Pneumothorax refers to the accumulation of air within the pleural space.
🦴 Anatomy
Our pleurae are serous membranes (mesothelial tissue lining internal cavities of the body and are lubricated by serous fluid) similar to the pericardium and peritoneum. They allow for efficient and effortless respiration.
They are made of 2 layers:
- Parietal pleura - the outer layer that lines the thoracic cavity. Detects pain (well localised), pressure and temperature as it is innervated by the phrenic and intercostal nerves.
- Visceral pleura - the inner layer that covers the lungs. Detects stretch and receives innervation from the pulmonary plexus.
These 2 layers are continuous and converge at the hilum of the lung.
The pleural cavity is the “potential space” between these 2 layers. It contains serous fluid which lubricates the pleurae to allow them to slide over each other. It also creates surface tension that ensures the 2 pleural layers pull together. This means that when the thoracic cavity expands, the parietal pleura will pull with it. This surface tension pulls the visceral pleura which is connected to the lung and therefore also pulls the lungs with it, allowing it to expand and fill with air. However, if air fills the pleural cavity then this surface tension is lost (i.e. a pneumothorax).
Pathophysiology
Let’s recap some of our pressures:
- Atmospheric pressure - 760mmHg.
- Intrapulmonary (intraalveolar) pressure - 760mmHg.
- Intrapleural pressure - 756mmHg
- Transpulmonary pressure - 760mmHg - 756mmHg = 4mmHg.
Normally the pressure in our lungs is equal to the atmospheric pressure and greater than our intrapleural pressure. If transpulmonary pressure = 0 then this means either that the lungs are removed from the chest or we have a pneumothorax.
An absent transpulmonary pressure means that the lungs collapse due to elastic recoil.
Let’s do a quick recap of our ventilation mechanics:
- Inhalation - diaphragm contraction causes the thoracic cavity to increase its volume, causing a decrease in intrapulmonary/intraalveolar pressure below that of atmospheric pressure. This causes the flow of air across the pressure gradient, allowing air into the lungs.
- Expiration - diaphragmatic and elastic recoil of our alveoli decreases intraalveolar and intrathoracic pressure above that of atmospheric pressure. This then causes a subsequent push of air out of the lungs.
However, if a communication between the pleural space and the atmosphere (compromised parietal pleura) or between the pleural space and the alveoli (compromised visceral pleura). This will allow the flow of gases from the higher intrapulmonary pressure or atmospheric pressure into the lower intrapleural pressure → a pneumothorax. This flow will continue until there is no pressure gradient (transpulmonary pressure of 0mmHg) or until the communication is sealed.
The more air entering the pleural space, the more difficult it is to inflate the lungs as there is a lack of space. This then causes our lungs to collapse, which is known as atelectasis.
🔢 Classification
We can classify pneumothorax into 4 types (TITS):
- Traumatic pneumothorax
- Iatrogenic pneumothorax
- Tension pneumothorax
- Spontaneous pneumothorax
- Primary spontaneous pneumothorax
- Secondary spontaneous pneumothorax
Spontaneous pneumothorax
As implied by the name, this is a pneumothorax that occurs without precipitating factors/trauma. There are 2 subtypes:
- Primary spontaneous pneumothorax (PSP) - a spontaneous PT occurring without any apparent pulmonary disease.
- Secondary spontaneous pneumothorax (SSP) - a spontaneous PT occurring due to a complication of pulmonary disease such as in emphysema when we have a ruptured bullae, or in asthma, TB, cystic fibrosis, cancer, thoracic endometriosis. It tends to be more severe than PSP.
Traumatic pneumothorax
This is due to blunt or penetrating trauma that causes air to enter the pleural cavity. Air will enter into the pleural cavity on inspiration and will exit on expiration.
It too can be subdivided into either open or closed.
- Open pneumothorax - if the parietal pleura is compromised and there is a break in the chest wall.
- Closed pneumothorax - the chest wall remains intact but the visceral pleura is compromised. This is due to a break in the alveoli of the lungs.
The causes of traumatic pneumothoraces include:
- Stabbings
- Mechanical ventilation and non-invasive ventilation
- Accidents
- Rib fractures
Iatrogenic pneumothorax
This is a pneumothorax that occurs due to medical interventions such as lung biopsy, thoracocentesis, mechanical ventilation with high positive end-expiratory pressure (PEEP), bronchoscopy.
Tension pneumothorax
This is a PT in which the intrapleural pressure exceeds atmospheric pressure as air is able to enter the pleural space on inspiration but is unable to exit as there is essentially a one-way valve that allows air in but doesn’t allow air out as the parenchyma creates a flap that closes when air tries to leave. Thus pressure continues to build up. It is a life-threatening condition as the pressure causes compression of the lungs, heart, major vessels and trachea → cardiovascular collapse → cardiac arrest.
A tension pneumothorax can develop with any type of PT, but mostly in traumatic chest injury or in those using mechanical ventilation.
⚠️ Risk factors
Primary spontaneous pneumothorax
- Smoking
- Tall height
- Thin body habitus
- Pregnancy
- Connective tissue disorders
- Familial PT
Tension pneumothorax
- Spontaneous PT
- NIV or mechanical ventilation
- Truama
- Lung disease
- Chest drain blockage
Secondary spontaneous pneumothorax
- COPD
- Asthma
- HIV with pneumocystis pneumonia
- TB
- Cystic fibrosis
- Severe ARDS
- Lung cancer
- Sarcoidiosis
- Thoracic endometriosis
- Pulmonary fibrosis
Traumatic pneumothorax
- Penetrating injury
- Blunt injury
😷 Presentation
There is a range of presentations from asymptomatic, all the way to haemodynamic instability.
Symptoms include:
- Dyspnoea and shortness of breath
- Ipsilateral pleuritic chest pain -
- Sweating
Some signs we may see include…
- Tachypnoea
- Tachycardia
- Reduced breath sounds ipsilaterally
- Hyperinflation and hyper-resonance on the affected side
- Hypoxia - a late sign mainly seen in tension PT.
- Asymmetry - with tension PT especially.
- Decreased vocal fremitus on auscultation.
- Subcutaneous emphysema
- P - Pleuritic chest pain
- T - Tracheal deviation
- H -Hyperresonance
- O - Onset sudden
- R - Reduced breath sounds and dyspnoea
- A - Absent fremitus
- X - X-ray shows collapse
🔍 Investigations
- 🥇🏆 CXR is first-line and the gold standard.
There are some things we can look for specifically to identify a pneumothorax, such as:
- Visible pleural edge - seen as a thin sharp white line with no lung markings peripheral to the line.
- Radiolucent peripheral space when compared to the other lung
- Collapsed lung
- Mediastinal shift
- Pneumomediastinum or subcutaneous emphysema may be present
- Hyperinflation
- Clotting profile - an INR <1.5 is needed before inserting a chest drain (management of pneumothorax).
🧰 Management
The management is dependant on the size of the rim of air present:
- <2cm rim of air:
- Discharge after observation (4-6 hours)
- Supplemental oxygen - aiming to keep SpO2 > 94% or 88-92% in CO2 retainers.
- >2cm rim of air:
- Decompression (percutaneous aspiration) - this is done with a 16-18G cannula, aspirating less than 2.5L.
- If unsuccessful → chest drain + admission.
- <1cm rim of air (small pneumothorax):
- Observation
- High-flow oxygen - unless there is a risk of CO2 retention as seen in type 2 respiratory failure.
- Admission to hospital
- 1-2cm rim of air (medium pneumothorax):
- Decompression
- If unsuccessful → chest drain + admission.
- High-flow oxygen
- >2cm rim of air (large pneumothorax) or patient is >50 years old:
- Chest drain - clotting abnormalities (such as an INR >1.5 or platelets <50 x 109/L) need to be corrected in the critically unwell.
- Hospital admission
The majority will resolve with observation but sometimes aspiration decompression may be needed. If the patient is ventilated or in some cases of severe COPD, a chest drain will be used.
- High-flow oxygen
- Observation
- Referral to thoracic surgery
We should not:
- Aspirate the traumatic pneumothorax.
- Leave the patient unattended as a tension pneumothorax may develop.
- Immediate decompression
- Supplemental oxygen
- Chest drain - immediately after decompression.
- Open thoracotomy - if the tension pneumothorax is secondary to trauma and if the expertise is available.
Base - 5th ICS
Posterior border - lateral edge of lat. dorsi.
Anterior border - lateral edge of pec. major.
Superior border - base of axilla.
A 14 or 16 gauge cannula is inserted into 1 of 2 sites:
- 2nd ICS MCL
- 4th/5th ICS MAL - if unsuccessful or if the patient has large amounts of fat/tissue.
- 🚭 Smoking - patients should avoid smoking to reduce risk of recurrence. The lifetime risk in healthy smokers is about 10% while in healthy non-smokers the risk Is 0.1%.
- 🛫 Flying - flying is an absolute contraindication according to the British Thoracic Society. Air travel should be avoided for at least 1 week post resolution on CXR.
- 🤿 Scuba diving - the British Thoracic Society states that scuba diving should be permanently avoided unless bilateral surgical pleurectomy has been performed and the patient has normal lung function and a normal chest CT post-operatively.