Acute Asthma Flashcards
Asthma is a common obstructive chronic respiratory condition.
What is asthma characterised by?
Asthma is characterised by recurrent episodes of dyspnoea, cough and wheeze caused by a reversible airway obstruction.
What are the 3 main underlying pathology in asthma which lead to airway narrowing?
- Bronchial muscle contraction triggered by various stimuli => airflow limitation
- Mucosal inflammation caused by mast cell and basophil degranulation resulting in the release of inflammatory mediators
- Increased mucus production
* In chronic asthma inflammation may be accompanied with irreversible airflow limitation due to airway wall remodelling.
Who does asthma affect?
Asthma commonly starts in childhood between 3-5 years => may worsen or improve during adolescence.
Westernised life-style / Developed countries
What is the atopic triad?
Who does this commonly affect?
Atopic triad:
=> Atopic Dermatitis,
=> Atopic Asthma,
=> Allergic Rhinitis
Atopic asthma is a childhood onset wheezing illness caused by inhaled allergic triggers.
What are the most common allergens in atopic asthma?
Dust mite
Animal danders particularly cats
Pollens
Fungi
Which age group does non-atopic asthma affect?
What extrinsic factors lead to asthma in this?
Middle aged individuals
Extrinsic causes:
Sensitisation to occupational agents
Intolerance to NSAIDs
Beta-adrenoreceptor blocking meds => block protective effect of endogenous catecholamines.
*Extrinsic causes must be considered in all cases of asthma and avoided.
What are the underlying theories behind allergic asthma?
Explain hygiene hypothesis in detail.
- Early childhood exposure to allergens and maternal smoking = major influence in IgE production
- Hygiene hypothesis: growing up in a ‘clean’ environment predispose towards IgE response to allergies
Conversely, growing up in a ‘dirtier’ environment allows the immune system to avoid allergic response
=> early life exposure to inhaled and ingested products of micro-organisms as seen in developing countries => reduces the risk of developing asthma/allergies.
*allergens involved in asthma similar to ones involved in rhinitis
What are the precipitating factors for asthma?
Exercise-induced
Cold air
Smoking & passive smoking
Emotions
Drugs i.e. NSAIDs, beta-adrenoceptor blocker
Environment exposure i.e. pollen, house dust-mite, fur
Irritants, dust, vapour, fumes
Atmospheric pollution
Viral infections i.e. rhinovirus, parainfluenza virus, RSV
Occupational sensitisers
Genetic factors
How does exercise or cold air induce asthma?
Exercise induced wheeze is driven by the release of histamine, prostaglandin and leukotrienes from mast cells.
Why are beta-adrenoceptor blockers contraindicated in asthma?
The airways have a direct parasympathetic innervation to produce broncho-constriction via beta2 receptors.
Non-selective beta-blockers i.e. propranolol => broncho-constriction and reduced airflow therefore, should be avoided in asthma.
Beta-1 receptor blockers may be given i.e. atenolol if needed in asthmatic patients
There are two broad types of occupational sensitisers.
I. Low molecular weight compounds i.e.
=> found in spray painting, welding, electronics industry,
=> wood dust,
=> bleaches and dyes,
=> complex metals i.e. nickel, platinum and chromium.
II. High molecular weight compounds
=> Antibiotics
=> Latex
=> Allergens from animals & insects inc. farmers, poultry workers, seafood processing industry, laboratory workers
INFO CARD
Occupational asthma depends on level of exposure.
Atopic individuals develop occupational asthma more quickly => development of specific IgE antibodies
Non-atopic individuals can also develop occupational asthma when exposed to occupational sensitisers for a longer time than atopic individuals.
What are the signs and symptoms of asthma?
Symptoms:
Wheezing attacks
Intermitted dyspnoea
Cough [nocturnal] => usually predominant feature in children and nocturnal cough may be the presenting symptom
Sputum
Signs:
Tachypnoea
Audible wheeze
Hyper-inflated chest
Hyper-resonant percussion
Reduced air entry
Widespread, polyphonic wheeze
What are the clinical features of a severe attack?
Inability to finish sentences
Pulse >110bpm
Respiratory rate >25/min
Peak expiratory flow: 30-50% predicted
What are the clinical features of a severe life-threatening attack?
Silent chest
Confusion
Exhaustion
Cyanosis <92% O2 sats
Bradycardia
Peak expiratory flow <33% predicted
Near fatal = high CO2
What are the 7 important information to establish during history-taking a suspecting asthma patient?
- Diurnal variation: vary throughout the day but marked peak flow drop is common during morning
- Exercise: quantify tolerance
- Disturbed sleep: quantify as nights per week (sign of severe asthma)
- Acid reflux: 40-60% of people with asthma have reflux => treating it improves spirometry but not symptoms
- Other atopic disease: eczema, hay-fever or family Hx?
- Home (especially bedroom): pets? carpets? feather pillows or duvet? soft furnitures i.e. floor cushions?
- Job: 15% of cases are job related, more for paint sprayers, food processors, welders and animal handlers.
If symptoms get better during weekends or holidays then work may be the trigger => ask patient to measure their peak flow at intervals at work and at home (at the same time of day) to confirm
How is initial diagnosis of asthma made in children?
High probability of asthma => trial asthma treatment
=> if successful, continue at minimum effective dose
=> if unsuccessful, assess inhaler technique/compliance
=> no further improvement = refer
Intermediate probability => lung function tests/atopy
=> if lung function test +ve, start asthma trial
=> if lung function test -ve, investigate/treat other cause/refer
Low probability => consider alternative cause
How is initial diagnosis of asthma made in adults?
Clinical investigation i.e. spirometry or peak flow
High probability of asthma => asthma treatment
=> if successful, continue at minimum effective dose
Intermediate probability
=> FEV1/FVC <0.7 = asthma treatment
=> FEV1/FVC >0.7 = consider alternative cause / refer
Which clinical features increase the probability of asthma?
Wheeze, shortness of breath, chest tightness
Diurnal variation
Response to exercise, allergen, cold air
Symptoms after aspirin or B-blocker
Hx of atopy
Family Hx of atopy/asthma
Widespread wheeze on auscultation
Unexplained low FEV1 or peak expiratory flow
Unexplained peripheral blood eosinophilia
Which clinical features lower the probability of asthma?
Prominent dizziness, lightheadedness, tingling
Chronic productive cough with no wheeze
Normal exam when symptomatic
Change in voice
Symptoms with colds only
Significant smoking hx >20 pack years
Cardiac disease
Normal peak expiratory flow when symptomatic
Which investigations are carried out in acute asthma attack?
Peak expiratory flow
Sputum culture (sputum eosinophilia = diagnostic finding)
Bloods: FBC (peripheral eosinophilia), U&E, CRP, blood cultures
ABG: usually shows significantly reduced CO2 and a normal or slightly low O2 => hyperventilating
=> if O2 is normal but patient is hyperventilating then monitor carefully and repeat ABG later
=> if CO2 normal or high and patient is hyperventilating then transfer to ITU for ventilation => indicates respiratory failure
Chest X-ray: to exclude infection / pneumothorax (complication of asthma)
Which investigations are carried out in chronic asthma attack?
Peak expiratory flow monitoring
Diurnal variation of >20% on >3days a week for 2wks
Spirometry: obstructive (reduced FEV1/FVC) => ~15% improvement in FEV1 after beta2 agonists or steroid trial.
Chest X-ray: hyper-inflation
Skin prick test: identify allergen
What is the purpose of a lung function test?
What are the two main lung function tests?
Describe them.
Lung function tests help diagnose and assess asthma reversibility, treatment effectiveness and severity.
- Peak respiratory flow rate (PEFR) measurements on walking, prior to taking a bronchodilator, before bed and after a bronchodilator
=> Demonstrates variable air-flow restriction which characterises asthma
=> Diurnal variation in PEFR = a good measure of asthma activity
- Spirometry assess reversibility => asthma can be diagnosed by showing >15% improvement in FEV1 or PEFR after inhaling bronchodilator
When should skin prick tests be performed?
What is the alternative and when should this test be performed?
Skin prick tests should be performed in all cases of asthma to help identify allergic triggers.
Alternative: allergen specific IgE measurement in serum.
This should only be performed if skin-prick test is not available, if patient taking anti-histamines or no suitable antigen extracts are available.
What is allergen provocation test for?
Allergen inhalation challenge ONLY indicated for patients suspected with occupational asthma, NOT ordinary asthma.
What are the differential diagnosis for asthma?
Pulmonary oedema (cardiac asthma)
COPD
Superior vena cava obstruction (wheezing/dyspnoea not episodic)
Pneumothorax
Pulmonary embolism
Bronchiectasis
Obliterative bronchiolitis (elderly)
What lifestyle changes are required to help improve asthma?
Stop smoking
Avoid triggers
Stop beta-blockers and NSAIDS
Weight loss if overweight
What specific advice is given to patients about asthma management?
Correct inhaler technique
Teach use of peak flow meter to monitor peak expiratory flow twice a day
Educate to enable self-management by altering their medications depending on their symptoms
Written plan on how to act in an emergency
Consider teaching relaxed breathing technique to avoid dysfunctional technique (Papworth method - use stomach area for breathing, not chest)
Which drugs are used for asthma management?
Beta-adrenoceptor agonists (short acting & long acting)
Inhaled & oral corticosteroids
Leukotriene receptor antagonists
Anti-muscurinic (anti-cholinergic) bronchodilators
Anti-inflammatory drugs
Monoclonal antibodies
What is the mechanism of action for Beta2-adrenoceptor agonists?
What are the two types of beta2-adrenoceptor agonists?
Examples?
What are the side effects?
Beta2-adrenoceptor agonists are selective for respiratory tract (doesn’t stimulate beta1 adrenoceptors of the myocardium).
=> They help relax the bronchial smooth muscles and help relieves symptoms by increasing CAMP
=> They have no affect on the underlying inflammation => only symptomatic control!!
2 types of beta2-adrenoceptor agonists:
=> Short-acting Beta agonists (SABA) : 2 puffs/day and can be taken as and when required i.e. salbutamol 100ug ; terbutaline 250ug
=> Long-acting Beta agonists (LABA) : once or twice daily by inhalation can help with nocturnal symptoms & reduce morning dips - effective up to 12h e.g. salmeterol => can be used as an alternative to increasing steroid dose
They should be given in combination with an inhaled corticosteroid e.g. salmeterol + fluticasone
Side effects: tachyarrythmias, decreased K+, tremor, anxiety + LABA = paradoxical breathing
What is the mechanism of action for corticosteroids? Examples?
When do you need oral corticosteroid?
Act over days to decrease bronchial mucosal inflammation i.e. Beclomethasone, fluticasone => inhaled to minimise systemic effects.
For all patients with symptoms, even mild.
Rinse mouth after inhaled steroids to prevent mouth candidiasis
Inhaled corticosteroid dose should be lowered once asthma is controlled
Oral corticosteroid is needed for acute exertions (high dose) and for long term use (small dose) when other meds don’t work e.g. prednisolone
What is the mechanism of action for leukotriene receptor antagonist? Examples?
Targets cysteinyl LT1 recceptor => blocking the effects of cysteinyl leukotrienes in the airway e.g. montelukast
=> only effective on a small proportion of asthma patients
=> should be trialled for 4 weeks before deciding on effectiveness
Leukotriene receptor antagonist should be tried on patients whose asthma is not controlled on low-medium dose of inhaled steroids
What is the mechanism of action for anticholinergic (anti-muscuric) broncho-dilators? Examples?
Muscurinic receptors are found in respiratory tract:
large airways = M3 receptors
Peripheral lung tissue = M1 & M3 receptors
=> nebulised short-acting antimuscurinic drug e.g. Ipratropium may be used in acute severe exacerbation of asthma
What is the mechanism of action for monoclonal antibodies? Examples?
Omalizumab, monoclonal antibody, directed against IgE to downregulate its number and activity of mast cells and basophils.
=> Given as subcutaneous injection every 2-4 weeks
=> Effective in eosinophilic asthma
What is cromoglicate and when can it be used?
Cromoglicate is a mast cell stabiliser (inhaled)
Can be used as prophylaxis in mild and exercise induced asthma in children
What is the prognosis for asthma?
Most childhood asthma improves by adolescence or is less severe as adults.
Significant number develop chronic asthma later in life.
In an acute severe asthma attack patients often present with acute breathlessness and wheeze.
What other features are present in a life-threatening attack?
Peak expiratory flow <33% of predicted or best
Silent chest, cyanosis, feeble respiratory effort
Arrhythmia or hypotension
Exhaustion, confusion or coma
ABG: normal/high CO2 ; low O2
What investigations should be done for a acute asthma attack?
Peak expiratory flow - may be difficult to obtain
ABG if O2 sats <92% or life-threatening features
Chest X-ray if suspicion of pneumothorax, infection or life-threatening attack
FBC, U&E
How do you manage acute asthma attack?
Assess severity of attack - warn ICU if severe or life-threatening
Immediate treatment:
O2 - maintain between 94-98%
Salbutamol 5mg nebuliser with oxygen
If severe/life-threatening, add in Ipratropium 0.5mg/6h to nebuliser
Hydrocortisone 100mg IV or prednisolone 40mg orally
=> Reassess every 15 mins
If peak expiratory flow <75% repeat salbutamol nebuliser every 15-30mins
Add Ipratropium if not already given
Monitor ECG for arrhythmias
Consider single dose of magnesium sulphate IV => in patients with severe/life-threatening features without good response to therapy (only done by senior)
How do you manage acute asthma attack?
Assess severity of attack - warn ICU if severe or life-threatening
Immediate treatment:
O2 - maintain between 94-98%
Salbutamol 5mg nebuliser with oxygen
If severe/life-threatening, add in Ipratropium 0.5mg/6h to nebuliser
Hydrocortisone 100mg IV or prednisolone 40mg orally
=> Reassess every 15 mins
If peak expiratory flow <75% repeat salbutamol nebuliser every 15-30mins
Add Ipratropium if not already given
Monitor ECG for arrhythmias
Consider single dose of magnesium sulphate IV => in patients with severe/life-threatening features without good response to therapy
What is the next step in management of acute asthma attack if patient is improving within half an hour of initial management?
Continue nebuliser salbutamol every 4-6h (+ipratropium if started)
Prednisolone for 5-7 days
Monitor peak flow and O2 (94-98%)
If peak expiratory flow >75% 1h after initial treatment, consider discharge with follow up appt
What is the next step in management of acute asthma attack if patient is not improving with initial management?
Refer to ITU for ventilatory support and additional meds i.e. aminophylline, IV salbutamol if patient has the following signs:
=>Deteriorating peak expiratory flow =>Persistent/worsening hypoxia =>Hypercapnia =>ABG shows low pH, high H+ =>Exhaustion, feeble respiration =>Drowsiness, confusion, altered conscious level =>Respiratory arrest
What are the differential diagnoses for acute asthma attack?
Acute infective exacerbation of COPD
Pulmonary oedema
Upper respiratory tract obstruction
Pulmonary embolus
Anaphylaxis
What steps should be met in a patient who was admitted for acute asthma attack before discharge?
Discharge patient once:
=> stable on discharge meds for 24h
=> inhaler technique checked
=> peak flow rate >75%
=> steroid (inhaled and oral) and bronchodilator therapy
=> their own peak flow meter and written management plan
=> GP appt within 2 days
=> respiratory clinic appt within 4wks
