhaled high-dose 2 -agonist and
anticholinergic by neb q 20 minutes or
continuously for 1 hour

• Oral corticosteroid

Initial Treatment (continued)
Impending or Actual Respiratory Arrest

• Intubation and mech ventilation with 100% O2

• Nebulized 2-agonist and anticholinergic

• IV corticosteroid

• Admit to hospital intensive care

2002 Update on Selected Topics

• Antibiotics not recommended for acute
asthma

• ICS are preferred treatment for children of
all ages with persistent asthma

• ICS + long-acting -agonist is the preferred
treatment for moderate or severe persistent
asthma in individuals age 6 and older
NAEPP, 2002

Factors associated with higher
risk of asthma death

Over-dependence on rapid-acting
inhaled B2-agonists.
 History of psychosocial problems or
denial of asthma or its severity.
 History of noncompliance with
asthma medication plan.

DIFFERENTIAL DIAGNOSIS

• • Upper airway disease • • Pulmonary embolism
• • Chronic bronchitis • • Cystic fibrosis
• emphysema • • Laryngeal/vocal cord
• • Obstruction of airways by dysfunction
foreign • • Obstruction of airways by
• • Congestive heart failure foreign body or tumour
• enlarged lymphnodes • • Swallowing dysfunction
• tumour • • Drug induced cough e.g. ACE
• • Viral or obliterative • •Gastroesophagial reflux
bronchiolitis inhibitors
• • Prolonged post-infection cough

Patients should immediately seek
medical care if...

• :The patient is breathless at rest,
• hunched forward,
• talks in words rather than sentences
• infant stops feeding
• agitated ,drowsy or confused,
• bradycardia,
• respiratory rate greater than 30 per minute.

Also needs imm. attention
Wheeze is loud or absent.
Pulse is greater than 120/min
(greater than 160/min for infants).
PEF is less than 60 percent of
predicted or personal best even after
initial treatment.
The patient is exhausted.

Also needs imm. attention

• The response to the initial bronchodilator treatment
is not prompt and sustained for at least 3 hours.
• There is no improvement within 2 to 6 hours after
oral glucocorticosteroid treatment is started.
• There is further deterioration.

• Asthma attacks require prompt treatment:

• Inhaled rapid-acting 2-agonists in adequate
doses are essential.

• If inhaled medications are not available, oral
bronchodilators

• Oral glucocorticosteroids introduced early in
the course of a moderate or severe attack
help to reverse the inflammation and speed
recovery.

• • Oxygen is given at health centers or
hospitals if the patient is hypoxemic.

• • Methylxanthines are not recommended if
used in addition to high doses of inhaled 2-
agonist.
• However, theophylline can be used if inhaled
B2-agonists are not available.
• Epinephrine (adrenaline) may be indicated
for acute treatment of anaphylaxis and
angioedema.

Therapies not recommended for
treating attacks include

• Sedatives (strictly avoid)
• Mucolytic drugs (may worsen cough)
• Chest physical therapy/physiotherapy (may increase
patient discomfort)
• Hydration with large volumes
• Antibiotics (do not treat attacks but are indicated for
patients who also have pneumonia or bacterial
infection such as sinusitis).

• Mild attacks can be treated at home
• Moderate attacks may require, and severe attacks
usually require hospitalisation

• oxygen saturation , arterial blood gas measurement --
in patients with suspected hypoventilation,
exhaustion, severe distress, or peakflow 30-50 percent
predicted.

Parameter Mild Moderate Severe Respiratory arrest
imminent

Posture Walking , can lie Difficulty in Upright Recumbent
down lying down, sitting
sitting

Talks in sentences phrases words monosyllables

Alertness May be agitated agitated agitated Confused or drowsy

Parameter Mild Moderate Severe Respiratory arrest
imminent

Respiratory Normal increased Increased Paradoxical
rate >30min

Accessory Not active Active active Thoracoabdominal
muscles paradox

Wheeze Moderate Loud Usually loud Absent breath
End expiratory sounds

Pulse/min <100 100-120 >120 Bradycardia

Parameter Mild Moderate Severe Respiratory
arrest imminent

PEFR >80% 60-80% <60% ?<40%
Response <2hrs

PaO2 Normal >60 mm Hg <60 mm hg ?
Possible
cyanosis

PaCO2 <45 mm hg <45 mm hg >45 mm hg ?
Possible resp.
failure

SaO2 >95 % 90-95% <90% ?
On room air

• Do not underestimate the severity of an
attack; severe asthma attack
• may be life threatening.

• Know you are where you
are not by accident, but by
the design of your Creator,
for your own development
or for the development of
those around you. - Abdu'l-
Baha

The British Thoracic Society Scottish Intercollegiate Guidelines Network

Pharmacological
management

All doses of inhaled steroids in this section refer to beclomethasone (BDP) given via
metered dose inhaler. Adjustment may be necessary for fluticasone and/or other devices

Pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92

Asthma control

Asthma control means:
• minimal symptoms during day and night
• minimal need for reliever medication
• no exacerbations
• no limitation of physical activity
• normal lung function (FEV1 and/or PEF >80% predicted or best)


Asthma control


Aim for early control, with stepping up or down as required


Asthma control


Aim for early control, with stepping up or down as required

Before initiating a new drug therapy:
• check compliance with existing therapies
• check inhaler technique
• eliminate trigger factors


Stepwise management of
asthma in adults

Step 1: Mild intermittent asthma
Inhaled short acting ß2 agonist as required


asthma in adults

Step 2: Regular preventer therapy

Add inhaled steroid 200-800mcg/day *
400mcg is an appropriate starting dose for many patients

Start at dose of inhaled
steroid appropriate to
severity of disease.
* BDP or equivalent



asthma in adults
Step 3: Add-on therapys
1. Add inhaled long-acting ß2 agonist (LABA)
2. Assess control of asthma:
• good response to LABA – continue LABA
• benefit from LABA but control still inadequate – continue LABA and increase inhaled steroid
dose to 800mcg/day * (if not already on this dose)
• no response to LABA – stop LABA and increase inhaled steroid to
800mcg/day *. If control still inadequate, institute trial of other therapies
(e.g. leukotriene receptor antagonist or SR theophylline)

Step 2: Regular preventer therapy steroid appropriate to
* BDP or equivalent


asthma in adults

Step 4: Persistent poor control
Consider trials of:
• increasing inhaled steroid up to 2000mcg/day *
• addition of fourth drug (e.g. leukotriene receptor
antagonist, SR theophylline, ß2 agonist tablet)

Step 3: Add-on therapy

* BDP or equivalent


asthma in adults
Step 5: Continuous or frequent use of oral steroids
Use daily steroid tablet in lowest dose providing adequate control
Maintain high dose inhaled steroid at 2000mcg/day *
Consider other treatments to minimise the use of steroid tablets
Refer patient for specialist care



* BDP or equivalent


asthma in adults

Step 5: Continuous or frequent use of oral
steroids



Step 2: Regular preventer therapy




Adults Children Children
5-12 years <5 years

Prescribe inhaled short-acting 2 agonist as short
term reliever therapy for all patients with symptomatic
A B D asthma

Review asthma management in patients with high
B D D usage of inhaled short acting 2 agonists


Step 2: Introduction of
regular preventer therapy

5-12 years <5 years

A A A Inhaled steroids are the recommended preventer drug

A D D Give inhaled steroids initially twice daily

If good control, once a day inhaled steroids at the
A D D same total daily dose can be considered


Step 2: Introduction of regular
preventer therapy (practice points)
Inhaled steroids should be prescribed for patients with recent exacerbations,
nocturnal asthma, impaired lung function or using inhaled 2 agonists more than
once a day

Start patients at inhaled steroid dose appropriate to disease severity (e.g. adults:
400mcg per day; children 5-12 years: 200mcg per day; children under 5 years: higher
doses may be required to ensure consistent drug delivery)

Use lowest dose at which effective control of asthma is maintained

Monitor children’s height on a regular basis

In children on inhaled steroids with decreased consciousness, check blood glucose
levels urgently and consider IM hydrocortisone


5-12 years <5 years

Try adding in other treatments before increasing the
A B  inhaled steroid dose (adults: >800mcg/day; children:
>400mcg/day)
Inhaled long-acting 2 agonist is first choice add-on therapy in
A B
adults and children (5-12 years)
If asthma control remains sub-optimal after addition of inhaled
D D long acting 2 agonist, increase dose of inhaled steroids to
800mcg/day (adults) or 400mcg/day (children)
If control still inadequate, consider sequential trial of other add-on therapy
(leukotriene receptor antagonists, theophyllines or slow release 2 agonist
 tablets)



Inadequate control on low dose inhaled steroids




Add inhaled long-acting ß2 agonist (LABA)





Assess control of asthma






Good response to LABA: Benefit from LABA but control still inadequate: No response to LABA:
• Continue LABA • Continue LABA • Stop LABA
• Increase inhaled steroid dose to • Increase inhaled steroid dose to
800mcg/day (adults) and 400mcg/day 800mcg/day (adults) and
(children 5-12 years) 400mcg/day (children
5-12 years)





• Continue LABA • Continue LABA • Stop LABA
5-12 years)

Control still inadequate:
• Trial of other add-on therapy, e.g.
leukotriene receptor antagonist or
theophylline





• Continue LABA • Continue LABA and • Stop LABA
5-12 years)

If control still inadequate go to Step 4 Control still inadequate:
• Trial of other add-on therapy, e.g.
leukotriene receptor antagonist or
theophylline

If control still inadequate go to Step 4


Step 4: Poor control on moderate
dose of inhaled steroid + add-on
Adults Children
5-12 years

If control inadequate with inhaled steroids (adult: 800mcg/day; children:
400mcg/day) plus long-acting 2 agonist, consider:

• increasing inhaled steroids to 2000mcg/day (adults) or 800mcg/day
(children)
D D • leukotriene receptor antagonists
• theophyllines
• slow release 2 agonist tablets (caution when used with long acting 2
agonists)

If intervention ineffective, stop the drug (or reduce to original steroid dose)


 Before proceeding to step 5, consider referring to specialist care


Step 5: Use of oral steroids

5-12 years <5 years

To eliminate or reduce the dose of steroid tablets, use inhaled
A D steroids (adults: up to 2000mcg/day; children aged
5-12years, up to 1000mcg/day)
Consider treatment with long-acting 2 agonists, leukotriene
receptor antagonists, and theophyllines for about 6 weeks,
D D D but stop if no improvement in symptoms/lung function or
reduction in oral steroids

After discussing risks/benefits, immunosuppressants, (methotrexate,
 cyclosporin or oral gold) may be given as a 3-month trial


Stepping down

 Important to review patients regularly as they step down

Patients should be maintained at the lowest possible dose of
inhaled steroid. Reductions should be considered every 3
 months, decreasing the dose by approximately 25-50% each time


Exercise-induced asthma
5-12 years <5 years

Exercise-induced asthma often indicates poorly
 controlled asthma

For patients taking inhaled steroids but with exercise-induced symptoms, consider
adding:

A C leukotriene receptor antagonists

A A long-acting 2 agonists

C C cromones

A A oral 2 agonists

C C theophyllines

Inhaled short-acting 2 agonists immediately before
A A  exercise


Allergic bronchopulmonary
aspergillosis

In adults with allergic bronchopulmonary aspergillosis, consider
C
4-month trial of itraconazole
 Monitor itraconazole side-effects (particularly hepatic)


Overview: Pharmacological
management

• Add inhaled long-acting 2 agonists rather than
increasing the dose of inhaled steroids (above
800mcg/day in adults and 400mcg/day in children)
• Step down therapy to lowest level consistent with
maintained control


Acute severe asthma
Initial Treatment

• Inhaled rapid-acting 2-agonist up to three
treatments in 1 hour.
• (Patients at high risk of asthma-related death
should contact physician promptly after initial
treatment.)

Response to Initial Treatment
Is...Good if...

• Symptoms subside • ACTIONS:
• after initial 2-agonist • • May continue B2-agonist
• 3-4 hrs for 1-2 days.
• relief is sustained
• for 4 hours. • • Contact physician

• PEF is greater than
• 80% predicted or
• personal best.

Response to Initial Treatment Is...
Incomplete if…
• Symptoms decrease • ACTIONS: urgently
• but return in less than 3 • • Add oral steroid.
hours after initial B2-
• • Repeat B2- agonist
agonist treatment.
• • Add inhaled anticholinergic.
• transport to hospital
• PEF is 60-80%
• predicted

Response to Initial Treatment Is...
Poor if…
• ACTIONS:
• Symptoms persist or • • Add oral
• worsen despite initial B2- • glucocorticosteroid.
agonist
• • Add inhaled
• PEF is less than 60% • anticholinergic.
• Of predicted
• •Continue 2-agonist.

• • Consult clinician
• urgently

Management of Asthma Attacks:
Hospital-Based Care

• Initial Assessment
• • History, physical examination auscultation,
use of accessory muscles, heart rate,
respiratory rate,
• PEF or FEV 1 ,
• oxygen saturation , arterial blood gas

Initial Treatment

• • Inhaled rapid-acting B2-agonist, usually by
nebulization, one dose every 20 minutes for 1 hour
• • Oxygen to achieve O2 saturation >90% (95% children)
• • Systemic steroids if no imm. response, or if patient
recently took oral steroids,
• or if episode is severe
• • Sedation is contraindicated in the treatment of attacks

Severe Episode

• PEF < 60% predicted/personal best
• • Physical exam: severe symptoms at rest,
chest retraction
• • History: high-risk patient
• • No improvement after initial treatment
• • Inhaled 2-agonist and inhaled
anticholinergic

Severe Episode
• • Oxygen
• • Systemic glucocorticosteroid
• • Consider subcutaneous, intramuscular, or
intravenous B2-agonist
• • Consider intravenous methylxanthines
• • Consider intravenous magnesium

Severe Episode

• Incomplete Response Within 1-2 Hours
• • Physical exam: mild to moderate symptoms
• • PEF < 70%
• • O2 saturation not improving

Admit to Hospital

• • Inh. B2-agonist ± inh. anticholinergic
• • Systemic steroids
• • Oxygen
• • Consider IV methylxanthines
• • Monitor PEF, O2 saturation,
• pulse, theophylline levels

Severe episode

• Poor Response Within 1 Hour
• • Physical exam: symptoms severe,
• drowsiness, confusion
• • PEF < 30%
• • PCO2 > 45 mmHg
• • PO2 < 60 mmHg

Admit to Intensive Care

• • Inhaled B2-agonist + anti-cholinergic
• • Intravenous steroids
• • Consider S/C , IM ,IV B2-agonists
• • Oxygen
• • Consider IV methylxanthines
• • ? intubation and mechanical ventilation

We can't solve problems
by using the same kind
of thinking we used
when we created
them. - Albert Einstein

Differential diagnosis

I (a) : Acute hypersensitivity pneumonitis )
I (b) : Subacute cellular interstitial pneumonitis
(c) : Pulmonary infiltrates and eosinophilia
I (d) : Organising pneumonia ± bronchiolitis obliterans (BOOP)
I (k) : Lung nodules
I (l)* : Diffuse alveolar damage
II (a) : Acute pulmonary edema
III (a) : Alveolar hemorrhage
IV (a) : Bronchospasm
V (d) : Pleural/pericardial thickening or effusion and positive
antinuclear/antihistone antibodies: the drug-induced lupus
syndrome
VII (a) : Enlarged hilar/mediastinal lymph nodes
VII (b) : Angioimmunoblastic lymphadenopathy-like syndrome
X (a) : Systemic hypersensitivity syndrome with a combination of
skin rash, eosinophilia, changes in liver chemistry and mental
disturbances

Mrs. AD 43 yrs female , housewife
diagnosed as Bronchial Asthma in
1983 was on T. Theoasthline & T.
Betnesol

In 1997 dyspnea fever cough
diagnosed as bacterial pnemonitis,
treated with antibiotics .
Course was uneventful except minor
symptoms till 2000.

• In 2000 had dyspnea, fever, cough diagnosed as
pul koch, started AKT took for some days.
• Fever persisted,nausea, vomit, admitted stopped
AKT, treated with antibiotics & was on
nebulisation,oral medications for asthma
• Patient lost follow up.

In 2003 presented with dyspnea,
fever,cough investigated, BAL
showed AFB , AKT started along
with steroids

There are only two
ways to live your life.
One is as though
nothing is a miracle.
The other is as though
everything is a
miracle. - Albert
Einstein

DIAGNOSTIC FEATURES OF
ABPA
Main
• Bronchial Asthma
• Pulmonary Infiltrates
• Peripheral Eosinophilia
• Immediate wheal & flare response response to A.
fumigatus
• Serum precipitins to A. fumigatus
• Elevated serum IgE
• Central Bronchiectasis

OTHER
•History of brownish plugs in sputum
•Culture of A. Fumigatus from sputum
•Elevated IgE &IgG class of Antibodies specific for
A.. fumigatus

TREATMENT
• CORTICOSTEROIDS- PREDNISOLONE 1 mg/kg OD FOR 1 WEEK, 0.5
mg/kg/day FOR 2 WEEKS, THEN ALTERNATE DAY
MAINTENANCE STEROIDS- MINIMUM FOR 3-6MNT
• ITRACONAZOLE-200mgBD PROPHYLAXIS
• INHALED CORTICOSTEROIDS-CONTROL SYMPTOMS OF ASTHMA
• INHALED ANTIFUNGAL AGENTS-NYSTATIN/ AMPHOTERICIN B-
TEMPORARY SUPRESSION OF COLONIZATION
• BRONCHIAL LAVAGE
• BRONCHODILATORS & PHYSIOTHERAPY WITH POSTURAL
DRAINAGE

Asthma is a disease where most
important pathophyisiological event
is

• 1) bronchospasm
• 2) airway inflammation
• 3) Mucus hypersecrterion
• 4) Infections

Usual starting dose for inhaled
budesonide is
• 1) 200 mcg daily
• 2) 800 mcg daily
• 3)1600 mcg daily
• 4)2000 mcg daily

Co prescription of aminophylline with
which drug is safest

• 1)Ranitidine
• 2)Ciprofloxacin
• 3)Pantoprazole
• 4)Warfarrin

Injection of a steroid starts working in
an asthma attack
• 1) within a minute
• 2)within 15 minutes
• 3) after a few hours
• 4) after 24 hours

PEFR reading in green zone means

• 1)PEFR >40 % of predicted
• 2) PEFR >60 % of predicted
• 3) PEFR >80 % of predicted
• 4) PEFR < 40 % of predicted

In an asthma attack management
most important support device you
look for is
• 1) Pulse oximeter
• 2) Oxygen cylinder
• 3) IV access
• 4) Intubation trolley

Spacer usage with a metered
dose inhaler
• Increases throat deposition of the drug
• Increases airway deposition of the drug
• Increases incidence of oropharyngeal
candidiasis
• Increases systemic absorption of the drug

PEFR means

• Peak exercise flow rate
• Peak expiratory flow rate
• Paediatric expiratory flow rate
• Peak expiratory forced ratio

Most important objective
evidence of asthma is

• Obstructive pattern on spirometry
• Restrictive pattern on spirometry
• Reversibility test – on PEF/ FEV1
• Auscultation of wheeze

Salbutamol metered dose inhaler
has a standard strength of

• 50 mcg / puff
• 100 mcg /puff
• 200 mcg /puff
• 400 mcg /puff

Propellent used for metered dose
inhaler in India currently is

• CFC-(Chloro fluoro carbons )
• HFA-(Hydro fluoro alkane )
• TNT-(Tri nitro toluidine )
• RDX-(you know that !)

Rotahaler achieves airway
deposition of ---- % of inhaled
medicine

• 5%
• 20-30%
• 50%
• 60 %

Spacer with a metered dose
inhaler can achieve comparable
airway deposition to a nebulizer

• True
• False

PEFR reading in red zone
means
• 1)very good asthma control
• 2)Acceptable asthma control
• 3)This has nothing to do with asthma control
• 4)Impending attack and a poor asthma
control

In a pregnant lady with asthma
most important issue is

• 1)risk of foetal malformations due to anti asthma
drugs
• 2)Poor control of asthma causing hypoxia in mother
and foetus
• 3)Hyperemesis is further aggravated by theophylline
use
• 4)Systemic steroid use will affect foetal HPA axis

Asthma deaths are often
associated with

• 1)excessive/high dose use of B2 agonists
• 2)Excessive use of systemic/ inhaled steroids
• 3)Lack of technology –viz-nebulizers,
ventilators, ICU care etc
• 4)None of the above

Latest addition in anti asthma
medicines is

• 1)Leucotriene modifiers
• 2)Long acting B2 agonists
• 3)Dry powder inhaler devices
• 4)Sustained release theophylline
preparations

On arrival in emergency room for
asthma which of these steps will
you order first ?

• 1)Connect pulse oximeter and start oxygen
• 2)Nebulize salbutamol
• 3)Inject 200 mg hydrocortisone
• 4)Inject 250 mg aminophylline IV slowly in 5
% dextrose over 5 minutes

Introduction
• Paradoxical vocal cord motion (PVCM)
– Episodic laryngeal dyskinesia, VCM
– Vocal cord adduction during inspiration/expiration causing a
functional extrathoracic airway obstruction.
– Symptoms include: wheeze, cough, dyspnea, SOB
– More common than is appreciated, diagnosis frequently not
considered.
– Often confused with asthma and misdiagnosed.
– Much morbidity caused from misdiagnosis.
» Newman et al studied 95 patients with proven PVCM
» Asthma was misdiagnosed an avg. 4.8 years, 28% intubated

Clinical Presentation
• Wide variety of symptoms including:
– Cough
– Inspiratory/expiratory wheeze
– Dyspnea with/without exertion
– Stridor
– Hoarseness
– Chest tightness
– Reflux
Study evaluating 90 patients with documented PVCM:
-- Cough most common reported in up to 77%.

Physical Exam – posterior
chinking

Differential Diagnosis
• Extensive, therefore separate by location and age group.
• Anatomic locations for extrathoracic airway obstruction
include the trachea, larynx, glottis, and thyroid.
• Endobronchial obstruction must also be suspected as a
foreign body, bronchial adenoma, bronchial carcinoid, or
bronchogenic carcinoma can all present with dyspnea
and/or wheezing.
• Because the site of obstruction is more specific to the
presenting symptoms than the actual cause of the
obstruction, it is helpful to develop a d/d according to age
group and location of obstruction.

• PFT’s with flow-volume loops have also been used to support the
diagnosis of PVCM in symptomatic patients.
• Flow-volume loops of patients with PVCM often show flattening of
the inspiratory curve, or a decrease in maximal inspiratory flow
during acute attacks, and are normal while asymptomatic

PFT studies cont’d
• Inspiratory blunting is sensitive for symptomatic
patients with PVCM but is not specific for VCD and
may be produced by most types of extrathoracic
airway obstruction.
• Parker et al evaluated 26 patients with PVCM
– exercise flow-volume loops indicated the upper airway as a
cause for symptoms in 74%
– 62% showed inspiratory flow limitation
• Primary use of PFT’s is to eliminate asthma from the
differential diagnosis.

PFT studies cont’d
• Expiratory adduction and obstruction has been shown
by laryngoscopy in these patients without evidence of
expiratory flow-volume abnormalities.
– Mechanism unknown, pursed-lip exhalation suspected
» Elevates soft palate to posterior nasopharyngeal wall
» Closes nasopharyngeal airway, increases resistance
» Creates sufficient back pressure to open vocal cords and
therefore shows no expiratory flow loop defect

Other lab studies
• Other PFT parameters have a high sensitivity and
specificity for detecting extrathoracic airway
obstruction but are not specific for VCD:
– FEF50/FIF50
– FEV1/FVC,
– SRaw (specific airway resistance)
• Chest x-rays show no evidence of lung hyperinflation
or peribronchial thickening.
• Low peripheral eosinophil count.

Diagnosis
• Difficult due to its episodic nature and presentation.
• Criteria for diagnosis:
– Laryngoscopic confirmed adduction of vocal cords during
inspiration, early expiration, or both inspiration and expiration with
evidence of post. glottic chinking.
» adduction occurring during only the last half of expiration is not
pathologic
– PVCM cannot be ruled out when asymptomatic.
» if the patient is asymptomatic, negative laryngoscopic findings due not
exclude the diagnosis
– Absence of gagging or coughing during laryngoscopy
» must not confuse PVCM with vocal cord motion produced by a
laryngoscope induced gag reflex

Treatment
• The cause of the PVCM must first be elicited.
• In PVCM secondary to preexisting organic disease states
the underlying disorder should be treated appropriately:
– brainstem compression, encephalopathy, stroke, ALS, myasthenia
gravis, GERD, etc.
• A history of previous exposure to irritants should be
obtained.
• With no obvious source of causative organic disease -
acute treatment is henceforth symptomatic.

Heliox therapy
• Gaseous mixture of oxygen and helium in ratios of 20/80
and 30/70 respectively.
– mixture is less dense than air
– inhalation reduces turbulence in the airway and eliminates
respiratory noise
• Recommended for immediate relief of respiratory distress
– reduces anxiety - the predisposing factor to many attacks
– provides short-term relief of dyspnea
– not effective for relief of symptoms due to asthma or other lower
airway disease

Other Acute Therapy
• IPPV and CPAP
– widen the rima glottidis and reduce turbulence
• Panting
– physiologically increasing the glottic aperture
• Benzodiazepines / Reassurance
– reduce anxiety and have been shown effective
• General anesthetic induction
– small doses of propofol can relieve acute attacks
• Intralaryngeal injection of botulinum toxin type A
– more invasive approach for severe exacerbation
• Conversely, therapy with bronchodilators / oxygen /
corticosteroids
– shown ineffective for relief in patients with PVCM

Long-term Management
• requires a multidisciplinary approach involving
speech therapy, psychiatric support and physician
education regarding the syndrome
• Speech therapy
– techniques aimed at focusing attention on expiration and
abdominal breathing rather than on inspiration and laryngeal
breathing
– early recognition of symptoms allows relaxation of neck,
shoulder and chest muscles promoting normal laryngeal
breathing

Long-term management cont’d
• Psychotherapy
– allows patient to explore for potential causes
– trains the patient with relaxation techniques
• Psychotherapy should be initiated if:
– insufficient improvement with speech therapy alone
– evident psychological tumult in the patient’s life
– at the patient’s request
• Education about the condition
– useful for reducing stress.
– Biofeedback training has been used as a long-term treatment
approach -not considered primary agent

Prognosis
• long-term outcome unknown
– most literature consists of case reports and
retrospective studies.
– One study followed three patients over a 10- year
period - all showed continued symptomatic VCD at
follow-up
• More trials needed before conclusions about
management efficacy can be drawn.

Prognosis cont’d
• Initial response to standard management
(speech, psychotherapy) is good:
– interview with 15 patients all diagnosed with PVCM
who had received prior therapy.
– took place an average of 20 months (range 11-62)
after initial diagnosis of the disorder.
– results showed most responded well with improved
functioning and fewer symptoms after intervention

Conclusion

• PVCM is an under recognized disorder that can result from
many different etiologies
– majority of patients are young to middle-aged females.
• Must have a high suspicion to make the diagnosis
• Many people every year are misdiagnosed and wrongly
treated for refractory asthma and anaphylaxis
– Inappropriate hospitalization, high doses of corticosteroids,
intubation, and tracheostomy
• Strong association between people with VCD and those
with asthma.

Conclusion cont’d
• The presentation of both patient groups can be identical
– the finding of one in a patient does not rule out the presence of the other - it
seems to make it more likely.
• Each disease carries its own unique treatment,
– asthma therapy is ineffective against symptoms of VCD and vice-versa.
– Success for both relies on correct diagnosis
Treatment of both must be maintained beyond resolution of the initial
exacerbation.
• Little data is available about the long-term effects of therapy, but
short-term studies have revealed promising results.
– As more clinicians become aware about the spectrum of presentation seen
with VCD, fewer misdiagnoses will be made.

Overview: Diagnosis
and natural history

• Diagnose before treating
• Try to confirm diagnosis with objective tests before long-term
therapy is started
• Differentiate from other respiratory and non-respiratory conditions
• Question the diagnosis if little response to treatment


Overview: Non-pharmacological
management

• Little evidence for effectiveness in preventing development
of asthma, or reducing its impact
• Early wheezing may be reduced with breast feeding and
smoke-free environment
• Allergen reduction may reduce impact of asthma
• No consistent evidence supporting use of complementary or
alternative treatments

Non-pharmacological management. Thorax 2003; 58 (Suppl I): i1-i92

Overview: Pharmacological
management

• Add inhaled long-acting ß2 agonists rather than
increasing the dose of inhaled steroids (above
800mcg/day in adults and 400mcg/day in children)
• Step down therapy to lowest level consistent with
maintained control


Overview: Inhaler devices

• pMDI + spacer is preferred delivery method in children
aged 0-5 years
• pMDI + spacer is as effective as other delivery methods
for other age groups
• Choice of inhaler should be based on patient preference
and ability to use

Inhaler devices. Thorax 2003; 58 (Suppl I): i1-i92

Overview: Management
of acute asthma

• Assess and act promptly in acute asthma
• Admit patients with any feature of a life threatening or near
fatal attack, or severe attack persisting after initial treatment
• Measure oxygen saturation
• Use steroid tablets
• Primary care follow up required promptly after acute asthma

Management of acute asthma. Thorax 2003; 58 (Suppl I): i1-i92

Overview: Asthma in pregnancy

• Continue treatment as usual
• Monitor pregnant women with asthma closely to ensure
therapy is appropriate for symptoms
• Acute severe asthma in pregnancy should be treated as
usual, but in a hospital setting
• If anaesthesia is required, regional blockade is preferred

Asthma in pregnancy. Thorax 2003; 58 (Suppl I): i1-i92

Overview: Occupational asthma

• Consider occupational causes in adults presenting
with asthma symptoms
• Objective confirmation required

Occupational asthma. Thorax 2003; 58 (Suppl I): i1-i92

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