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Preparation for Board Examination
Decompression Accidents I:Pathophysiology
Definition and Classification

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.

  • Gas nuclei serve as a nidus for bubble formation.
  • Tribonucleation is a mechanism of viscous adhesion resulting in gas nuclei due to tissue motion. This is thought to be  a form of mechanical supersaturation from very high pressures causing the bubble formation. This same process causes gas cavities in joints of non-divers (knuckle-cracking). These silent bubbles are also called vacuum phenomenon. Autochthonous (spontaneous) bubble formation has been noted in studies of the spinal cord.
The location of the bubble in the tissues is responsible for the signs and symptoms of DCS. Bubbles in or near a joint thus cause pressure on the pain receptors resulting in the classical "bend". A bubble that obstructs a spinal vessel can lead to immediate pain or paralysis. The mechanical effects of the bubbles then cause a more complex array of events to occur: complement activation, kinin production, platelet activation, white cell adherence and blood sludging. This injury then leads to microvascular injury with extravasation of fluid, proteins and blood due to increased permeability. This is also thought to be associated with free radical injury to the vascular endothelium, similar to a reperfusion injury.
Bubble growth is enhanced the presence of nitrogen and other gases. It is decreased in size by an increase in barometric pressure (Boyle's Law).


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


               Blotchy rash
               Paralysis or weakness
               Coughing spasms
               Staggering or instability


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

  Early Management

  • Immediate oxygen breathing, continue even if person improves markedly
  • CPR, if required
  • Open airway, prevent aspiration, intubate if trained person available
  • Give O2, remove only to open airway or if convulsions ensue.
  • If conscious, give nonalcoholic liquids
  • Place in horizontal, neutral position
  • Restrain convulsing person loosely and resume O2 as soon as airway is open.
  • Protect from excessive cold, heat, water or fumes.
  • Transport to nearest ER for evaluation and stabilization in preparation for removal to the nearest recompression chamber.
  • Call DAN (919-684-9111) or your own preferred emergency number
  • Air evacuation should be at sea level pressure or as low as possible in unpressurized aircraft
  • Contact hyperbaric chamber, send diver's profile with the diver,and send all diving equipment for examination or have it examined locally.
  • Urgent recompression after stabilization in trauma facility
  • Early recompression treatment for all forms of decompression sickness 
Decompression Accidents

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