QuestionSBA
QuestionChoice
The role of inhaled corticosteroids as an adjunct in asthma exacerbations has not been well established. As the patient has already received high dose IV steroids, this would not be of additional benefit
32196
d
Inhaled corticosteroids
QuestionChoice
The patient has features of a life-threatening asthma attack and would benefit from an early ICU review. Patients with a normal pCO2 are at risk of quick deterioration to type 2 respiratory failure due to exhaustion and hypoventilation. The patient should be assessed for consideration of intubation and mechanical ventilation
32193
a
Intensive care unit (ICU) review
QuestionChoice
This would not be appropriate at this stage although the blood gas results seem relatively reassuring. As the patient has a normal pCO2, they are at risk of exhaustion and hypoventilation, and should be considered for early escalation and senior review
32194
b
Watch and observe
QuestionChoice
Uncontrolled oxygen delivery may be dangerous in the deteriorating asthmatic patient as it may cause over-oxygenation and worsening hypercapnia if the patient hypoventilates. Controlled supplementary oxygen should be given to maintain oxygen saturations above 94%, with close pulse oximetry monitoring
32195
c
High flow oxygen via non-rebreathe mask
QuestionChoice
This is not likely to result in an additional bronchodilator effect compared with inhaled bronchodilators and steroids. It should only be administered after consultation with a senior as it would require close monitoring of levels
32197
e
IV theophylline
Concept
Chapter
# Summary

Asthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack”), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations for all adults with suspected asthma are fractional exhaled nitric oxide (FeNO) or a full blood count looking for eosinophilia. If neither of these are confirmatory, patients should be assessed with spirometry including bronchodilator reversibility. Management involves a stepwise approach to medications, starting with “reliever therapy” (usually short-acting beta-2 agonists such as salbutamol inhalers) in combination with “preventer therapy” medications including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-2 agonist inhalers. Allergen avoidance, smoking cessation, regular peak flow monitoring and inhaler technique are all key to good asthma control.

# Definition

Asthma is a common disease in both adults and children, characterised by intermittent "asthma attacks" with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.

# Epidemiology

In the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.

On average, three people die from an asthma attack each day in the UK. The majority of these deaths are preventable, with an estimated 7/10 people with asthma not receiving basic preventative care such as inhaler technique checks and a personalised asthma plan.

People experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.

# Pathophysiology

Asthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:

- Cold air and exercise
- Pollution and cigarette smoke
- Allergens such as animal dander, dust mites and pollen
- Irritants such as perfumes, paints or air fresheners
- Medications such as NSAIDs or beta-blockers

These trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.

This inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.

# Risk factors

- Family history of asthma or atopy
- Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)
- Exposure to smoke, including maternal smoking in pregnancy
- Respiratory infections in infancy
- Prematurity and low birth weight
- Obesity
- Social deprivation
- Occupational exposures (e.g. flour dust, isocyanates from paint)

# Symptoms

- Wheeze
- Dyspnoea
- Cough
- Chest tightness

The above symptoms should be episodic and usually show **diurnal variation** (worse at night or in the early morning). The patient may be able to identify specific triggers as listed above.

# Signs

In between asthma exacerbations, clinical examination may be normal. If asthma is poorly controlled or during an exacerbation, signs include:

- Tachypnoea
- Increased work of breathing
- Hyperinflated chest
- Expiratory polyphonic wheeze throughout the lung fields
- Decreased air entry (if severe)


# Differential diagnosis

- **Bronchiectasis** - usually associated with a productive cough, patients get frequent chest infections and coarse crackles rather than wheeze predominate on examination.
- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.
- **Chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.
- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.
- **Eosinophilic Granulomatosis with Polyangiitis** (Churg-Strauss syndrome) - small vessel vasculitis associated with pANCA, aside from asthma symptoms include nasal polyps, sinusitis, purpuric rashes and peripheral neuropathy.

# Investigations 

- **FeNO (fractional exhaled nitric oxide) testing:** offer this **or** blood eosinophil count to all adults to confirm eosinophilic airway inflammation, asthma can be diagnosed if this is >50 parts per billion.
- **Full blood count** to check **eosinophil count:** offer this **or** FeNO first-line to all adults - asthma can be diagnosed if this is above the normal reference range.
- If neither of these confirm asthma, **spirometry** with **bronchodilator reversibility** should be offered to confirm airway obstruction (i.e. FEV1/FVC<70%). A bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is diagnostic of asthma.
- If spirometry is delayed or not available, patients may be asked to monitor their peak flow twice a day for 2 weeks and keep a diary of the readings. This is then used to assess **peak flow variability** (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result.
- If none of the above are confirmatory, patients may be referred to specialist services for a **direct bronchial challenge test**, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.

Note: All of the above tests may be falsely negative in patients treated with inhaled corticosteroids.

# Management of Chronic asthma

The aim of chronic asthma management is to achieve complete control over symptoms, with no need for rescue medications and no restrictions on physical activity. All patients should have a personalised asthma action plan which should be reviewed at least annually. Components of management include:

## Non-pharmacological

- Teach good inhaler technique and review this regularly
- Spacer devices can be used to optimise medication delivery
- Regular peak flow monitoring
- Smoking cessation
- Advice on avoiding triggers where possible (e.g. allergens, certain medications)
- Ensure vaccinations are up to date, including annual influenza vaccination
- Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected

## Pharmacological

- Prescribe all patients a combination inhaler with a **long-acting beta-2 agonist** (LABA) i.e. formoterol and a low-dose **inhaled corticosteroid** (ICS) i.e. budesonide to use as a reliever inhaler (i.e. PRN) - this is referred to as anti-inflammatory reliever (AIR) therapy.
- Patients who do not respond adequately to AIR therapy, who are highly symptomatic at presentation or who present with a severe asthma exacerbation should be started on a low-dose **maintenance and reliever therapy inhaler** (MART). MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler (PRN) and as maintenance treatment (usually twice daily).
- The next step would be increasing the ICS dose from low to **moderate** in the MART inhaler.
- At this stage if asthma is not controlled, check FeNO and blood eosinophil count and refer to specialist asthma services if either are raised.
- If neither are raised, consider adding either a **leukotriene receptor antagonist** (LTRA) such as montelukast (this is a tablet taken every night) or a **long-acting muscarinic agonist** (LAMA) such as tiotropium.
- One of these should be trialled for 8-12 weeks alongside the moderate-dose MART - if asthma is well-controlled it can be continued.
- If there is some improvement in control but this is still inadequate, the other medication can be trialled in addition (i.e. moderate dose MART + LTRA + LAMA).
- If control has not improved, stop the medication and try the other one - if this is not successful refer to specialist services.
- Options in specialist clinics include therapies such as **biologics** (e.g. omalizumab, which targets IgE).

Other than patients who are not responding to treatment, the following situations shold also prompt a secondary care referral:

- Uncertainty regarding diagnosis
- Suspected occupational asthma
- Severe or life-threatening asthma requiring admission to hospital
- Multiple exacerbations requiring oral steroid treatment per year

# Acute asthma

Acute asthma exacerbations are graded in severity as below:


| Severity | Clinical Features |
|-----------------------|-----------------------------------------------|
| Moderate | PEFR > 50% of predicted or best |
| | No features of severe/life-threatening asthma |
| Severe | PEFR 33-50% of predicted or best |
| | Heart rate > 110 |
| | Respiratory rate > 25 |
| | Unable to complete sentences in one breath. |
| | Accessory muscle use |
| Life-threatening | PEFR < 33% of predicted or best |
| | Oxygen saturation < 92% or cyanosis |
| | Altered conciousness/confusion |
| | Exhaustion/poor respiratory effort |
| | Cardiac arrhythmia |
| | Hypotension |
| | Silent chest |


## Investigations 

- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.
- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.
- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.

## Management 

- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment
- Titrate oxygen to maintain saturations of 94-98%
- Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)
- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide
- Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow
- Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers
- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)

Follow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management.

# NICE Guidelines

[NICE - Asthma: diagnosis, monitoring and chronic asthma management](https://www.nice.org.uk/guidance/ng245)

# References

[NICE CKS](https://cks.nice.org.uk/topics/asthma/)

[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)

[Guideline on severe asthma in primary care](https://www.pcrs-uk.org/sites/default/files/pcru/articles/2019-Autumn-Issue-18-SevereAsthmaReferral.pdf)




334
3418
Asthma
Topic
20
Respiratory Physiology
6439
A 75 year old lady is admitted to the general medical ward with a 2 day history of worsening shortness of breath and a productive cough. She has a background of asthma since childhood and is known to be poorly compliant with her inhalers.


On examination, she is drowsy and has reduced breath sounds bilaterally.


Observations:


 - Temperature 38.5°C
 - pulse 115
 - BP 110/70
 - respiratory rate 16
 - SpO<sub>2</sub> 96% on 8L oxygen


Arterial blood gas:

||||
|--------------|:-------:|------------------|
|pH|7.37|7.35 - 7.45|
|PaO₂|11.5 kPa|11 - 15|
|PaCO₂|5.1 kPa|4.6 - 6.4|
|Bicarbonate|23 mmol/L|22 - 30|


She has been started on nebulised salbutamol and ipratropium, and has been given IV hydrocortisone and magnesium sulphate. Which is the next most appropriate management?
a