Pneumothorax: Clinical practice

The pleura is the blanket that covers our lungs, and it’s made of two layers, the inner visceral pleura and the outer parietal pleura. In between those two layers is a space.

If air gets in that space, it’s called a pneumothorax. Pneumothoraces can be classified into two broad categories: spontaneous or traumatic.

Spontaneous pneumothorax is further subclassified into primary and secondary. A primary spontaneous pneumothorax occurs without a triggering event in an otherwise normal lung.

Most commonly, an individual at risk of primary spontaneous pneumothorax is a tall, thin, young male presenting with symptoms that started at rest.

This is because there are more mechanical shear forces at the apex of the lung, that can make the pleura rupture, especially after for some reason holding their breath like diving or inhaling and holding a recreational drug or medication in their lungs.

Another risk factor for a primary pneumothorax is smoking cigarettes and systemic syndromes like Marfan disease.

Then there’s a secondary pneumothorax; that is a spontaneous pneumothorax that occurs in a lung with pre-existing lung disease, like chronic obstructive pulmonary disease or COPD, asthma, interstitial lung disease, tuberculosis, cystic fibrosis, or lung cancer.

In COPD, destruction of the alveolar sacs leads to formation of large alveolar blebs, which are small balloons that can eventually rupture, leaking air into the pleural space.

Traumatic pneumothorax occurs secondary to injury of the pleura after blunt or penetrating trauma to the chest like a stab wound, or as a complication of a procedure, such as a lung biopsy, thoracentesis, central line insertion, or mechanical ventilation.

Now, any pneumothorax, regardless of how it forms, can potentially become a tension pneumothorax, but it most often happens in a traumatic pneumothorax, which most often occurs due to a punctured lung.

Causes can include a broken rib puncturing through the pleural space, or even after CPR. Tension pneumothorax is when the injured pleura forms a one-way valve, allowing air to go in, but not go out.

This means that with every breath, the pneumothorax gets bigger and bigger. Now, in cases of a tension pneumothorax, it can compress the right atrium of the heart and the vena cavae, decreasing venous return.

This results in decreased cardiac output manifesting as hypotension, altered mental status and an elevation of the jugular venous pressure, and this is typical of obstructive shock.

In fact, because of the external pressure, sometimes the right ventricle can’t move into the pericardial space, so the extra volume pushes the interventricular septum toward the left.

This leads to a reduction in left ventricular diastolic volume, a lower stroke volume, and a drop in systolic blood pressure during inspiration.

A decrease in the systolic pressure of greater than 10 mm mercury is called pulsus paradoxus. Additionally, in a tension pneumothorax, the mediastinum and trachea may be shifted to the contralateral side.

In terms of symptoms, a small pneumothorax may cause no symptoms, but typically a pneumothorax causes a sudden-onset of shortness of breath and unilateral pleuritic chest pain; which is a sharp knife-like pain that worsens with inspiration due to irritation of the parietal pleura by the expanding lung.

It also typically causes tachycardia, tachypnea, or hypoxemia. Examination of the chest reveals decreased air entry or absent breath sounds on auscultation and hyperresonance on percussion of the affected area.

The diagnosis of a pneumothorax is generally confirmed by a chest x-ray, which shows a visible “white” visceral pleural line that’s separated from the parietal pleura by pitch “black” gas.

It’s important to distinguish the pleural line from the border of the scapula on a chest X-ray. Additionally, the normal pulmonary vessel markings that branch from the hilum of the lung suddenly disappear beyond that visceral line.

This is why we obtain these films during expiration, because when the individual breathes out air from their lungs, the lungs will shrink a bit, making it easier to detect even small pneumothoraces.

Additional findings include flattening of the normally convex hemidiaphragm, and deepening of the costophrenic angle, which is the angle between the pleura covering the ribs and the pleura covering the diaphragm.

In secondary spontaneous pneumothorax, other findings of underlying lung disease will be present, such as hyperinflation in COPD.

Now, in a non-tension pneumothorax, you may also see mediastinal shift toward the side of the pneumothorax; while in a tension pneumothorax, mediastinal shift will be away from the pneumothorax.

Now initially, all patients with a spontaneous pneumothorax are put on supplemental oxygen, even if they’re not hypoxemic.

The idea behind this is that the air in both the alveoli and the pneumothorax is mostly composed of nitrogen - about 78%. So by giving oxygen, we make the alveolar air mostly contain oxygen with very little nitrogen.

This increases the nitrogen gradient between the pleural space and alveoli, so nitrogen in the pneumothorax will just diffuse from the pleural space to the alveoli, allowing the individual to essentially breathe most of the air in the pneumothorax right out.

Alright, now the subsequent steps of management depend on the size of the pneumothorax on chest x-ray, and the stability of the symptoms.

Definition of stability must include a respiratory rate lower than 24 breaths per minute, a heart rate between 60 and 120 beats per minute, a normal blood pressure with cutoff values that are not established, room air oxygen saturation higher than 90 percent, and have the ability to speak in whole sentences.