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Obstructive Airway Disease Obstructive Airway Disease

Obstructive Airway Disease - PowerPoint Presentation

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Obstructive Airway Disease - PPT Presentation

Asthma amp COPD Rachel Ventre FY1 Spirometry PFT Obstructive FEV1FVC ratio Asthma COPD Bronchiectasis CF Restrictive FVC amp FEV1 Normal or ratio KyphosisScoliosis ID: 237049

lung asthma www copd asthma lung copd www fev1 chronic amp pefr severity http clinical allergens org wheeze pulmonary

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Presentation Transcript

Slide1

Obstructive Airway Disease

Asthma & COPD

Rachel Ventre FY1Slide2

Spirometry/ PFT

Obstructive – 

FEV1/FVC ratio

Asthma

COPD

Bronchiectasis

CF

Restrictive –

FVC & FEV1. Normal or

ratio.

Kyphosis/Scoliosis

ILD

Connective tissue diseases

Infection - pneumoniaSlide3

AsthmaSlide4

Definitions

AsthmaCommon, chronic inflammatory airway disease, characterised by variable (diurnal)

reversible

airflow

obstruction

, airway hyper-responsiveness, bronchial inflammation and bronchospasm.Slide5

Aetiology

Environmentmaternal smoking during pregnancy

low air quality (pollution)

sterile environment (Hygiene hypothesis)

occupational allergens (isocyanates, epoxy resins)

Genetic

FHx of atopy. +ve twin studies.Slide6

Asthma Triggers?Slide7

Pathophysiology

3

main

features:

Airway narrowing – bronchiole constriction

Irritation – inflammation of

mucosal liningBlockage – excess mucous production forming plugsSlide8

Epidemiology

Increasing prevalence in

UK

FHx

of

atopy

B>G 3:2 in children but equal in adultsOnset – any ageAtopy?Type I hypersensitivity to allergensIncreased tendency for T lymphocyte’s to drive IgE production on allergen exposureAssociated with Asthma, Eczema and Allergic Rhinitis (Hayfever). Runs in families.Slide9

Symptoms

Signs

Presentation

Symptoms

Signs

Cough

WheezeChest tightnessOccasional sputum productionDyspnoea (mild – severe)Pattern  worse at night, exacerbated by exercise, cold, allergens and physiological stress. Drugs (NSAIDs and βblockers)Common allergens  animal dander, cats, dust mites, flour, paints, varnishes and detergentsTachypnoeaAccessory muscle useAudible wheeze polyphonicHyperinflated

chestHyperesonant percussionReduced air entryProlonged expiratory phaseSlide10

Investigations

Initial

Dx & assess

severity

Bedside:

PEFR – with diary showing diurnal variation (>20%), morning dipPulse oximetryBlood:ABG – acidotic?Eosinophil levels, Aspergillus antibodyFBC (WCC), CRP, U&EBlood and sputum culturesRadiology:CXR – hyperinflation, pneumothorax, pneumonia?Special tests:Pulmonary function testsFEV1/FVC < 80%Spirometry – Flow volume loop showing obstructive picture15% improvement post – salbutamolSkin prick tests – allergen identificationBTS uses a ‘response to therapy’ approach to asthma Dx.Chronic monitoring: PEFR – best comparisonSlide11

Management

Conservative:

Smoking cessation

Check inhaler technique

Patient education – avoid allergens/precipitants

Emergency plan – acute exacerbations

Vaccinations – pneumococcal and influenzaMedical: BTS guidelinesStart at appropriate level for severity. Move up if necessary and step down if good control for 3 months. Rescue steroids if required in exacerbations.Slide12

Stepwise RxSlide13

Acute Asthma

Acute exacerbations are

common

Medical emergency

Responsible

for 1000-2000

deaths/yr??Slide14

Management

Resuscitate

ABCDE

Monitor

O2

sats, ABG and PEFRHigh flow 100% Oxygen (15L via non-rebreathable mask) aim sats 94-98%NebulisersSABA (Salbutamol 5mg continuously then 2-4hourly) + Ipatropium Bromide 0.5mg QDSSystemic corticosteroidshydrocortisone 100-200mg IV then Prednisalone 40mg PO for 5/7Magnesium sulphate 2g over 20mins IVBronchodilators IV (ITU only, need cardiac monitoring)Aminophylline or SalbutamolAssess severity (ventilation)Consider ITU or intubation if worsening hypoxia and PEFR despite RxHypercapnia, resp acidosis, coma, resp drepression/arrest. Also if patient is tiring!Consider patient performance status (poor  poor ITU prognosis)Rx underlying cause – infection (ABx) or pneumothorax.Slide15

COPD

Chronic obstructive pulmonary diseaseSlide16

Definitions

COPDChronic progressive lung disorder, characterised by (mostly)

irreversible

airflow

obstruction

, FEV1 <80% predicted and FEV1/FVC ratio <70%.

Chronic bronchitis = clinicalCough & sputum, most days, 3/12 over 2yearsChronic inflam of bronchi (medium)Emphysema = histopathological, CXR/CT changesPermanent destructive enlargement of airspacesDistal to terminal bronchioles (alveolar) = bullaeSlide17

Aetiology

Bronchial

and alveolar damage caused by environmental toxins

Cigarette smoking

Process not fully understood. Processes causing lung damage include

:

GeneticAlpha 1 antitrypsin deficiency (<1%)  EmphysemaPersistent airway inflammationCytokine release due to inflammation, body responds to irritant particlesOxidant/antioxidant capacity imbalanceOxidative stress produced by high free radical concentration in tobacco smokeProtease/antiprotease imbalance in lungsSmoke and free radicals impair activity of antiprotease enzymes (e.g. Alpha 1 antitrypsin). Proteases damage lung.Slide18

Epidemiology

Very common, many undiagnosedMore common in lower socioeconomic status (relates to smoking prevalence)

Presents in middle age or later

M>F due to smoking tendencies in pastSlide19

Presentation

SymptomsChronic productive cough

Following colds and in winter months

Increase severity and frequency over time

Sputum – can be blood stained in advanced disease

Recurrent respiratory infections

Exertional dyspnoea & reduced exercise toleranceRegular morning coughWheezeSlide20

Presentation

Signs:

Inspection

Percussion

Wheeze on forced expiration

Tracheal tug

Tracheal descent in inspiration, reduced cricosternal distanceAccessory muscle usesternocleidomastoid and scalenesSuprasternal and supraclavical fossae excavation (prominent)Indrawn costal margins and intercostal spacesPursed lip breathinghyperinflation/barrel chestIncreased AP diameterWeight lossCentral cyanosisCO2 flapping tremor and bounding pulse (

hypercapnia)Hyper-resonant percussionLoss of liver and cardiac dullnessAuscultationQuiet breath soundsProlonged expirationWheezeCrepitations if infectedSlide21

Investigations

Bedside

:

PEFR

– reduced

Blood:

Secondary polycythaemiaABG - Hypoxia, normal or raised CO2Radiology:CXRChest CT – bullae and lung volumesSpecial tests:Pulmonary function testsSpirometry – reduced FEV1 <80%FEV1/FVC ratio – reduced <70% (see below)Increased lung volumesCO gas transfer coefficient decreased when significant alveolar destructionECG/Echo – cor pulmonale?Sputum/blood cultureSlide22

CXR

Hypertranslucent lung fields

Low flat diaphragm

Bullae

Hyperinflation

>6ribs ant

 peripheral lung markingsElongated cardiac shadowSlide23

Diagnosis/Severity

4 classifications of severity of COPD:Slide24

Management

Conservative:Avoid bronchial irritation

Smoking cessation

limits FEV1 decline

Occupational allergens

ExercisePulmonary rehabilitationWeight loss – correct obesity, nutritional improvementRx depression/social isolation – often associatedSlide25

Management - medicalSlide26

Management

Surgery:Lung transplant in lung patients with alpha 1 antitrypsin deficiency

Bullaectomy

lung volume reduction surgery (Lobectomy – now close off the lobe using a filter)Slide27

Acute COPD Mx

Rescusitation

– ABCDE

24%

O2

, 2L via nasal cannula or non-variable flow venture

mask.If Type II resp failure target 88-92%Nebulisers - bronchodilatorsCorticosteroids (oral/IV)FluidsTheophylline IVEmpirical ABx IV if infection (+/- pseudomonal cover? Tazocin, Meropenum, Gentamycin)Consider ventilationConsider NIV, intubation or ITU in severe cases.Indication for NIV  persistent hypercapnia type II RF, deterioration despite 1hr best medical Rx and patient tiring.Slide28

Video by Asthma UK PEFR

http

://www.youtube.com/watch?v=DxBDfqPmaZUSlide29

Video Asthma UKInhaler technique

MDI

http://www.youtube.com/watch?v=FqztOZLqFhE

All other inhalers

http://www.asthma.org.uk/knowledge-bank-treatment-and-medicines-using-your-inhalersSlide30

LTOT

Indications:Chronic hypoxaemia e.g COPD, ILD, Lung Ca

PaO2 <7.3kPa on air when clinically stable

PaO2 7.3-8kPa if 2* polycythaemia or pulmonary hypertension (clinical/echo)

Nocturnal hypoventilation

e.g obesity, OSA, chest wall disease

Specialist referral. Usually with CPAP or NIV.Palliative careFor Rx of dyspnoea in terminal illness.Assessed by respiratory physiologistsrequires ABG on and off O2.Slide31

Any QuestionsSlide32

References

BTS guidelines asthma -

http

://

www.brit-thoracic.org.uk/Portals/0/Guidelines/AsthmaGuidelines/qrg101%202011.pdf

BTS guideline COPD

- http://www.nice.org.uk/nicemedia/live/13029/49399/49399.pdfBTS guidlein LTOT - http://www.brit-thoracic.org.uk/Portals/0/Clinical%20Information/Home%20Oxygen%20Service/clinical%20adultoxygenjan06.pdfSpirometry guideline - http://www.brit-thoracic.org.uk/Portals/0/Clinical%20Information/COPD/COPD%20Consortium/spirometry_in_practice051.pdfAsthma UKPatient.co.uk – professionalAcutemed.co.ukhttp://www.eguidelines.co.uk/eguidelinesmain/gip/vol_13/aug_10/jones_copd_aug10.php#.UlqCeBDZIa8Good books for finals: Clinical cases uncovered