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CO2 Soda Bubbles
CO2 Soda Bubbles

Before English chemist, William Henry, took his own life in 1836, he discovered a simple physics law to explain how gas behaves in solution. This gas law, now appropriately known as Henry’s Law, together with Boyle’s Law, form the basis of the pathophysiology and treatment for Decompression Illness. Henry’s Law states that the amount of a particular gas dissolved in solution is proportional to the partial pressure of that gas over the solution. A common, everyday example of this scientific law in action occurs every time you open a carbonated beverage.  Anglo-Irish chemist, Robert Boyle, published the gas law bearing his name in 1662, when he explained the inverse relationship between the volume and pressure of gases at a constant temperature. Simply put, gas expands (volume increases) as pressure diminishes. An everyday example of this scientific principle occurs every time you feel your ears pop upon changing altitudes in an airplane.

Although somewhat dated, this historical video produced by the U.S. Navy is entertaining as a tribute to cinematography from an era of distant past, yet also remains informative on the topic it addresses.

Most people know that SCUBA divers are at risk for developing ‘the bends’.  Although considerably less frequent than divers, high-altitude aviators and astronauts are also at risk for this serious medical condition. The bends are actually one variant of a medical syndrome known as Decompression Sickness (not to be confused with Decompression Illness). Decompression Illness (DCI) is a comprehensive term that captures all medical conditions that may occur when living organisms are exposed to hypobaric changes (going from higher to lower ambient pressure). DCI is routinely divided into two separate conditions that differ by respective pathophysiology- Decompression Sickness (DCS) and Arterial Gas Embolism (AGE). DCS occurs when a person is rapidly exposed to hypobaric changes causing inert gases (usually nitrogen) previously dissolved in the blood to come out of solution into their gaseous state as bubbles. This occurs in accordance with Henry’s Law as stated above. AGE is also due to the effects of bubbles in the vasculature, but the mechanism for their formation differs. In AGE, gas bubbles are introduced to the body suddenly, usually by pulmonary barotrauma (rupture of lung tissue) when lung alveoli expand to the point of failure and release gases directly into pulmonary arteries. This proceeds in accordance with Boyle’s Law, also stated above. This most commonly occurs when a diver holds their breath during ascent or when an aircraft experiences rapid decompression, though other causes do exist. AGE will be covered in detail by a separate post at a later time.

Cutis Marmorata
Cutis Marmorata

Decompression Sickness was initially categorized as either Type I (less severe) or Type II (more severe). Although the US Navy continues to use the Type I/Type II classification in it’s Dive Manual, this annotation has generally been supplanted by a simple description of the organ effects and symptom constellation caused by intravascular bubbles. The four basic varieties based on effected organ systems, followed by the respective common eponym are:

1. Cutaneous (Skin) – Creeps
2. Arthopathy (Joint) – Bends
3. Cardiopulmonary (Heart/Lungs) – Chokes
4. Neurologic (Brain/Spinal Cord) – Staggers

A SCUBA diver rapidly ascending from a dive continually experiences less external pressure as the volume of water molecules surrounding their body decreases. Similarly, a pilot experiencing a sudden loss of cabin pressure is suddenly thrust into an environment at the altitude of the aircraft, which is likely to be a significant decrease in surrounding ambient pressure. Once a person is exposed to a much greater hypobaric environment, bubbles that were previous dissolved in liquid may supersaturate and enlarge through either coalescence or the effects of Boyle’s Law. Bubbles in the blood vessels act as emboli, traveling to end organs where they are thought to cause mechanical effects, ischemia, and immmune-mediated inflammatory responses. The various symptoms caused depend on the end organs affected and will usually present in one or several of the above categories. The chokes and staggers are the most serious presentations and in the worst case may even be life-threatening.

It is important to note the manifestations of DCI in divers cannot be assumed to be identical to that of fliers. For the purposes of this post, the remainder of content will refer only to DCI as it applies to aviation. For fliers, risk of developing DCS is directly tied to the absolute altitude achieved. Even the best cabin pressurization systems have limits and at some point, cabin pressure cannot maintain a low enough ambient pressure to necessarily prevent DCS. Most airplanes attempt to maintain a cabin pressure of no more than 8,000 feet (2438 m). Although pressurization systems will differ based on whether they are low or high-differential systems, most aircraft can sustain cabin pressures in a safe range as long as they fly below 40,000 feet (12,192 m). A later post will cover cabin pressure systems in greater detail. Although there is no ‘safe’ altitude, it is highly unlikely that an aviator will experience DCS without a hypobaric exposure equivalent to 18,000 feet (5,486 m) or greater. This fact places a much higher DCS risk on high-altitude military pilots and astronauts, which is why these unique aviators must wear fully or partially pressurized suits. Other factors that increase one’s risk of developing DCS are duration of exposure, level of activity at exposure, presence of a patent foramen ovale (PFO), and previous exposure to either altitude or hyperbaric (diving) environments.

In the vast majority of DCS cases associated with aviation, symptoms will completely resolve upon descent. There are times, however, when symptoms persist at O AGL. In rare cases, symptoms will not be present until hours after landing. Almost all of these cases will present within the first 24 hours. If symptoms suggestive of DCS persist or arise in a person with a recent (previous 24 hours) exposure, treatment will depend on the severity of the symptoms. The mainstay of treatment for Decompression Sickness is 100% oxygen and hyperbaric therapy. In some mild cases, 100% ground oxygen treatment (GLO) will resolve all symptoms through denitrogenating (replacement of excess nitrogen in the body) the blood and tissues. More commonly, a patient with symptoms suggestive of DCS will be transported to a hyperbaric chamber for oxygen therapy under hyperbaric conditions.  Although there do exist competing hyperbaric treatment tables, the vast majority of Hyperbaricist Physicians (specialty focusing on hyperbaric medicine) uses the US Navy Treatment Tables 5, 6 and more rarely 7, developed by Goodman & Workman in 1965 and adopted by the US Navy in 1967. Of note, hyperbaric medicine has demonstrated effectiveness for wound care treatment  and also claims to treat many other diseases and medical conditions, though with less scientific validity.

Hyperbaric Chamber
Hyperbaric Chamber

Lastly, the flight medicine doctor needs to determine how a case of DCS may affect a flyer’s ability to fly in the future. This decision may have strict guidance to follow for a military flight surgeon or may require a clinical decision based on persistent symptoms for the civilian Aviation Medical Examiner.

Regardless, flying after diving should always be discouraged by both flight medicine and dive medicine physicians as participating in these two activities within 24 hours significantly increases one’s risk for developing DCI.


1. Fundamentals of Aerospace Medicine (Ed. 4) by Jeffrey R. Davis (Editor), Robert Johnson (Editor), Jan Stepanek (Editor), Jennifer A. Fogarty (Editor).