The lungs are an elastic organ that expand in size with each breath we take. We do not force air into our lungs (positive pressure breathing); our lungs work on a negative pressure system. When we breathe, our muscles expand our chest wall volume. As our chest wall increases in size, it pulls the lungs outward with them. As the lungs expand, the pressure within them drops below atmospheric levels. Air then rushes in from a higher pressure zone (the atmosphere) into our lower pressure lungs. We repeat this process 8 to 15 times per minutes to keep our blood saturated with oxygen and properly balanced with just the right amount of carbon dioxide.
The rigid chest wall not only surrounds and protects the lungs, but it also guides and pulls them apart. A thin layer of fluid sliding between the lungs and inner chest wall serves as a “water seal,” creating a suction effect not unlike a wet dish clinging to a counter top surface. However, when air is introduced underneath the dish, the suction is broken and the dish immediately released. Similarly, when air is introduced into the chest, the suction effect between the lungs and chest wall is broken, and the lungs are released from the chest wall. Since the lungs are elastic, they collapse and either partially or completely stop working since the pressure is no longer changing inside of them every time we breathe.
As we will see, spontaneous lung collapse (pneumothorax) tends to happen to two very different segments of our population.
For reasons that are poorly understood, the healthiest members of our families sometimes develop air pockets called (Emphysema Like Changes or ELCs). These tiny air blisters are found in perfectly healthy, tall, thin, athletically-built young men and women. ELCs sit atop the lungs and sometimes rupture, leaking air into the chest cavity. When this happens, the water seal is broken and the lung collapses. Interestingly, these young athletes rarely complain of shortness of breath. Their other lung functions so well and provides so much reserve capacity that they typically notice fatigue only when they exert themselves. More commonly they present with chest pain, which they experience because the lining of the lung and chest wall are sensitive to separation. Please be aware that for these patients, the lung collapse is only very rarely dangerous or life threatening. However, if the lung is not properly reflated, it can lead to a permanent loss of lung function and exercise capacity. Think of the lungs in these healthy young patients as an expensive high performance sports car…with flat tires. After treatment, the lungs and athletic performance returns completely to normal. Would you trade in a Porsche because of its flat tires? Patients with primary pneumothorax have been followed for more than 10 years after treatment have lung function that is 100% of what is expected of their age and demographic group.
At the other end of the population is a second group of individuals who also experience spontaneous lung collapse. However this group tends to be much older, has an extensive history of smoking, and usually has a history of emphysema as well. In these patients, smoking has destroyed the upper portion of the upper lobes and has caused large air bubbles to form and coalesce. These large bubbles are fragile and can also sometimes rupture and leak air - thus leading to lung collapse. However, unlike the first population of primary pneuomothorax patients, the remaining lung is not normal and healthy. It is emphysematous and usually incapable of supplying all metabolic needs by itself. Therefore, these patients are typically quite short of breath when they are brought into the emergency room. Lung collapse for them is a medical emergency and the expeditious re-inflating of their lung is of paramount importance. Even one presentation of spontaneous lung collapse can be a dramatic life changing event for these patients with diseased and badly injured lungs. Essentially, you could say that spontaneous lung collapse is a manifestation of emphysema and a long term consequence of heavy cigarette use.
For primary pneumothorax patients, treatment for the intial episode can be observation if the lung collapse is quite small. Sometimes the lung is re-inflated with a soft flexible suction tube (chest tube) that is left in place for a day or two. If pneumothorax recurs in the same lung, then statistically the problem is highly likely to continue to recur. After 1 episode, the likelihood of recurrence is between 30-50%. After a second however, the chance of a 3rd episode climbs to 85% if the problem is not dealt with definitively. The Standard of Care is therefore to cause the lungs to adhere to the chest wall and a procedure that accomplishes this is typically offered after the 2nd event. The most successful procedure is a minimally invasive removal of the leaking air blister and a mechanical irritation of the inner chest wall (VATS Wedge resection and mechanical pleurodesis). This procedure is highly efficacious (95% long term success rate), takes 30 minutes, is accomplished with 2 or 3 small incisions, and usually only requires a 2 day hospital stay afterwards. While typically offered for a second episode, sometimes it is offered for an initial presentation in patients with high risk features such as those with dangerous occupations or hobbies such as airline personnel, scuba divers, distant hikers, the medically co-morbid, or those who live far from medical care.
For patients with secondary pneumothorax, the treatment for an initial episode is typically minimally invasive removal of the leaking air bubble (bleb) and a mechanical irritation of the inner chest wall. This is because these patients often present to the emergency Room in extremis, and the excellent safety profile of the procedure far exceeds the risk of another episode of lung collapse in these pulmonary compromised patients. Other alternatives exist for these patients who are sometimes too frail to go to the operating room. For example, talc or doxycycline instillation through a chest tube at bedside can avoid the operating room but typically has a much lower success rate.
The success rate of a VATS wedge resection and mechanical pleurodesis is approximately 95% or better. Therefore we take a patient that may have an expected pneumothorax recurrence rate of 85% or higher…and convert them to a patient with an expected rate of 5% or less. Primary pneumothorax patients can expect to be in the hospital for 2-3 days after the procedure and stay off work for 1 to 2 weeks, depending on their occupation. The chance of a significant complication for primary pneumothorax patient is about 1%. Secondary pneumothorax patients are often in the hospital for 3 to 5 days after the procedure -due to their older age, emphysema, and other medical problems. Their complication rate is approximately 20% due to these issues. The most common problems we see in this population after the procedure are pneumonia and prolonged air leaks but these are usually easily managed with antibiotics and judicious management of the chest tube.