AIR EMBOLISM

An air embolism occurs when there is a rupture in the barrier between the microscopic air space of a lung and its corresponding blood vessel, which carries oxygenated blood back to the heart (where it can be distributed to the body). In effect, bubbles of air are released into the arterial bloodstream, where they act as physical barriers to circulation, and can cause a stroke (see page 144), heart attack (see page 50), headache, and/or confusion. Typically, the victim is a scuba (self-contained underwater breathing apparatus) diver who ascends too rapidly without exhaling, thus allowing overexpansion of the lungs—and rupture of the tissue—as the external water pressure decreases with ascent. In other words, as a diver ascends from the depths, the air in his lungs (which was delivered from the scuba tank through a regulator at a pressure equal to the surrounding water pressure on the lungs, thereby allowing lung expansion) expands. If the rate of exhalation does not keep pace with the lung expansion, the increased pressure within the lungs causes air to be forced through the lung tissue, where it appears in the bloodstream in bubble form and travels directly to the heart. From the heart, the air circulates to and may occlude critical small blood vessels that supply the heart, brain, and spinal cord.

The most common symptoms are unconsciousness, confusion or disorientation, seizures, and/or chest pain immediately on surfacing. Others include dizziness, visual blurring, loss of vision, headache, abnormal personality, confusion, total or partial paralysis, and weakness. Any disorder that appears in a previously normal diver more than 10 minutes after surfacing is probably not due to air embolism.

Anyone suspected of having suffered an air embolism should be placed in a head-down position (with the body at a 15- to 30-degree tilt), turned onto his left side, assisted with breathing if necessary (see page 29), and immediately transported to an emergency facility. If oxygen (see page 431) is available, it should be administered by facemask at a flow rate of 10 liters per minute. The treatment for arterial gas embolism is recompression in a hyperbaric oxygen chamber, which pressurizes the victim’s environment and shrinks the bubbles. This must be accomplished as rapidly as possible to save the victim’s life and to minimize disability. A portable recompression chamber manned by trained personnel may be used to initiate field treatment. If the victim is capable of purposeful swallowing, administer one adult aspirin by mouth.

If the air that expands on ascent does not rupture into a blood vessel and become an air embolism, it can rupture into the actual lung tissues or into the pleural space between the lung and the inside of the chest wall, and cause a collapsed lung (pneumothorax) (see page 41). Other symptoms include air that escapes into the soft tissues, so that there is swelling of the chest and neck, and sometimes a “Rice Krispies” feel to the skin. If the air dissects into the neck, it can cause hoarseness, difficulty swallowing, and sore throat. In this case, oxygen administration is advised. Recompression in a hyperbaric chamber is not advised for a pneumothorax unless there are also severe symptoms associated with an air embolism.

When transporting a victim of air embolism, it is recommended that you use an aircraft that can be pressurized to 1 atmosphere (such as a Lear jet, Hercules C-130, or Cessna Citation), or keep the flight altitude (in an unpressurized aircraft) below 1,000 ft (305 m).

The Divers Alert Network at Duke University Medical Center (919-684-4326 collect or 919-684-8111 toll) provides a 24-hour hotline to assist in the management of all significant diving accidents, as well as evacuation to a facility with a hyperbaric chamber.

DECOMPRESSION SICKNESS (THE “BENDS”)

When a scuba diver descends in the water, nitrogen present in the compressed air he breathes is absorbed into the tissues of his body. This process is analogous to the introduction of carbon dioxide into a beverage for the purpose of carbonation. In the human case, there is a limit to the time and depth that a diver can tolerate before exceeding the amount of nitrogen he can absorb safely without a staged decompression (ascent). If this limit is exceeded, and/or if the diver ascends too rapidly, this nitrogen leaves his tissues and enters his bloodstream in the form of microscopic bubbles (like opening a bottle of soda pop).

The signs and symptoms caused by these bubbles in the body represent decompression sickness, also known as the “bends.” Symptoms may begin immediately after ascent from a dive or may be delayed by a number of hours. These include deep boring joint pain without swelling-warmth-redness, numbness and tingling of the arms and legs, difficulty walking, back pain, fatigue, weakness, inability to control the bladder or bowels (spinal cord “hit”), paralysis, double vision, diminished vision, headache, confusion, dizziness, nausea, vomiting, difficulty in speaking, itching, skin mottling (“marbling”), shortness of breath, cough, and collapse. A rapid, simplified neurologic exam (see page 145), such as administered to a suspected stroke victim, may identify a subtle abnormality.

If you suspect someone of suffering the bends, immediately have him begin to breathe oxygen (at a flow rate of 10 liters per minute by facemask) (see page 431