Dysbaric osteonecrosis

Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen embolism (blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers.[1] Although the definitive pathologic process is poorly understood, there are several hypotheses:

Process

The diagnosis is made by x-ray/MRI appearance and has five juxta-articular classifications and forehead, neck, and shaft classifications indicating early radiological signs.[2]

Early on there is flattening of articular surfaces, thinning of cartilage with osteophyte (spur) formation. In juxta-articular lesions without symptoms, there is dead bone and marrow separated from living bone by a line of dense collagen. Microscopic cysts form, fill with necrotic material and there is massive necrosis with replacement by cancellous bone with collapse of the lesions.

The lesion begins as a random finding on x-ray without symptoms. Symptomatic lesions usually involve joint surfaces and fracture with attempted healing occurs. This process takes place over months to years and eventually causes disabling arthritis, particularly of the femoral head (hip).

The following staging system is sometimes useful when managing lesions.[1]

In a study of bone lesions in 281 compressed air workers done by Walder in 1969, 29% of the lesions were in the humeral head (shoulder), 16% in the femoral head (hip), 40% in the lower end of the femur (lower thigh at the knee) and 15% in the upper tibia (knee below the knee cap).

Worsening of the condition from continued decompression in an asymptomatic x-ray finding may occur.

Prevalence

Dysbaric osteonecrosis is a significant occupational hazard, occurring in 50% of commercial Japanese divers, 65% of Hawaiian fishermen and 16% of commercial and caisson divers in the UK.[3][4] Its relationship to compressed air is strong in that it may follow a single exposure to compressed air, may occur with no history of DCS but is usually associated with significant compressed air exposure.[5] The distribution of lesions differs with the type of exposure - the juxta-articular lesions being more common in caisson workers than in divers.[1][6] There is a definite relationship between length of time exposed to extreme depths and the percentage of divers with bone lesions.[1][7] Evidence does not suggest that dysbaric osteonecrosis is a significant risk in recreational scuba diving.[8]

Treatment

Treatment is difficult, often requiring a joint replacement. Spontaneous improvement occasionally happens and some juxta-articular lesions do not progress to collapse. Other treatments include immobilization and osteotomy of the femur. Cancellous bone grafts are of little help.

Prevention

Prevention is a more successful strategy than treatment. By using the safest decompression table possible, the risk of DON is reduced. Prompt treatment of any symptoms of decompression sickness (DCS) with recompression and hyperbaric oxygen also reduce the risk of subsequent DON.

Prognosis

If the diver has not been exposed to excessive depth and decompression and presents as DON, there may be a predisposition for the condition. Diving should be restricted to shallow depths. Divers who have suffered from DON are at increased risk of future fracture of a juxta-articular lesion during a dive, and may face complications with future joint replacements. Because of the young age of the population normally affected, little data is available regarding joint replacement complications.

There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental or helium diving. Physically stressful diving should probably be restricted, both in sport diving and work diving due to the possibility of unnecessary stress to the joint. Any diving should be less than 40 feet/12 meters. These risks are affected by the degree of disability, and the type of lesion; juxtaarticular or shaft.

References

  1. ↑ 1.0 1.1 1.2 1.3 Brubakk, Alf O; Neuman. Tom S (2003). Bennett and Elliott's physiology and medicine of diving, 5th Rev ed. United States: Saunders Ltd. p. 800. ISBN 0-7020-2571-2.
  2. ↑ Coulthard, A; Pooley, J; Reed J; Walder, D (1996). "Pathophysiology of dysbaric osteonecrosis: a magnetic resonance imaging study". Undersea Hyperbaric Medicine 23 (2): 119–20. ISSN 1066-2936. OCLC 26915585. PMID 8840481. Retrieved 2008-04-26.
  3. ↑ Ohta, Yoshimi; Matsunaga, Hitoshi (Feb 1974). "Bone lesions in divers". Journal of Bone and Joint Surgery (Br) (British Editorial Society of Bone and Joint Surgery) 56B (1): 3–15. Retrieved 2008-04-26.
  4. ↑ Wade, CE; Hayashi, EM; Cashman, TM; Beckman, EL (1978). "Incidence of dysbaric osteonecrosis in Hawaii's diving fishermen". Undersea Biomedical Research 5 (2): 137–47. ISSN 1066-2936. OCLC 26915585. PMID 675879. Retrieved 2008-04-26.
  5. ↑ British Medical Research Council Decompression Sickness Central Registry and Radiological Panel (1981). "Aseptic bone necrosis in commercial divers. A report from the Decompression Sickness Central Registry and Radiological Panel". Lancet 2 (8243): 384–8. PMID 6115158.
  6. ↑ Zhang, LD; Kang, JF; Xue, HL (July 1990). "Distribution of lesions in the head and neck of the humerus and the femur in dysbaric osteonecrosis". Undersea Biomedical Research 17 (4): 353–8. ISSN 0093-5387. OCLC 2068005. PMID 2396333. Retrieved 2008-04-06.
  7. ↑ Cimsit, M; Ilgezdi, S; Cimsit, C; Uzun, G (December 2007). "Dysbaric osteonecrosis in experienced dive masters and instructors". Aviation, Space, and Environmental Medicine 78 (12): 1150–1154. doi:10.3357/ASEM.2109.2007. PMID 18064920. Retrieved 2008-06-06.
  8. ↑ Kenney IJ, Sonksen C (2010). "Dysbaric osteonecrosis in recreational divers: a study using magnetic resonance imaging". Undersea & Hyperbaric Medicine : Journal of the Undersea and Hyperbaric Medical Society, Inc 37 (5): 281–8. PMID 20929185. Retrieved 2012-01-07.

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