Compression Arthralgia and Diving


Called ‘Compression Pains’ in the new U.S. Navy Diving Manual (3- 10.8). it is referred to as compression arthralgia in other texts (Edmonds and Bove). It is the result from increases in external pressure surrounding the body. These pains affect the joints and may occur in almost any diver. They have been experienced in the knees, shoulders, fingers, back, hips, neck, and ribs. Occasionally, severe low back pain or xiphisternal pain may occur (Bove). The pains are often described as deep aching pains, similar to those of Type I decompression sickness. However, the pains may be relatively sudden in onset and initially intense. These pains may be accompanied by “popping” of joints or a dry, “gritty” feeling within the joint.

Symptoms are dependent on depth, rate of compression, and individual susceptibility and usually come on at 200 fsw (60 msw), increasing with depth and aggravated by exercise. While primarily a problem encountered in saturation diving, symptoms may occur as shallow as 100 fsw at rapid compression rates, such as seen in air diving. In deep, helium saturation dives with slower compression rates, symptoms are more commonly seen deeper than 300 fsw. Deeper than 600 fsw, compression pains may occur even at very slow rates of compression. These pains may be severe enough to limit diver activity, travel rate and depths during downward excursions. Improvement is generally noted as time is spent at depth but, on occasion, these pains may last well into the decompression phase of the dive until shallower depths are reached. They can be distinguished from decompression sickness pain because they were present before decompression was started and do not increase in intensity with decreasing depth.

Mechanism of Action

The mechanism of compression pain is unknown, but is thought to result from the sudden increase in tissue gas tension surrounding the joints causing fluid shifts and interfering with joint lubrication. Edmonds describes this as a gas induced osmosis producing cavitation due to a relative imbalance between the inert gas in the blood and that in the synovial fluid and articular cartilage, causing a water shift from the joint to the higher osmolarity blood.


The symptoms usually disappear in reverse order as the diver ascends or decompressed. Unless damaged during the activities at depth, the joint pain disappears, requiring no treatment. If damage occurs at depth from load bearing exercise, then the pains on the surface might be difficult to differentiate from the pain of decompression illness. Recompression would improve DCS pain.


Ernest S. Campbell, M.D., FACS

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