Figure 6 Walruses on the Ice Flow

MEDICAL DISORDERS RELATED TO DIVING

AND

THE HYPERBARIC ENVIRONMENT

Mark W. Tuccillo

Eric Johnson

Principle Contributors

Objectives:

Describe the medical disorders that may result from scuba diving, how they are caused, and how they may be prevented.

Some medical considerations and risks are inherent in all water-related activities. The foremost concern is hypoxic asphyxiation or drowning. Other concerns include sunburn, physical trauma, motion sickness, infectious diseases, and allergies

Water has about twenty-five times the heat conductivity of air, and—more importantly—about 3,500 times the volumetric heat capacity of air. (To raise the temperature of a specific volume of water a specific amount requires 3,500 times as much heat as would be required to raise an identical volume of air the same amount.) Because water is usually cooler than body temperature, it conducts heat away from the body, and hypothermia can easily occur. Shipwrecked sailors have become hypothermic and died following immersion in 85ºF (30ºC) water for more than twenty-four hours. Any water temperature below 70ºF (21ºC) poses a significant threat of hypothermia. However, these conditions are not unique to diving and are not addressed in this discussion.

The medical disorders associated with diving are related to the increase in pressure. At a depth of approximately 33 feet in seawater the pressure is twice sea level pressure. (A comparable pressure change in air requires an elevation change of 18,000 feet.) At 100 feet the pressure is four times greater. (In fresh water the pressure doubles at about 34 feet.)

Some disorders are related to the relative rather than the absolute pressure change. (At a depth of 33 feet the pressure has increased 100 percent, but descending from 33 to 100 feet only increases the pressure another 100 percent.) Such disorders typically occur close to the surface where the relative pressure is changing much faster—approximately 25 percent in the first 8 feet; another 20 percent or a total of 50 percent in the next 8 feet.

BAROTRAUMA

Air-filled spaces are most susceptible to injury by pressure changes (barotrauma) and most problems occur during compression, both during diving and descending from terrestrial altitudes. When the external pressure increases as the result of descent, a pressure differential between the air filled structures and the external pressure can develop. Unless the pressure can be equalized, the structural integrity of the air-filled spaces eventually fails. The middle ear, paranasal sinuses, gastrointestinal tract, and the lungs are all susceptible to barotrauma.

The middle ear is separated from the outside world by the thin tympanic membrane or eardrum. The Eustachian tube provides a vent that normally equalizes the pressure across the eardrum. If equalization fails, as little as 2.5 feet of descent below the surface can produce enough of a pressure gradient, 65 mmHg, to cause ear pain. At 4 feet the eustachian tube collapses and equalization is nearly impossible. Rupture of the membrane can occur at between 5 and 17 feet. As water enters the middle ear vertigo can occur and may cause disorientation that could result in drowning.

Yawning or swallowing may open the Eustachian tube and allow the pressure to equalize. However, most divers must achieve equalization with a modified Valsalva maneuver, pinching the nose shut and attempting to exhale.

If attempts to forcefully equalize the middle ear pressure by Valsalva occur once the Eustachian tube is blocked, pressure can be exerted on the middle ear from the inner ear, which can rupture the round or oval windows. Such rupture produces more severe disequilibrium and can result in permanent disability.

Blocking the nasal ostia, usually the result of mucus plugging, tissue congestion, or a mass obstructing the passage, typically is the cause of paranasal sinus barotrauma. The duct to the frontal sinuses is the longest and most tortuous, and most injuries involve those sinuses. Negative pressure (in comparison with the increased external pressure) developing during descent increases edema and may cause blood to collect in the sinus cavity. On ascent, the increased pressure of pressurized air trapped in a sinus cavity causes pain and possibly epistaxis.

Use of decongestants by divers with colds, sinusitis, or similar upper respiratory infections is not recommended. The decongestant may wear off during the dive, and some decongestants contain antihistamines that could lead to diminished alertness. Divers with chronic nasal allergies or other conditions that lead to continuous mucosal edema should consult an otolaryngologist familiar with the effect of scuba diving on such disorders.

Changes in ambient pressure can result in dental pain due to compression when there is a small amount of gas trapped under a filling, crown, or an area of caries. Conversely, gas can diffuse into the same cavity while submerged, resulting in painful expansion of gas pockets during ascent.

Mask squeeze is a form of barotrauma that occurs when the air cavity within a facemask is compressed during descent. If the pressure is not equalized (by simply exhaling into the mask) negative pressure develops because the structure of the mask prevents further compression. The resulting hemorrhages into the skin and he conjunctiva have a gruesome appearance but the medical consequences are of little significance. Small pockets of air that form under a wet suit can cause similar hemorrhages.

Swallowed gas during a dive expands during decompression and could cause stomach rupture if the differential exceeds about 100mm of Hg, the pressure exerted by slightly more than 4 feet of seawater. However, such events are quite rare.

AIR EMBOLISM

During ascent, air in the lung expands. Breath holding during ascent, usually the result of panic by an inexperienced diver, can produce tears in the lung tissues. Hemoptysis and chest pain often result.

Air can be extruded into the mediastinum, producing mediastinal emphysema that is most readily detected outside of a medical facility when the air extends into the neck and produces subcutaneous emphysema with crepitus.

Air can be extruded into the pleural space and produce a pneumothorax.

More significantly air can enter pulmonary veins leading to air embolism. The bubbles follow a path determined by buoyancy and typically localize in the cerebral or coronary circulation, although any vascular bed may be involved.

Symptoms tend to arise from showers of bubbles in a crescendo-decrescendo pattern rather than from a single large bubble. Usually the symptoms are noted during ascent or very shortly after surfacing. Typical features are a rapidly developing stroke-like syndrome ranging from focal deficits to unconsciousness and death. Myocardial ischemia or disrhythmias caused by coronary artery obstruction may dominate the presentation.

Treatment consists of high flow oxygen, hydration, and transfer for hyperbaric therapy as rapidly as possible.

THE GAS LAWS

Understanding the problems with gas mixtures under pressure requires an understanding of the way gases interact with each other, and how they act within the body. Pressure-volume relationships, partial pressures, and solubilities are addressed by Boyle's, Charles', Dalton's, and Henry's Laws.

Boyles Law most directly influences decompression phenomena and bubble formation. At any given temperature, the product of the pressure and the volume of a specific mass of a gas or mixture of gases is constant. If the pressure doubles, the volume halves. The actual diameter of a bubble changes more slowly, decreasing by about one fifth. (The volume of a sphere equals one-sixth pi (p) times the diameter cubed. Reducing the volume of a two-inch sphere by half reduces the diameter to slightly less than 1.6 inches. The diameter of a three-inch sphere would be reduced to approximately 2.5 inches.) Shrinking a bubble requires a lot of pressure.

Charles' Law states that at any given pressure, the product of the temperature and the volume of a specific mass of a gas or mixture of gases is constant. The general gas law conveniently combines these two laws and can be expressed by the formula: P 1 V 1 /T 1 = P 2 V 2 /T 2

Dalton's Law deals with the behavior of a single gas in a mixture of gases. The total pressure exerted by a mixture of gases is the sum of the pressures that would be exerted by each gas if it occupied the total volume by itself.

Henry's Law deals with the movement of a gas into or out of a liquid. The amount of a gas (mass or number of molecules) that dissolves in a liquid at a given temperature is proportional to its partial pressure.

DECOMPRESSION ILLNESS

In order to breathe more than three feet below the surface, the pressure of inspired air must equal the ambient pressure. For each 33 feet of seawater the ambient pressure increases by one atmosphere (760 mmHg or 14.7 lb/in 2 .) A standard two-stage scuba regulator allows a gas mixture to be delivered at an ambient pressure by using the pressure of the water to regulate flow through a series of mechanical levers.

In accordance with the gas laws, the pressure increase decreases the volume so that the product of the two is a constant. The inspiration of this more dense gas mixture causes passive diffusion, first into the blood, then into the tissues, called “on gassing.” The rate of diffusion depends on the surface area of the interface, the pressure gradient caused by the partial pressure of the gas, and the lipid solubility of the individual gas.

Problems arise as the ambient pressure decreases with ascent. The gas that has gone into solution during compression now begins to come out of solution, “off gassing”. If the gas comes out of solution and expands before it reaches the lungs, bubbles form. The gas reacts only with tissue at the bubble's interface, its surface, rather than as individual molecules. Therefore, the molecules can not diffuse from one tissue to another as readily, and local function and circulation is impaired.

The gas that causes decompression sickness is nitrogen, which makes up 78 percent of the atmosphere. It has high lipid solubility in comparison with other inert gases. Fat has relatively poor circulation and on-gassing is slow. But adipose tissue has a great capacity to absorb nitrogen. Once off-gassing begins the poor circulation in fat allows the gas to expand and bubbles to form before the nitrogen can be transported to the lungs.

Physical disruption of tissues, obstruction of blood flow, and triggering the clotting cascade can produce injury.

Where bubbles form determines where the symptoms arise. Decompression illness has traditional been classified by the site affected. Type I produces musculoskeletal, dermal, and constitutional symptoms. Type II produces pulmonary, neurologic, and vestibular symptoms.

Musculoskeletal pain is the classic form of decompression sickness and has been recognized for over one hundred years. From this form the term “bends” arises. A deep aching pain that is poorly localized and often progressive is characteristic. Previously injured sites are predisposed to bubble formation. It occurs within six hours of surfacing 95 percent of the time.

Gas can be absorbed into the sweat glands and pores, and upon decompression, bubbles form in these structures. Pruritis, vasodilatation, and vascular stasis typically occur in the trunk, ears, wrists and hands.

Constitutional symptoms can be very non-specific. Headache and fatigue are common symptoms after diving. That they signify decompression illness is usually determined in retrospect. Subtle changes in personality or neuropsychiatric performance are hard to assess unless base line testing has been done beforehand.

If bubbles form in the central nervous system, an air embolus may be created, impairing circulation to that tissue and causing a CVA.

Divers Alert Network (DAN) found the following incidence of symptoms:

Pain       34.4%

Numbness     21.9%

Dizziness     7.5%

Weakness     6.4%

Headache     5.9%

Extreme Fatigue     4.2%

Nausea       4.2%

Itching       3.6%

If the gas comes out of solution with sufficient vigor it can actually impair circulation through the lungs to such an extent that no effective movement of blood take place throughout the vascular system. The first condition is survivable; the second, known as “The Chokes,” is lethal.

Some bubble formation always takes place. Ascending slowly enough to allow the gas to diffuse out of the tissues before a significant number of gas bubbles are formed prevents decompression sickness. Following prolonged deep dives, decompression stages during ascent are advisable. Such stages consist at stopping at levels ten to twenty feet below the surface for periods of five, ten, or twenty minutes, depending on the depth and duration of the dive. (Additional air tanks may have to be lowered to the level of decompression to allow a diver to remain under water.) Decompression is boring; usually nothing can be seen but the bottom of the boat. Divers occasionally abbreviate or skip decompression stages altogether.

Detailed decompression profiles have been developed to guide ascent based on the depth and duration of the dive. However, the failure rate for the various tables varies from .01 percent to 1 percent. Age, body composition and fitness, and hydration status probably all play a role in developing decompression illness.

Over half of the divers who develop decompression illness have done everything correctly. About one to two divers per 100,000 are affected. Contributing elements are deep dives, repetitive diving, missed decompression dives, and multiple no-decompression dives. Data gathered in 1995 indicated that 85 percent of divers developing decompression illness had made no-decompression dives, 72 percent had gone deeper than 80 feet, 62 percent had made multilevel dives, 61 percent had made repeat dives, and 59 percent had exerted themselves during the dive.

Treatment of decompression illness focuses on speeding the elimination of nitrogen from the tissues and minimizing the number and size of bubbles. Recompression to or beyond previous maximum depth prevents further bubble formation, and shrinks the bubbles that already exist. Oxygen is used to increase the diffusion gradient of nitrogen across the tissues, and speed it's elimination. Risks of toxicity with hyperbaric oxygen are discussed below.

DIVING AND ALTITUDE

Decompression profiles are based on sea level atmospheric pressures. Ascent to higher altitudes, most commonly by flying in transport aircraft, further lowers the atmospheric pressure and increases the tendency for dissolved gases to come out of solution. Similar problems are encountered during dives at high-altitude, fresh-water lakes, such as Lake Titicaca on the border between Peru and Bolivia, which is located at an altitude of 12,500 feet.

Special precautions must be observed in these situations. Waiting for twenty-four hours after diving before flying is widely recommended.

NITROGEN NARCOSIS

Nitrogen narcosis, also known as “Rapture of the Deep,” is the intoxicating effect of nitrogen when inhaled at a high partial pressure. This syndrome is more correctly described as inert gas narcosis. It can be produced by any inert gas. Susceptibility varies with lipid solubility of the individual gas. For nitrogen, symptoms can begin at around three atmospheres of pressure or 100 feet of seawater, but individual susceptibility varies widely. By three hundred feet of seawater incapacitation is almost universal.

Like intoxication with any other substance there is a sense of euphoria, impaired neuromuscular coordination, and errors in judgment. However, subjective improvement may be felt shortly after arrival at depth. Objective testing shows no change, which is strikingly similar to the effects of alcohol ingestion. Individuals may appear to perform in a perfectly normal fashion but have no memory of events. They may acknowledge commands but not act on them. Mistakes, erroneous judgment, or risky behavior may result, and problems are produced by aberrant actions or by inaction. Simply ascending a short distance diminishes the narcotic effects.

OXYGEN TOXICITY

Too little oxygen is obviously incompatible with life. Too much oxygen likewise is not tolerated well. With the increasing popularity of oxygen enriched gas mixtures for both recreational and commercial diving, oxygen toxicity is becoming more common. The body's systems can be overwhelmed by the production of free radicals. The pulmonary and central nervous systems are most readily affected.

Pulmonary toxicity typically takes more time to develop than could be expected during a dive. The fibrosis that occurs in the lungs develops slowly and, at least at first, is reversible. It does not cause acute incapacitation, but gradual loss of vital capacity, lung compliance, and oxygen diffusion. At one atmosphere of oxygen, symptoms can appear after as little as four hours of exposure.

Central nervous system oxygen toxicity is less predictable. It may present with muscle fasciculations, ataxia, unconsciousness, or seizures. Milder symptoms can not be expected to precede the more severe. Only a hyperbaric environment potentially provides enough oxygen to affect the central nervous system. Oxygen becomes potentially toxic to the central nervous system when the partial pressure exceeds 1.6 atmospheres while at rest, and possibly as low as 1.3 atmospheres with exertion.

HIGH PRESSURE NERVOUS SYNDROME

High Pressure Nervous Syndrome is a general excitation of the central nervous system. It is associated with marked tremor, dizziness, nausea, and sometimes vomiting. The onset of HPNS is strongly affected by the rate of compression—the rate of descent. The symptoms are more severe during more rapid compression. Unlike nitrogen narcosis, measurable improvement of symptoms appears with time at depth. This syndrome does not occur at less than 600ft of seawater. For most it is of academic interest only, but the industrial dive community is conducting operations beyond this depth with increasing frequency. The treatment is to add a small amount of nitrogen to the Heli-Ox mixture typically used for deep diving

DIVERS ALERT NETWORK (DAN)

The Divers Alert Network is an institution established at Duke University Medical Center to provide round-the-clock emergency assistance to divers. (Educational programs are also provided, investigational studies are carried out, and other services are maintained.) If any uncertainty exists about the diagnosis or treatment of diving related medical disorders, telephone consultation is always available and should be utilized. DAN also maintains a list of hyperbaric chambers so that the facility nearest the site of a diving emergency can be immediately determined.

The telephone number for consultation about diving emergencies is 919-684-8111. Information about DAN can be obtained by calling 919-684-2948. The DAN Website is http://www.diversalertnetwork.org .

DAN covers all of North America including Canada. DAN International organizations cover Europe, Southern Asia including Japan, and Southern Africa.