Scuba Diving and Dysbarism

Background and Importance

Underwater free diving has been practiced for more than 5000 years both commercially and for recreation. Diving bells physically provided access to air and protection from pressure at depths to divers and have been described as far back as the 4th century bce . The earliest artificial underwater breathing devices were restrictive to shallow water because of pressure constraints. In the 1940s, Cousteau and Gagnan introduced a self-contained underwater apparatus (SCUBA) and buoyancy control device (BCD), which revolutionized the ability of divers to safely dive to moderate depths. Diving has increased exponentially since that time among commercial, military, and especially recreational activities which now account for approximately 9 million participants per year in the United States alone, with several hundred thousand new divers trained per year. As a result of its recreational popularity, injuries related to diving have also increased. ^, According to the Divers Alert Network (DAN), which is the diving industry’s largest association dedicated to diving safety, there are approximately three injuries of any kind per 100 dives and up to 10% of these are fatal. This represents a small but clinically relevant subpopulation of dives.

The symptoms and signs of diving-related illness, also known as dysbarisms, began to be recognized as diving became increasingly accessible. The ailment became known as caisson disease, named after the large diving bell commonly used for submersion. Construction workers on the Brooklyn Bridge (constructed between 1870–1880) termed the disorder “the bends,” because the symptoms often caused the victim to bend forward in pain. The first clinical description by Bert in 1878 correctly attributed the disease to nitrogen gas coming out of solution in the tissues during decompression, which led to the recommendation of slow ascents for pressurized workers and the development of the first recompression chambers.

Most divers use compressed air, open-circuit scuba equipment at depths of less than 130 feet of seawater (fsw). Systems with artificial mixtures of various gases, however, are used to extend the depths to which divers can descend or the duration that a diver may safely remain submerged. Other variations of supplying air for divers include closed-circuit and semiclosed-circuit diving apparatus (called “rebreathers”) that use calcium hydroxide to absorb expired carbon dioxide and add oxygen to the decarboxylated gas before rebreathing and allow more efficient and safe diving.

Physiology and Pathophysiology

The leading cause of death among divers is from drowning accidents. Scuba divers may also encounter emergencies common to environmental exposures (e.g., hypothermia, sun exposure, motion sickness, bites, envenomation, and physical trauma). They are also subject to the unique injuries related to pressure at depth. The pathophysiologic mechanism of diving or dysbarisms can be separated into two broad categories: (1) Barotrauma which is related to pressure and; (2) Decompression illness which is related to gas bubbles. Barotrauma can be related to the speed of descent and ascent but is almost completely independent of time of depth. Bubble formation (primarily nitrogen) during and immediately after ascent as well as nitrogen narcosis are both dependent on being at depth for an extended period of time. Therefore, it is useful when treating a patient with an acute diving injury to know the recent dive history because it can assist the clinician in narrowing down the differential diagnoses. For instance, a recreational diver who was at a moderate depth for only a few minutes can still have a major barotrauma-related dive injury but would not have had time to accumulate enough gas or nitrogen in their tissues to cause symptoms.

Familiarity with several of the laws of physics that define the properties of liquids and gases ( Table 131.1 ; Figs. 131.1 to 131.5 ) is useful when discussing diving pathophysiology. Boyle’s law explains diver-related barotrauma and states that at constant temperature, the absolute pressure, and the volume of gas are inversely proportional ( PV = k ). In other words, as pressure increases (with descent), the gas volume is reduced; as the pressure is reduced (with ascent), the gas volume increases. A diver needs to descend only 33 feet in seawater to double the atmospheric pressure, an increase of 23 mm Hg per foot of depth. Abrupt changes in the volume of air-containing parts of the body (e.g., ears, sinuses, and lungs) are at risk of barotrauma with the extreme pressure changes of the environment. These include barotrauma associated with an inability to equalize, mask squeeze, or barotrauma to the ears and sinuses during descent, as well as barotrauma related to ascent (usually associated with breath-holding) including pneumomediastinum, pneumothorax, and arterial gas embolism. Fractional changes in volume are greater near where the proportional pressure changes are highest, which is generally in more shallow water.

Henry’s law explains decompression illness and states that the amount of any gas that dissolves in a liquid at a given temperature is directly proportional to the partial pressure of that gas. At higher ambient pressures, an increasing concentration of each component gas of the inhaled air will dissolve in solution until a new steady-state concentration is achieved. Therefore, the length of time the diver is breathing the gas at the increased pressure and the inherent solubility of the gas also govern the quantity of a particular gas that dissolves. The dissolved gas remains in solution as long as the pressure is maintained. As the diver ascends, however, increasingly more of the dissolved gas comes out of solution. A rapid ascent may reduce the pressure at a rate higher than the body can accommodate, and the bubbles (particularly nitrogen) may accumulate and disrupt body tissues and systems, a phenomenon termed decompression sickness (DCS). This is similar to the rapid opening of a bottle of a carbonated beverage which allows bubbles of carbon dioxide to rapidly come out of solution.

Safe diving practice includes a controlled ascent rate (i.e., through the use of safe decompression tables or submersible dive computers), during which the gas is carried to the lung vascular bed and is exhaled before it accumulates to form significantly large or numerous bubbles in the tissues. This is similar to how opening of a soda bottle slowly reduces agitated bubbling of the contained carbonated liquid.

Disorders Related to Descent/Barotrauma

Middle Ear Barotrauma

Middle ear barotrauma (MEBT), also known as barotitis or ear squeeze, is the most common complaint of scuba divers. In a survey of over 750 recreational divers, over half experienced pain related to mild ear barotrauma multiple times during their dives. Most of these were minor pains associated with descent that resolve with equalization maneuvers with no long-term effects.

The middle ear is an air-filled space with solid bone walls except for the tympanic membrane ( Fig. 131.6 ). In the auditory system, the eustachian tube is the only anatomic passage to the external environment. During descent, there is an increase in external pressure that exerts inward pressure against the tympanic membrane (TM). This occurs when the eustachian tube (ET) does not effectively allow air to flow into the middle ear space to equalize pressure. The ET can become blocked and eventually locked in place by a combination of pressure differential and tissue inflammation or edema.

During a diving descent, there is increasing external and inward pressure against the tympanic membrane unless air enters the middle ear via the eustachian tube (ET) to maintain equal pressure across the tympanic membrane. Typically, a diver performs various equalization maneuvers to force air into the middle ear through the ET. The ET may become blocked or collapse related to the pressure differential or inflammation, making subsequent attempts at equalization virtually impossible. This is typically painful and may be associated with tinnitus; some patients develop transient vertigo. Further descent without successful equalization can cause the TM to collapse inward and rupture. The pain may or may not resolve as the TM ruptures. Rupture of TM can cause asymmetric caloric stimulation by exposure of the middle ear to cold water, inducing a transient nystagmus and vertigo. This can become life-threatening if the diver panics or becomes disoriented. The pressure of the water in the middle ear may also lead to a facial palsy in certain individuals where the seventh cranial nerve passes through this space.

Disorders Arising at Depth