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 ofasthma in adults

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

Some of symptoms of asthma are shared with diseases of other systems

Numerous relatively common lung diseases

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

Differential diagnoses include:

• COPD• cardiac disease• laryngeal, tracheal or lung tumour• bronchiectasis• foreign body

• interstitial lung disease• pulmonary emboli• aspiration• vocal cord dysfunction• hyperventilation

Indications for referral ofadults 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 inadults: practice points


Record presence of wheeze in patient’s notes

Try to confirm diagnosis with objective tests beforelong-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

ED and Hospital Management: 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

ED and Hospital Management: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

ED and Hospital Management: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 �• Chronic bronchitis �• emphysema• Obstruction of airways by �

foreign• Congestive heart failure�• enlarged lymphnodes • tumour• Viral or obliterative �

bronchiolitis

• Pulmonary embolism�• Cystic fibrosis �• Laryngeal/vocal cord dysfunction�• Obstruction of airways by foreign �

body or tumour• Swallowing dysfunction�• Drug induced cough e.g. ACE�• Gastroesophagial reflux 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.

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

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 down

Difficulty in lying down, sitting

Upright sitting

Recumbent

Talks in sentences phrases words monosyllables

Alertness May be agitated

agitated agitated Confused or drowsy


Respiratory rate

Normal increased Increased>30min

Paradoxical

Accessorymuscles

Not active Active active Thoracoabdominal paradox

Wheeze ModerateEnd expiratory

Loud Usually loud Absent breath sounds

Pulse/min <100 100-120 >120 Bradycardia


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

?<40%

PaO2 Normal >60 mm Hg <60 mm hgPossible cyanosis

?

PaCO2 <45 mm hg <45 mm hg >45 mm hgPossible resp. failure

?

SaO2On room air

>95 % 90-95% <90% ?

• 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

Pharmacological management

The British Thoracic Society Scottish Intercollegiate Guidelines Network

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

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

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

Step 1: Mild intermittent asthma

Inhaled short acting ß2 agonist as required

Stepwise management ofasthma 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


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


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



Step 5: Continuous or frequent use of oral steroidsUse daily steroid tablet in lowest dose providing adequate controlMaintain high dose inhaled steroid at 2000mcg/day *Consider other treatments to minimise the use of steroid tabletsRefer patient for specialist care









Step 5: Continuous or frequent use of oral steroids



Step 2: Regular preventer therapy



A B D

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

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

Adults Children 5-12 years

Children <5 years

Step 2: Introduction ofregular preventer therapy


A A A Inhaled steroids are the recommended preventer drug

A D D Give inhaled steroids initially twice daily

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


Children <5 years

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


A B Try adding in other treatments before increasing the inhaled steroid dose (adults: >800mcg/day; children: >400mcg/day)

A B Inhaled long-acting 2 agonist is first choice add-on therapy in adults and children (5-12 years)

D DIf asthma control remains sub-optimal after addition of inhaled 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)




Children <5 years



Inadequate control on low dose inhaled steroids




Add inhaled long-acting ß2 agonist (LABA)




Assess control of asthma




Good response to LABA:• Continue LABA




Benefit from LABA but control still inadequate:• Continue LABA• Increase inhaled steroid dose to

800mcg/day (adults) and 400mcg/day (children 5-12 years)

No response to LABA:• Stop LABA• Increase inhaled steroid dose to

800mcg/day (adults) and 400mcg/day (children5-12 years)






Benefit from LABA but control still inadequate:• Continue LABA• Increase inhaled steroid dose to


Control still inadequate:• Trial of other add-on therapy, e.g.

leukotriene receptor antagonist or theophylline




Step 3: Add-on therapyInadequate control on low dose inhaled steroids

If control still inadequate go to Step 4


Benefit from LABA but control still inadequate:• Continue LABA and• Increase inhaled steroid dose to


Control still inadequate:• Trial of other add-on therapy, e.g.

leukotriene receptor antagonist or theophylline

If control still inadequate go to Step 4






D D

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)

• 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 4: Poor control on moderate dose of inhaled steroid + add-on



A DTo eliminate or reduce the dose of steroid tablets, use inhaled steroids (adults: up to 2000mcg/day; children aged5-12years, up to 1000mcg/day)

D D D

Consider treatment with long-acting 2 agonists, leukotriene receptor antagonists, and theophyllines for about 6 weeks, 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

Step 5: Use of oral steroids



Children <5 years

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

Stepping down


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

A A Inhaled short-acting 2 agonists immediately before exercise

Exercise-induced asthma



Children <5 years

C In adults with allergic bronchopulmonary aspergillosis, consider 4-month trial of itraconazole

Monitor itraconazole side-effects (particularly hepatic)

Allergic bronchopulmonary aspergillosis


Overview: Pharmacologicalmanagement


• 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 asthmaInitial 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• after initial 2-agonist

• relief is sustained• for 4 hours.

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

• ACTIONS:• • May continue B2-agonist• 3-4 hrs for 1-2 days.

• • Contact physician

Response to Initial Treatment Is... Incomplete if…

• Symptoms decrease• but return in less

than 3 hours after initial B2-agonist treatment.

• PEF is 60-80%• predicted

• ACTIONS: urgently• • Add oral steroid.• • Repeat B2- agonist • • Add inhaled anticholinergic.• transport to hospital

Response to Initial Treatment Is... Poor if…

• Symptoms persist or• worsen despite initial

B2-agonist

• PEF is less than 60%• Of predicted

• ACTIONS:• • Add oral• glucocorticosteroid.

• • Add inhaled• anticholinergic.

• •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• • History: high-risk patient• • 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• • History: high-risk patient• • 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

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

Differential diagnosis

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

Management Summary

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 diagnosisTreatment 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: Diagnosisand 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-pharmacologicalmanagement

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

• 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

Overview: Pharmacologicalmanagement


• 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

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

• 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

Overview: Managementof acute asthma

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

• 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

Overview: Asthma in pregnancy

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

• 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

Overview: Occupational asthma

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

• Consider occupational causes in adults presenting with asthma symptoms

• Objective confirmation required

Asthma

Health & Medicine

metered dose

acute treatment

preferred

age group

initial treatment

objective

term therapy

hospital management