“Breathing through a straw”

Carrie Nicholas

Keelyjo Hindhaugh

Dorothy Millar

Miss L.W

33 year old female, admitted SGH 28/07/03, 19:15 PC:

• Increasing shortness of breath

HPC: • 1/52 productive cough, white sputum

• rhintis

• Amoxicillin started by GP

Miss L.W

HPC:• Increasing chest tightness throughout the day

• Mid-afternoon SOB “breathing through a straw”

• Inhalers gave no relief

• 1 previous hospital admission

• No previous admission to ITU

Miss L.W

PMH:• Asthma

• Hayfever

• Nasal polyps

Drug history• Seretide 250

• Salbutamol

• Flixonase

ALLERGIES: Aspirin Acute Asthma

Miss L.W

Family history• Mother

• Grandmother

Social history• Lives with mother

• Non-smoker, no-one in house smokes

• Occasional alcohol

• Pets: Dogs, 4 Cats, Bird Garden

Systems enquiry unremarkable

A & E Management

RR 30 Unable to complete sentences Use of accessory muscles Diffuse wheeze, no crackles/consolidation

– High dose O2 (4L)

– 5mg Salbutamol nebulized

– 500mg Atrovent nebulized

– 40mg Prednisolone (oral)

– CXR to exclude pneumothorax

Examination

General:• Apyrexial

• Overweight

Respiratory• RR 25/min, no use of accessory muscles

• chest clear, no crepitations, trachea central

• PEFR: Pre-nebs - 190

Post-nebs - 350

Normal - 400

Examination

Cardiovascular• Pulse: 112 regular• Blood pressure: 140/70• JVP not elevated• Heart sounds normal. No murmurs• No oedema

Abdominal• Soft and non-tender• No organomegaly• No masses• Bowel sounds present

Investigations

Bloods: Na: 142 Hb: 13.9 Neut: 20.1

K: 4.5 WBC: 24.6 Lymph: 1.8

Urea: 4.9 Plt: 345

Creat: 73 MCV: 82

CRP: 29.2

ECG: Sinus Tachycardia CXR: Poor expansion. No pneumothorax, no

consolidation, no effusion

Investigations - ABG’s

Admission +4hrs +8hrs +12hrspH 7.472 7.52 7.46 7.46PCO2 3.90 4.06 4.39 4.3PO2 8.87 7.91 7.54 9.32O2 Sats 95.2% 92.8% 90.5% 93.0%Base XS -2.0 -2.4 -0.6HCO3

- 23.5 23.0 22.8

Management

Regular nebulisers ABG’s Daily predisolone 40mg PO Monitoring clinical picture

Hospital Course

• Improvement of PEFR back to 400

• Afebrile

• Occasional wheeze

• Asthma nurse specialist

• No morning dip

• Converted to inhalers

• Steroid dose tapered

• GP to continue care

• Discharged on same medication as admission

Peak Flow Chart

Asthma

5-8% of the population Three characteristics:

– Airflow limitation; usually reversible– Airway hyper-responsiveness– Inflammation of the bronchi

Can occur at any time in life, although most commonly develops during childhood.

Prevalence is increasing Highest prevalence in affluent, westernized

populations

Pathogenesis

Bronchial inflammation (eosinophils, neutrophils, T lymphocytes, mast cells)

Environmental factors Genetic predisposition

Bronchial hypereactivity + Trigger factors

OedemaBronchoconstrictionMucous production

Airway narrowing and symptoms

TriggersEnvironmental Exposure to allergen

Genetic Factors

Occupational sensitizers:Isocyanates, Colophony fumes

Atmospheric Pollution:Sulphur Dioxide, Ozone, Diesel exhaust

Drugs (oral/topical):NSAIDS, Beta Blockers

Viral Infections:Rhinovirus, Parainfluenza, RSV

Cold air

Emotion

Irritant dusts, vapour and fumes:Perfume, cigarette smoke

Dermatophagoides pteronyssinus, grass pollen, pets

Aspirin Induced Asthma

Triad consisting of:– Asthma– ASA insensitivity– Nasal Polyps

5-30% asthmatics sensitive to aspirin Sensitivity develops between 30-50yrs Non allergenic mechanisms involved

Aspirin induced asthma; pathophysiology: Defect in the oxidative metabolism of

arachidonic acid Causes cysteinyl leukotreine formation Potent inflammatory mediator Produces

– bronchoconstriction– mucous secretion– airway oedema

Clinical presentation

Wheezing, nasal symptoms Facial flushing, angioedema, GI symptoms Tend to have more severe asthma Nasal polyposis often more troubling

Diagnosis

From hx of analgesic use Definitive diagnosis - pulmonary function

monitoring following ASA challenge Also urinary leukotrienes

Treatment Usual guidelines for asthma therapy NSAID avoidance COX-2 inhibitors safe to use Address sinus & nasal disease, aggressive use of

nasal steroids: – retard polyp growth and promote regression

Leukotriene modifiers:– better PEFR in AM, improved symptoms, decreased use

of rescue medications

ACUTE ASTHMA MANAGEMENT

Uncontrolled features

Nocturnal symptoms interrupting sleep - cough, dyspnoea

Worsening cough Increased use of beta-agonists Decreased efficacy of rescue

medication

Features of severe asthma

Peak flow <50% predicted or best achieved by Pt

Tachypnoea (>25 breaths/min) Tachycardia (>110 beats/min) Unable to complete full sentences

Features of potentially fatal asthma Peak flow <33% predicted or best

achieved by Pt Silent chest on auscultation Bradycardia Hypotension Cyanosis / Hypoxia

Monitoring

Measure ABG on admission Pulse oximetry to monitor Pts oxygen

sats Record peak flow on initial assessment,

before and after bronchodilator Rx, & again after at least 1-2 hrs

Oxygen

Most Pts will have low arterial oxygen tension so give high concentration of oxygen at flow rate of 6l/min

Ventimask should not be used

Bronchodilators

Start asap via oxygen-driven nebuliser, e.g. 2.5mg salbutamol

If no improvement, repeat this dose at 15 min intervals

Nebulised ipratropium bromide (250mcg) helps in ~30% Pts

IV bronchodilators only indicated in Pts who fail to respond to repeated nebulised Rx

Corticosteroids Hydrocortisone 200mg IV or prednisolone

30-60mg orally as soon as initial assessment made

If hydrocortisone given, same dose should be repeated every 6hrs for 12hrs then 100mg 6hr’ly

Whichever steroid given initially, after 2 days all Pts should be taking 20-30mg oral prednisolone daily for 14-21 days

Magnesium

Pts with severe asthma who respond poorly to nebulised bronchodilators, give iv Mg at dose of 2g (8mmol) in 250ml of NaCl 0.9% over 1hr

Hydration

Pts tend to become under-hydrated because of decreased fluid intake & extra loss through hyperventilation

This may increase the tenaciousness of the bronchial secretions

Give iv fluids Monitor electrolytes, particularly K

Aminophylline

Only rarely given in acute asthma because difficult to use & has limited efficacy

Administration limited to Pts in whom all other Rx’s failed and Pt continues to deteriorate and intubation is imminent

Therapeutic monitoring essential

Inpatient management

Progressive improvement in morning peak flow should be seen before discharge

Transfer from nebulised to aerosol Rx 24hrs after admission & start on inhaled steroids

Check inhaler technique

Discharge

Discharge on inhaled &/or oral steroids F/U after 2-3wks Home peak flow monitoring

MANAGEMENT OF CHRONIC ASTHMA

Step 1: Occasional relief bronchodilators Inhaled short-acting beta agonist (up to

once daily)

Step 2: Regular inhaled preventer therapy

As Step 1 PLUS Regular standard dose inhaled

corticosteroid

OR Regular cromoglycate or nedocromil

Step 3: High-dose inhaled corticosteroids or standard-dose corticosteroids + long-acting inhaled beta agonist

As Step 2 PLUS Regular inhaled long-acting beta

agonist - salmeterol 50mcg 2x daily or (>18yrs) formoterol 12 mcg 2x daily

Step 4: High-dose inhaled corticosteroids + regular bronchodilators

Inhaled short-acting beta agonist as required

WITH Regular high-dose inhaled

corticosteroid

PLUS sequential therapeutic trial of 1 or more of:

• Inhaled long-acting beta agonist• Modified-release oral theophylline• Inhaled ipratropium or, in adults, oxitropium• Modified-release oral beta agonist• High-dose inhaled bronchodilators• Cromoglicate or nedocromil

Step 5: Regular corticosteroid tablets

As Step 4 PLUS Regular prednisolone tablets (as single

daily dose)

Stepping down

Review Rx every 3-6 mths If control achieved stepwise reduction may

be possible If Rx started recently at Step 4 or 5 reduction

may take place after short interval Other Pts, 1-3 mth or longer stabilising

period required before slow stepwise reduction undertaken