Respiratory

Question 1

How is an asthma exacerbation classified?

Answer 1

An acute exacerbation of asthma can be classified based on the patient’s PEFR, arterial oxygen saturation (SpOâ‚‚), partial arterial pressure of oxygen (PaOâ‚‚), and partial arterial pressure of carbon dioxide (PaCOâ‚‚).

Question 2

What is moderate acute asthma exacerbation ?

Answer 2

Increasing symptoms.
PEFR >50-75% of the patient’s best or predicted score.
No features of acute severe asthma.

Question 3

What is considered severe asthma exacerbation?

Answer 3

PEFR 33-50% of the patient’s best or predicted score.
Respiratory rate (RR) ≥ 25 breaths per minute.
Heart rate (HR) ≥ 110 beats per minute.
Inability to complete sentences in one breath.

Question 4

What is considered a life-threatening asthma exacerbation?

Answer 4

PEFR <33% of the patient’s best or predicted score.
SpOâ‚‚ <92%.
In life-threatening asthma exacerbations, PaCOâ‚‚ will be normal. If the PaCOâ‚‚ rises, then this is now classed as a near-fatal asthma exacerbation.
PaOâ‚‚ <8kPa.
Absence of audible breath sounds over the chest (silent chest).
Cyanosis (usually of the lips).
Reduced respiratory effort.
New-onset arrhythmia.
Exhaustion.
Reduced Glasgow coma score (GCS).
Hypotension.

Question 5

What is considered a near-fatal asthma exacerbation?

Answer 5

Raised PaCOâ‚‚ (>6kPa) and/or need for mechanical ventilation.

Question 6

Differential diagnosis for acute asthma exacerbation?

Answer 6

Exacerbation of COPD

Pneumothorax (usually you would get pain which is not classically seen in pneumothorax)

Foreign body aspiration

Vocal cord dysfunction - clinically presents with dyspnoea and stridor

PE

Question 7

How should exacerbation of asthma be managed?

Answer 7

severe - admit to hospital if fails to respond to treatment
Near-fatal / life threatening - admit to hospital

If low oxygen - supplemental oxygen

High dose inhaled SABA (salbutamol) - if features of life threatening/near fatal this should be given nebulised.
Repeat administration every 20-30 minutes

if poor response to salbutamol add in nebulised ipratropium bromide
- all patients should be given 40mg of PO prednisolone daily

IV Magnesium and IV aminophylline may be used in near fatal or life threatening asthma

• If news not available.- use a pressurised metered dose inhaler with a large volume spare
  4 puffs initially followed by 2 puffs every 2 minutes - up to 10 puffs - repeat every 10 - 20 minutes if clinically necessary.

Mechanical ventilation
findings such as severe fatigue, cardiovascular compromise and pneumothorax may be useful in decision making about mechanical ventilation. Mechanical ventilation can be helpful in treating acute exacerbations of asthma but there is also a high rate of complications associated

Question 8

What is acute respiratory distress syndrome?

Answer 8

Acute respiratory distress syndrome (ARDS) is caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema. It is a serious condition that has a mortality of around 40% and is associated with significant morbidity in those who survive.

Question 9

what are the causes of ARDS?

Answer 9

infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
cardio-pulmonary bypass

Question 10

What are the clinical features of acute respiratory distress syndrome?

Answer 10

acute onset of hypoxemia and bilateral pulmonary infiltrates in the absence of cardiac failure.
Symptoms usually develop within 1 week after an inciting event or worsening of an existing condition

• dyspnoea - usually the first symptom and often very severe
• Hypoxema
• Tachypnoea
• Crackles
• Tachycardia
• use of accessory muscles
• cyanosis

Question 11

How is ARDS diagnosed?

Answer 11

Criteria (American-European Consensus Conference)
acute onset (within 1 week of a known risk factor)
pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
pO2/FiO2 < 40kPa (200 mmHg)

Question 12

How is ARDS managed?

Answer 12

due to the severity of the condition patients are generally managed in ITU
oxygenation/ventilation to treat the hypoxaemia
general organ support e.g. vasopressors as needed
treatment of the underlying cause e.g. antibiotics for sepsis
certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS

Question 13

What may trigger exacerbation of COPD?

Answer 13

Infections
- bacterial - strept pneumoniae, Haemophilus influenzae, moraxella catarrhalis
- Viral - rhinovirus, influenza virus, parainfluenza virus, coronavirus, respiratory syncytial virus (RSV), and human metapneumovirus.

Non-infectious
- Air pollution
- allergens
- PE
- Medication non-compliance

Question 14

What is the pathophysiology of exacerbation of COPD?

Answer 14

Increased inflammation, mucosal oedema and bronchospasm further limit expiratory flow
Gas trapping worsens, increasing ventilation-perfusion mismatch
The resulting hypoxia and hypercapnia trigger the neural drive to increase ventilation
Respiratory muscles fatigue, leading to a ‘neuromechanical decoupling’ that reduces the ventilatory drive
Existing cardiac dysfunction worsens due to increasing pulmonary vascular resistance

Question 15

what is the criteria for diagnosis of exacerbation of COPD?

Answer 15

The modified Anthonisen criteria suggest that a diagnosis of an exacerbation of COPD can be made if there are at least 2 of the major symptoms or at least one major and one minor symptom:

Major symptoms - dyspnoea, increased sputum volume, increased sputum purulence
Minor symptoms - cough, wheeze, nasal discharge, sore throat, pyrexia

Question 16

Signs of an acute exacerbation of COPD?

Answer 16

Increased respiratory effort (Tachypnoea, nasal flaring, use of accessory muscles, paradoxical chest wall movement)
Tachycardia
Reduced breath sounds
Prolongation of the expiratory phase with wheezing
Crackles which could indicate an infective component

Question 17

When should an exacerbation of COPD be managed in hospital?

Answer 17

Rapid onset of symptoms and/or severe breathlessness
Poor baseline functional status:
Poor level of activity or confined to bed
Unable to cope at home
Receiving long-term oxygen therapy (LTOT)
Presence of comorbidities:
Cardiac disease
Insulin-dependent diabetes mellitus
Findings on physical examination that indicate hypoxia and hypercapnia:
SpO2 < 90% on pulse oximetry
Presence of cyanosis
Worsening peripheral oedema (which could indicate worsening renal hypoxia)
Acute confusion and/or impaired level of consciousness

Question 18

Differential diagnosis for ECOPD

Answer 18

• pneumonia
• PE
• pulmonary oedema

Question 19

How is acute exacerbation of COPD management?

Answer 19

1. provision of respiratory support
   - if there is persistent hypercapnia and respiratory acidosis despite optimal management - need to be started on NIV. (acidosis < 7.35, Hypercapnia pCO2 >6.5, RR > 23)
   mechanical ventilation may be required if there isn’t an improvement in pH in 4 hours of NIV.
2. pharmacological management
   - SABA and or SAMA inhaled/nebulised
   - NICE recommends that IV theophylline may be used if the response is inadequate and levels should be checked 24 hours after commencing treatment
   - steroids - 5 days of pre
   - Abx - should be given if they have all 3 of the major symptoms with increasing sputum purulence being one of them
   Choice of antibiotic - penicillin e.g. amoxicillin, macrolides e.g. clarithromycin and tetracyclines e.g. doxycycline are most commonly prescribed due to their effectiveness against Haemophilus influenzae and Streptococcus pneumoniae

ABG measurements should be taken upon arrival in hospital and repeated after 30-60 minutes.

Question 20

What can be done to prevent exacerbations of COPD?

Answer 20

Smoking cessation
Influenza and pneumococcal vaccination
Pulmonary rehabilitation
Vitamin D supplementation
Long term macrolide (azithromycin)
Mucoregulators - N-acetylcystine and carbocysteine

Augmentation of long-acting bronchodilation with anti-inflammatory therapy
Inhaled corticosteroids - particularly effective with blood eosinophil counts of ≥ 100 cells/µL
Roflumilast (phosphodiesterase-4 inhibitor) - can be used as an alternative to inhaled corticosteroids if blood eosinophil counts < 100 cells/µL or added on to the medication of patients already on a combination of LABA, LAMA and ICS if they have been hospitalised for an exacerbation in the past year

Question 21

What is a pneumothorax?

Answer 21

presence of air within the pleural space , disrupting the negative intrapleural pressure and leading to a partial or complete lung collapse

Question 22

risk factors for pneumothorax?

Answer 22

Risk factors
primary spontaneous pneumothoraces are more prevalent in tall, lean males and are often linked to subpleural bleb rupture
pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
ventilation, including non-invasive ventilation
catamenial pneumothorax is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax

Question 23

what is the classification of pneumothorax?

Answer 23

spontaneous pneumothorax
- primary spontaneous (without any underlying lung disease)
- secondary spontaneous pneumothorax (in patients with pre-existing lung disease)

Traumatic pneumothorax - results from penetrating or blunt chest trauma

Iatrogenic pneumothorax - occurs a complication of medical procedures - such as thoracentesis, central venous catheter, ventilation, lung biopsy

Important clinical entity is tension pneumothorax - results in the displacement of mediastinal structures that may result in severe respiratory distress and haemodynamic collapse.

Question 24

what is a catamenial pneumothorax?

Answer 24

Catamenial pneumothorax is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax.

Question 25

Clinical features of tension pneumothorax?

Answer 25

sudden onset pleuritic chest pain and dyspnea

Clinical examination
diminished breath sounds
Hyper resonance on percussion
decreased chest wall movement on the affected side

Severe cases
hypoxia, tachypnea, tachycardia and hypotension

Tension pneumothorax is a life-threatening condition
- may present with severe respiratory distress, tracheal deviation, jugular venous distension and haemodynamic instability

Question 26

Investigation for Pneumothorax?

Answer 26

CXR in PA and lateral views
if CXR inconclusive - CT chest
Point of care USS

Question 27

Differential diagnosis for pneumothorax ?

Answer 27

Pleural effusion - Physical examination often reveals decreased breath sounds, dullness to percussion and reduced tactile fremitus on the affected side - contrasting with hyperresonance and decreased or absent breath sounds found in pneumothorax.

Pneumonia - typically exhibit systemic symptoms such as fever, malaise and productive cough with purulent sputum, Auscultation may reveal crackles or bronchial breath sounds, unlike the decreased breath sounds observed in pneumothorax.

Acute respiratory distress Syndrome - Patients with ARDS present acutely with severe dyspnoea, hypoxaemia and bilateral infiltrates on chest imaging. The onset is usually within a week of a known clinical insult. In contrast, pneumothorax can occur spontaneously without an apparent trigger and typically shows unilateral lung involvement on imaging.

Question 28

Management of Pneumothorax?

Answer 28

the BTS define minimal symptoms as ‘no significant pain or breathlessness and no physiological compromise’
no or minimal symptoms → conservative care, regardless of pneumothorax size
symptomatic → assess for high-risk characteristics

high-risk characteristics are defined as follows:
haemodynamic compromise (suggesting a tension pneumothorax)
significant hypoxia
bilateral pneumothorax
underlying lung disease
≥ 50 years of age with significant smoking history
haemothorax

if no high-risk characteristics are present, and it is safe to intervene, then there is a choice of intervention:
conservative care
ambulatory device
needle aspiration
if high-risk characteristics are present, and it is safe to intervene → chest drain

Question 29

what is conservative management for pneumothorax?

Answer 29

patients with a primary spontaneous pneumothorax that is managed conservatively should be reviewed every 2-4 days as an outpatient
patients with a secondary spontaneous pneumothorax that is managed conservatively should be monitored as an inpatient
if stable, follow-up in the outpatients department in 2-4 weeks

Question 30

what is ambulatory device for pneumothorax ?

Answer 30

an example of an ambulatory device is the Rocket Pleural Vent
it includes an 8FG catheter mounted on an 18G needle and a pigtail catheter to minimize the risk of occlusion
ambulatory devices typically have a one-way valve and vent to prevent air and fluid return to the pleural space while allowing for controlled escape of air and drainage of fluid
many devices also have an indication diaphragm that signals when the catheter tip enters the pleural space and continues to fluctuate with respiration, aiding in the assessment of pneumothorax resolution

Question 31

How can persistent /recurrent pneumothorax be managed?

Answer 31

If a patient has a persistent air leak or insufficient lung reexpansion despite chest drain insertion, or the patient has recurrent pneumothoraces, then video-assisted thoracoscopic surgery (VATS) should be considered to allow for mechanical/chemical pleurodesis +/- bullectomy.

Question 32

Discharge advice for pneumothorax?

Answer 32

smoking cessation

Not fit to fly - the CAA suggests patients may travel 2 weeks after successful drainage if there is no residual air.
The BTS recommend not fit to fly for 1 week post XR

Scuba diving - permanently avoided unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively