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Preparation for Board Examination
Decompression Accidents I:Pathophysiology

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On the earth's surface, the human body is exposed to an ambient pressure which is the result of the combined partial pressures of all the gases in the earth's atmosphere. At sea level, the force of this pressure is described as 1 atmosphere absolute (ATA). As a diver descends, exposure to increasing pressure forces more gas to dissolve in the bodily fluids and tissues, as described by natural gas laws. Upon ascent through the water column, the solubility decreases again. Rapid ascent may lead to bubble formation and decompression sickness (DCS) or alveolar rupture ("Pulmonary Overinflation Syndrome" [POIS]), with resultant bubbles in the arterial circulation (arterial gas embolism [AGE]).

DCS, AGE, and all of their presentations are grouped together under the heading "decompression illness" (DCI). Treatment consists of recompression in a chamber using air or a combination of helium-oxygen. Bubbles may form in blood vessels, where they may cause ischemia and infarct, and in tissues, where they may initiate an inflammatory response. Inflammatory changes can lead to extravasation into the tissues, further compromising the circulation and resulting in edema.

Hyperbaric exposures (situations where there are elevated pressures) can occur during construction and tunneling projects, in hyperbaric oxygen treatment facilities and hypobaric exposures in aviation. (The airman is subject to the same problem as divers, except that the situation is reversed--bubbles form on ascent, due to a decrease in pressure and supersaturation. Returning to the ground increases pressure and is analogous to recompression. However, DCS symptoms may occur after returning to the ground and sometimes require additional recompression.)

Recreational scuba diving is the most common type of hyperbaric exposure, especially since the explosive growth of sports scuba (self-contained underwater breathing apparatus) diving in the past decade. Hyperbaric oxygen (HBO) treatment is gaining popularity as the definitive therapy for a growing number of disorders, including decompression sickness, AGE, CO poisoning, clostridial infections, crush injuries, diabetic leg ulcers, skin graft failures, refractory osteomyelitis, thermal burns, necrotizing soft tissue infections, and osteoradionecrosis.

First described in 1841, decompression sickness has gradually become better understood. Sport divers have provided a large body of material to study causing us to be able to learn more about the illness. It's safe to say that DCS is caused by the production of nitrogen bubbles in the circulation, and this is related to the depth and time of a dive and to rate at which the diver ascends from depth. DCS and AGE combined form what is known as "decompression illness".

Called "bends" by early investigators, it is now classically divided into Type I, Type II and biphasic or "Type III" (a phrase coined by Bove and Neumann to describe a combination of DCS and arterial gas embolism). Type I DCS includes cutaneous manifestations and minor joint pain, or "pain only"; Type II includes severe symptoms related to the cardiopulmonary and neurological systems. Type III is a combination of AGE and DCS with neurologic symptoms. Specific organ systems are affected by bubbles and the syndromes are given names; pulmonary DCS is "chokes", skin DCS is 'cutis marmorata', ENT organs are named as 'inner ear DCS'.

Pain syndromes spot the pain in the limbs-not the central skeleton. It is dull, difficult to characterize and localize and is located in the shoulders, elbows and hands in divers. Compressed air workers more often have more pain in their lower extremities. Pain in the central parts of the trunk are generally Type II and are neurological.

It is caused by bubbles, intravascular and extravascular with large gas stores in the fatty bone marrow. This is a cause of dysbaric osteonecrosis.

Neurologic syndromes are increasing in sport divers and the spinal cord is the most commonly
involved site. Symptoms include abdominal, low back, lower extremity pain, weakness and loss of
feeling and function. Cerebral involvement is much more common than previously thought and
may account for a portion of the "spinal cord" lesions. Peripheral nerves can also be involved
causing numbness, limb pains and weakness.

As the surrounding pressure is decreased, nitrogen already in solution is released (as from opening a can of pressurized soda pop) and bubbles form. The actual cause of the bubbles is really not known but there are several camps advancing their theories.

Onset

Type I bends may present within minutes of surfacing or hours later. Pain peaks within 12 to 24 hours, gradually lessening thereafter. Type II decompression accidents usually has it's onset within a few minutes or a few hours of surfacing; most neurologic cases occur within the first hour. The diagnosis should be very simple but is made difficult by diver delay. Any joint pain or neurologic complaint occurring within 24 hours after surfacing should be considered a decompression accident until proven otherwise.

Recognition *Symptoms usually appear 15 minutes to 12 hours after surfacing

  Signs

               Blotchy rash
               Paralysis or weakness
               Coughing spasms
               Staggering or instability
               Unconsciousness

  Symptoms

               Tired feeling
               Itching
               Pain, arms, legs or trunk
               Dizziness
               Numbness, tingling or paralysis
               Chest compression or shortness of breath

  Early Management