Updated: Nov 04, 2015
  • Author: Joseph Kaplan, MD, MS, FACEP; Chief Editor: Joe Alcock, MD, MS  more...
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Diving as a profession can be traced back more than 5000 years, yet diving-related disease was not described until Paul Bert wrote about caisson disease in 1878. Symptoms of caisson disease were noted among bridge workers after finishing their shifts underwater and coming back to the surface. These symptoms included dizzy spells, difficulty breathing, and sharp pain in the joints or abdomen. The caisson workers often noted that they felt better while working. This was usually attributed to their being rested at the beginning of the shift as opposed to being tired when the workday was through. The workers would often have severe back pain that left them bent over, which is how caisson disease earned the nickname "the bends."

Diving barotrauma can present with various manifestations, from ear, face or mouth pain and headaches to major joint pain, paralysis, coma, and death. As a result of the wide variety of presentations, these disorders must be considered in any patient who has recently been exposed to a significant change in barometric pressure. The three major manifestations of barotrauma include (1) sinus or middle ear effects, (2) decompression sickness (DCS), and (3) arterial gas emboli. There have also been minor sequelae to include isolated nerve involvement and facial baroparesis. [1] Most commonly, the sinuses and middle ear are affected, and this can occur from relatively shallow dives, from deep dives, and in diver’s training.

Barotrauma has also reportedly been caused by an airbag rupturing during deployment, forcing high-pressure gas into a person's lungs. [2] It has also reportedly been associated with rapid ascent in military aircraft and with pressure changes associated with space exploration. Barotrauma has also been reported with both tracheal intubation and fiberoptic endotracheal intubation. Fiberoptic endotracheal intubation requires insufflated oxygen, which increases airway pressure. This leads to alveolar rupture with pneumothorax and subcutaneous emphysema. [3]

The most current research in barotrauma has been dealing with ventilator-associated barotrauma and barotrauma prevention.

Recently, there has been a significant rise in articles dealing with combat-associated barotrauma. These articles deal mainly with blast injury patterns and ballistics. This is an extensive subject and is not covered in this article.



Injuries caused by pressure changes are generally governed by the Boyle and Henry laws of physics.

The Boyle law states, "For any gas at a constant temperature, the volume of the gas will vary inversely with the pressure," or P1 X V1 = P2 X V2. Pressure rises by 1 atmosphere for every 33 ft (10 m) of seawater depth. This means that a balloon (or lungs) containing a volume of 1 cubic foot of gas at 33 ft of seawater depth will have a volume of gas of 2 cubic feet at the surface. If this air is trapped, as occurs when a person holds his or her breath during rapid ascent, it expands with great force against the walls of that space (reverse squeeze). During rapid ascent, incidents of pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can occur. Sinus squeeze occurs with eustachian tube dysfunction, which may result in inner ear hemorrhage, tearing of the labyrinthine membrane, or perilymphatic fistula.

The Henry law states that the solubility of a gas in a liquid is directly proportional to the pressure exerted upon the gas and liquid. Thus, when the cap is removed from a bottle of soda pop, the soda begins to bubble as gas is released from the liquid. In addition, when nitrogen in a diver's air tank dissolves in the diver's fatty tissues or synovial fluids at depth, nitrogen will be released from those tissues as the diver ascends to a lower pressure environment. This occurs slowly and gradually if the diver ascends slowly and gradually, and the nitrogen enters the bloodstream to the lungs and is exhaled. However, should the diver ascend rapidly, nitrogen exits tissues rapidly and forms gas bubbles.

Once bubbles are formed, they can affect tissues in many ways. They can simply obstruct blood vessels leading to ischemic injury. This can be devastating when occurring in critical areas in the brain. The bubbles can also form a surface to which proteins in the bloodstream can cling, unravel, and begin a clotting/inflammatory cascade. This cascade can lead to endothelial breakdown and permanent tissue damage.

Decompression sickness

Decompression sickness (DCS) usually results from the formation of gas bubbles, which can travel to any part of the body, accounting for many disorders. A gas bubble forming in the back or joints can cause localized pain (the bends). In the spinal cord or peripheral nerve tissues, a bubble may cause paresthesias, neurapraxia, or paralysis. A bubble forming in the circulatory system can lead to pulmonary or cerebral gas emboli. [4]

Some gases are more soluble in fats. Nitrogen, for example, is 5 times more soluble in fat than in water. Approximately 40-50% of serious DCS injuries involve the central nervous system (CNS). Women may be at an increased risk of DCS because they have more fat in their bodies. DCS also may occur at high altitudes. Those who dive in mountain lakes or combine diving with subsequent flying are at increased risk as well.

DCS is classified into 2 types. Type I is milder, is not life threatening, and is characterized by pain in the joints and muscles and swelling in the lymph nodes. The most common symptom of DCS is joint pain, which begins mildly and worsens over time and with movement. DCS type II is serious and life threatening. Manifestations may include respiratory, circulatory, and, most commonly, peripheral nerve and/or CNS compromise. [5]

Arterial gas embolism (AGE) is the most dangerous manifestation of DCS type II. AGE occurs after a rapid ascent, when a gas bubble forms in the arterial blood supply and travels to the brain, heart, or lungs. This is immediately life threatening and can occur even after ascent from relatively shallow depths. However, AGE can also occur from iatrogenic causes.

Patients with a patent foramen ovale (up to 30% of the population) are at higher risk of gas passing from a right-to-left shunt and causing CNS injuries. [6, 7]




United States

The average risk of severe (type II) DCS is 2.28 cases per 10,000 dives. The number of minor (type I) injures is not known because many divers do not seek treatment. Risk of DCS is increased in divers with asthma or pulmonary blebs. Risk of DCS type II is increased 2.5 times in patients with a patent foramen ovale. Deaths due to DCS in military aircraft have been reported to occur at a rate of 0.024 per million hours of flight time. [8] Rates of decompression incidents for civilian aviation average about 35 per year, and less than half are significant.


No information is available on the incidence of diving barotrauma worldwide. The Australian defense force has averaged 82 incidents per million hours of flying time.


No significant differences in the incidence of dive-related injuries have been associated with race.


Because of a generally greater percentage of body fat, females have a theoretically higher incidence of barotrauma injuries than males. However, no data support this hypothesis.


Although no direct correlation exists with age and frequency of barotrauma, the most common group affected ranges between 21 and 40 years. However, direct correlation does exist between age and residual effects of barotrauma, which significantly rises after age 50 years. [9]