Update in Airway Diseases for Internal Medicine Resident 2010

8/7/2019 Update in Airway Diseases for Internal Medicine Resident 2010

1/78

Update in Airway Diseasesfor Internal Medicine ResidentCOPD/ Asthma

F

F F


2/78

Pathogenesis of asthma

Diagnosis of asthma Guideline for asthma management

Asthma in special situationOccupational asthmaExercise induced bronchoconstrictionAsthma and pregnancy, GERD, AR

Interesting Topics in Asthma


3/78

A chronic inflammatory disorder of the airways

Many cells and cellular elements play a role Chronic inflammation leads to an increase inairway hyper-responsiveness with recurrentepisodes of wheezing, coughing and shortnessof breath, particularly at night and earlymorning

Widespread, variable and often reversibleairflow limitation

GINA guidelines, 2006.

Definition of asthma


4/78

Inducers

Allergens, Chemical sensitisers,Air pollutants, Virus infections

Inflammation

TriggersAllergens,Exercise

Cold Air, SO2

Particulates

Symptoms

Cough WheezeChest tightness

Dyspnoea

Airway

HyperresponsivenessAirflow Limitation

Barnes PJ

Host FactorsGenetics predisposing

Prevention of smoking exposure

(both in utero and after birth) mayprevent asthma development


5/78

Asthma vs. COPD


6/78

Th2 in allergic disease

IL-4,IL-5,IL-13


7/78

Question

Cells induced sputum F

asthma A. Eosinophils

B. NeutrophilsC. Alveolar macrophage

D. LymphocyteE. Epithelial cells


8/78

Inflammations in asthma


9/78

Most abundant cells in induced sputum ofhealthy subjects and asthma is neutrophils

Asthma with sputum eosinophilia (>3% of cells) Thickening of basement membrane

More likely responsive to corticosteroids Asthma with sputum neutrophilia (>60-65%) In non-allergic asthma

In patients with acute exacerbation More severe obstruction/ severity of asthma Less likely to response to corticosteriods

Inflammations in asthma

Proc Am Thorac Soc Vol 6. pp 256259, 2009


10/78

Asthma diagnosis

iagnosis of

sthmaF asthma


11/78

CXR chronic infection, lung cancer

To support the diagnosis of reversible airwayobstruction

1. Spirometry (pre-post bronchodilator)2. PER3. Bronchial provocative test4. Methacholine or histamine challenge

Investigation for diagnosis of asthma


12/78

Asthma diagnosis

iagnosis of

sthma

History

PT/ PE

Bronchialprovocative

test


13/78

Peak flow measurementPeak flow measurement eak low eter


14/78

Asthma diagnosis

eak low

ariation or diagnosis of asthma by peak flow variability

assessmentpeak flow variability =PEReveningPERmorning x 100

1/2(PERevening + PERmorning) > 20% suggest asthma (variable obstruction)

In diagnosed asthma cases, peak flow can be used forself monitoring and self management plans, assessseverity.


15/78

Asthma diagnosis

eak low

ariability

310/700:44%


16/78

Asthma diagnosis

ronchial

hallengesl (bronchial

hyperresponsiveness)lF methacholine or histamine

lPC20 FF methacholine FEV1 20% baseline F

lF PC20 lFFF asthma PT


17/78

Asthma diagnosis

ronchial

hallenge

Positive bronchial challenge = asthma


18/78


19/78

Late/ short onset of wheezing

Localizing wheezingNot respond to corticosteroids/LABA

May be position relatedNo history of previous allergic diseasePrevious historyo f TB

Clues from CXR or PT

Large airway obstruction


20/78


21/78


22/78


23/78

er r


24/78

10

8

6

4

2

0

-2

-4

-6

0 1 2 3 4 5 6

Flow

(L/s)

Volume (L)

Identify discordance between FEV1 and PEF

F 48 yrs 1.64 m

FVC 3.03 L, FEV1 2.63 L,FEV1% = 87%, PEF = 3.97 L/s

F/P = 11.0

FEV1 in mls > 10 UAOUAO

PEF in L/min

Empey D. Br Med J 1972; 3: 503-505.

Miller MR et al. Q J Med 1990; 74: 177-188.

low Volume LoopSimple approach for interpreting PTPE curves pper irway

bstruction


25/78


26/78


27/78

Cough Variant Asthma

In a subgroup of asthmatic patients cough isthe predominant or sole symptom.Thiscondition has been termed cough variantasthma (CVA).

Patients with CVA comprise a distinctsubgroup of individuals with asthma, ratherthan simply being asthmatic patients who

cough. Patients with CVA have a significantly moresensitive cough reflex. But with a lesser

degree of bronchial hyperresponsiveness


28/78

Cough Variant Asthma

In patient with CVA, bronchoprovocationtesting with inhaled methacholine should beused to document the presence of bronchialhyperresponsiveness and, therefore, thediagnosis of asthma.

The presence of bronchialhyperresponsiveness in a patient with chronic

cough is consistent with, but is not diagnosticof, CVA. A definitive diagnosis of CVA canonly be made after the documented resolution

of cough with specific treatment of asthma.


29/78

Early vs late onset asthma

Early onset asthma: since childhood (


30/78

Exercise induced asthma

Exercise is the most common trigger factor of

broncho-spasm in asthmatic patient Exercise induced bronchospasm also occursin 10% of non-atopic, no asthma patients

Usually indicate poor control asthma Can be prevented by adequate asthma

control or using bronchoditor prior to exercise Anti-leuketriene can also prevent exerciseinduced bronchospasm

a uati th a


31/78

GINA guidelines, 2006.

ontrol

guidelineCharacteristic Controlled

(All of the following)Partly Controlled(Any measurepresent in any week)

Uncontrolled

Daytime symptoms None(twice or less/wk) More than twice/week Three or morefeatures of partlycontrolled asthmapresent in any weekLimitations ofactivities

None Any

Nocturnal symptoms None AnyNeed for reliever/rescue medication

None(twice or less/ week)

More than twice/week

Lung function (PE orEV1)

Normal


32/78

ACT= asthma control testCut off 19 from 25 (5 )

Associated conditions that can


33/78

Allergic rhinitis/ post nasal drip

GERD Drugs ( beta-blocker, ACEI)

Sinusitis

Associated conditions that can

aggravate asthma


34/78

Aspirin induced asthma

Triads: asthma, ASA intolerance, sinusitiswith nasal polyps

Asthma is usually severe and poorly respondto inhaled corticosteriods

Rhinorrhea and nasal congestion usuallyproceed asthma+ASA intolerance for 1-5 yrs Patient usually has asthma attack wiht rhinitis

and conjunctival injection within 3 hours afteringestion of ASA or NSAIDS

Antileukotriene can be use to controlsymptoms


35/78

REDUCE INCREASE

Asthma education

Environmental controlAs-needed rapid-

acting 2-agonistAs-needed rapid-acting 2-agonist

Controller

options

Select oneSelect one Select oneSelect one Add one or moreAdd one or more Add one or bothAdd one or both

Low-dose inhaled

ICS

Low-dose ICS pluslong-acting

2-agonist

Medium-or high-dose ICS plus long-

acting 2-agonist

Oralglucocorticosteroid

(lowest dose)

Leukotriene

modifier

Medium-or high-

dose ICS

Leukotriene

modifierAnti-IgE treatment

Low-dose ICS plusleukotriene modifier

Sustained releasetheophylline

Low-dose ICS plus

sustained release

theophylline

Treatmentsteps

Step 1 Step 2 Step 3 Step 4 Step 5

GINA Report 2007 (www.ginasthma.org)

Budesonide


36/78

NEJM 1994;331:700-705

1200 mcg/day

Budesonide 400

mcg/day


37/78


38/78

Step down of Controller

If symptom is stable for3 months can try

step down If on moderate to high dose ICS, reduce doseto 50%

If on low dose ICS, may try once daily If low dose ICS and controlled for one year

may consider stop medication

If ICS+ LABA, try reduce ICS 50%

If ICS + other controller, try reduce ICS 50%


39/78

Asthma control

Symptoms based

A th T t t St t i


40/78

Sont JK et al, Am J Respir Crit Care Med 1999

Asthma Treatment Strategies



41/78

Pre Post

Reference-strategy

4

6

8

10

12

ReticularLayer

Thickness

(m)

Pre Post

AHR-strategy

Sont JK et al, Am J Respir Crit Care Med 1999

p = 0.3 p = 0.005

p = 0.03


Anti IgE in Asthma


42/78

B-cellB-cell

IgE

omalizumab complexes

with free IgE

XolairMast cell

Allergen-drivenB-cell secretes IgE

FcRI

Anti IgE in Asthma

Anti IgE in Asthma


43/78

Add-on therapy to improve asthma control in adults andadolescents (12 years) with severe persistent allergicasthma positive skin test or serum IgE to a perennialaeroallergen or high IgE level 30 and 700 IU andwho have reduced lung function (EV1


44/78

Total dose (mg) per 28 days

Body weight (kg)BaselineIgE (IU/mL) 2025 >2530 >3040 >4050 >5060 >6070 >7080 >8090 >90125 >125150

30100 75 75 75 150 150 150 150 150 300 300

>100200 150 150 150 300 300 300 300 300 450 600

>200300 150 150 225 300 300 450 450 450 600 750

>300400 225 225 300 450 450 450 600 600

>400500 225 300 450 450 600 600 750 750

>500600 300 300 450 600 600 750 DO NOT ADMINISTER

>600700 300 450 450 600 750

Q4 wks

Q2 wks

BW X IgE level X 0.016 (not more than 750 mg/ 4 week)if dose < 300mg 4 wks > 300 mg 2 wks

Anti IgE in Asthma

Clinical eatures of NA


45/78

Clinical eatures of NA


46/78


47/78

x

in acute severes


48/78

Asthma diagnosis

x c asthma

agnesium

agnesium ebuli ed

ddinganticholinergic

vs nebuli er

same

Interesting Topics in COPD


49/78

Smoking cessation

Pathogenesis of COPD Diagnosis of asthmaPT Management of COPDStable COPDAcute exacerbation

Interesting Topics in COPD

COPD Definition 2010


50/78


COPD is a preventable and treatable

disease with some significant extra-pulmonary effects that may

contribute to the severity in individualpatients.

Its pulmonary component ischaracterized by airflow limitation

that is not fully reversible.



51/78


The airflow limitation is usually both

progressive and associated with anabnormal inflammatory response of

the lungs to noxious particles orgases.

COPD Definition


52/78

COPD Definition

Susceptible

patient

Noxious stimuli

Other factors:Infections

:Environmentetc.

Airflow limitationbnormal inflammation

i


53/78

essation 5l Ask

l Advise/Educate

l Assessment l Assist

l Arrange ollow-up

FF


54/78

1 regnant smoker

2 actating

3 mokelesscigarette

4 dolescent

5 moke 10

tt

COPD Diagnostic/staging


55/78

COPD Diagnostic/staging

COPD


56/78

Breathlessness

InactivityDeconditioningDeconditioningReduced exercise capacity

ExacerbationsExacerbations

Expiratory flow limitationsAir trapping/

hyperinflation

HRQL

Extrapulmonary manifestations

DisabilityDisability MortalityProgressive loss of lung

function

Systemic Inflammations in COPD


57/78

Systemic Inflammations in COPD

Consequences of systemic


58/78

The systemic inflammation is probably related to

several systemic effects of COPD:

1) involuntary weight loss;

2) muscle wasting;

3) reduced functional capacity and health

status;

4) increased cardiovascular morbidityand mortality;5) Impaired bone metabolism.

q y

inflammation in COPD

COPD staging


59/78

g g

Severity Post BDFEV1

MILD 80%

MODERATE 50%FEV1


60/78

1. Airways inflammation

2. Airway obstruction and air trapping3. Respiratory impairment and

deconditioning/ lung functiondecline

4. requent exacerbations5. Multisystem (extrapulmonary)

involvement

Stop smoking/ noxious stimuli

Bronchodilator: shortand long acting

Anti-inflammation: ICS

Rehabilitation+ Rx co-existing diseaseVaccination


61/78

Treatment: Stage 2


62/78

Regular SABA


63/78

Meptin


64/78

Components of pulmonary


65/78

rehabilitation in chronic lung disease

Treatment: Stage 3


66/78

Stage 3/4 Stage 2


67/78

Long acting bronchodilator 1-2

SABA 1-2 + theophylline + rehab.

LABA + inhaled corticosteroids

Inhaled corticosteroids alone

> 1 Severe exacerbation in past 12 months

LABA: salmeterol, formoterol LAMA: tiotropium

Treatment: Stage 1


68/78

Treatment: Stage 4


69/78

COPD

Long Term Oxygen Therapy


70/78

>15 hr/day

PaO2 < 55 . SaO2 < 88%

PaO2 55-60 . SaO2 89-90%

cor pulmonale pulmonary hypertension erythrocytosis (Hct > 55%)

Prevention of AECB

Prevention of COPD exacerbation


71/78

Sapey E. Thorax 2006;61:250-258

Influenza vaccination

Pulmonary rehabilitationStop smokingLong acting bronchodilator

Inhaled corticosteroids (EV1


72/78

Wood-Baker RR. Cochrane Database Syst Rev 2005; (1): CD001288Ten randomised trials comparing parenteral or oral corticostersoid

with placebo Date of last search August 2004 ewer treatment failure within 30 days, OR 0.84 (95%CI, 0.34 to 0.68) Necessary to treat 9 patients (95%CI, 6 to 14) with systemic

corticosteroids to avoid one treatment failure Early EV1, up to 72 hr. showed significant treatment

benefit (EV1 140 ml) Significant improvement breathlessness and blood gases

6-72 hr. after treatmentRisk of hyperglycemia was significantly increased, OR 5.48; 95% CI 1.58

to 18.96

Exacerbation: ClassificationPrevention of AECB

Classification Exacerbation


73/78

Anthonisen NR et al Ann Intern Med 1987 ;106:196-204

Increase in:Dyspnea

Sputum volumeSputum purulence

Type IAll three present,antibiotic

recommended

Type IITwo of three present,antibiotic

recommendedif includes purulence

Type IIIOne of threepresent,

antibiotic notrecommended

in


74/78

l F NPVV COPD AR ,

F( several multicenter, randomizedcontrolled trials)l

success rate 58-93%l first-line intervention in eligibleCOPD with AR

l combination of CPAP and IPVV is preferred.l COPD CH Pneumonia FF

COPD with acute exacerbation.

in


75/78

Noninvasive positive pressure ventilation (NPPV)should be offered to patients with exacerbations

when, after optimal medical therapy andoxygenation, respiratory acidosis (pH


76/78

Ventilator Management


77/78

Large endotracheal tube (oral route)

Adequate sedationShort I-time, prolong expiratory time

Increase inspiratory flow, decreaserespiratory rate, sedationPermissive hypercapnea

Accept high peak airway pressure (keepplateau pressure < 35 cmH2O)

VC may be preferable to PC

Ventilator Management


78/78

Monitor for air trapping/ auto-PEEP

Aggressive bronchodilator via MDI ornebulizerConsider PEEP to counter act auto-

PEEP ( trigger F)

May require bronchoscopic for mucousremoval

Date post:	09-Apr-2018
Category:	Documents
Upload:	sariddet-charoenchai
View:	215 times
Download:	0 times

Update in Airway Diseases for Internal Medicine Resident 2010

Documents