| Dysbaric osteonecrosis | |
|---|---|
| Specialty | Diving medicine,occupational medicine  |
Dysbaric osteonecrosis orDON is a form ofavascular necrosis where there is death of a portion of thebone that is thought to be caused bynitrogen (N2)embolism (blockage of theblood 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:
Dysbaric osteonecrosis is associated with exposure to large ambient pressure changes, but the underlying etiology remains uncertain. Dysbaric osteonecrosis is radiologally indistinguishable from similar lesions not associated with pressure changes.[2]
The prevalent hypothesis is that gas bubbles which block the flow of blood are the cause, but there is not always symptomatic decompression sickness recorded in bones where dysbaric osteonecrosis later occurs. It is therefore considered possible that there may be other factors increasing the effects of gas bubbles on the affected bone. It has been suggested that rapid comression may impede intramedullary venous drainage and increase the risk of DO.[2]
Thelesion begins as a localised area ofinfarction, usually without symptoms. Early identification of lesions byradiography is not possible, but over time areas of radiographic opacity develop in association with the damaged bone. Symptomatic lesions usually involve joint surfaces, andfracture where attempted healing occurs. This process takes place over months to years and eventually causes disablingarthritis, particularly of the femoral head (hip).[3]
Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of thefemur and at the proximal end of thehumerus. Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure, andaetiology is uncertain.[3]
Thediagnosis is made byx-ray/MRI appearance and has five juxta-articular classifications and forehead, neck, and shaft classifications indicating earlyradiological signs.[4]
Early on there is flattening of articular surfaces, thinning ofcartilage withosteophyte (spur) formation. In juxta-articular lesions withoutsymptoms, there is dead bone and marrow separated from living bone by a line of dense collagen. Microscopiccysts form, fill withnecrotic material and there is massive necrosis with replacement bycancellous bone with collapse of the lesions.[clarification needed]
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,[clarification needed] 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).
It is possible that the condition can worsen even after the initial diagnostic x-ray shows no symptoms, given continued exposure to decompression.
Prevention is a more successful strategy than treatment. By using the most conservative decompression schedule reasonably practicable, and by minimizing the number of major decompression exposures, the risk of DON may be reduced.[citation needed] Prompt treatment of any symptoms ofdecompression sickness (DCS) with recompression andhyperbaric oxygen also reduce the risk of subsequent DON.[citation needed]
Treatment is difficult, often requiring a joint replacement.[citation needed] Spontaneous improvement occasionally happens and some juxta-articular lesions do not progress to collapse.[citation needed] Other treatments include immobilization and osteotomy of thefemur.[citation needed] Cancellous bone grafts are of little help.[citation needed]
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.[citation needed] 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.[citation needed] Because of the young age of the population normally affected, little data is available regarding joint replacement complications.[citation needed]
There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental orhelium diving.[citation needed] 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.[citation needed] These risks are affected by the degree of disability and by the type of lesion (juxta-articular or shaft).
Dysbaric osteonecrosis is a significant occupational hazard, occurring in 50% of commercial Japanese divers, 65% of Hawaiian diving fishermen and 16% of commercial and caisson divers in the UK.[5][6]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.[7] The distribution of lesions differs with the type of exposure - the juxta-articular lesions being more common in caisson workers than in divers.[1][8]There is a definite relationship between length of time exposed to extreme depths and the percentage of divers with bone lesions.[1][9] Evidence does not suggest that dysbaric osteonecrosis is a significant risk in recreational scuba diving.[10]
