Although healing is seen histologically, the possibility of resolution of radiologically positive asymptomatic lesions is less clear, although there are occasional reports in the literature. Nevertheless, the treatment of juxta-articular (A) lesions should be based on the finding that DON often progresses through the stages outlined later. One interesting study of the long-term outcome in affected divers who cease hyperbaric exposure after diagnosis suggests a high likelihood of further progression of lesions, and it has been suggested that progress may be unrelated to further diving exposure10. The asymptomatic head, neck and shaft lesions require no active therapy.
Hyperbaric oxygen therapy has been used successfully to treat the early stages of avascular necrosis (Ficat stages 1 and 2 – see the next section), but it is not clear whether DON is likely to respond in the same way.
Surgical treatment of disabling aseptic osteonecrosis must be based on the aetiology and may therefore have a rational basis in DON that is absent in idiopathic disease. Conversely, most surgical experience is with idiopathic osteonecrosis of the femoral head – the site at which osteonecrosis produces the most devastating disability. It is not yet clear whether the same approach will be more or less successful following DON. The type of treatment is determined by the staging of the disease process (as described by Ficat11), the age of the patient and the joints involved.
STAGING (FROM FICAT11)
0 – Asymptomatic, pre-radiological (i.e. high index of suspicion confirmed by raised intramedullary pressure or positive scan).
1 – Symptomatic, pre-radiological.
2 – Symptomatic, radiological pre-destruction.
3 – Collapse of articular surface.
4 – Destruction of joint.
Core decompression has its advocates, but the value of the procedure is still questionable. If accepted, it is indicated for stage 0 to 2. The results are, as expected, better for the earliest stages.
Vascularized fibular graft procedure has been used for stage 0 to 2 disease, mainly that affecting the hip. One comparative study suggests that results are better with this procedure than with core decompression12.
When gross damage to the articular surfaces exists, reconstructive techniques offer the best chance of rehabilitation.
Osteotomy of the femoral neck, either rotation or wedge, endeavours to move the weight-bearing axis away from a localized necrotic area.
Arthrodesis is possible for a young patient, with destruction of one hip only.
Arthroplasty is indicated for ‘end-stage’ joints especially if the patient is old or the disease is bilateral. Total joint replacement has proved useful in replacing severely affected hip and shoulder joints. The concern about this form of surgery is that the life of the prosthesis is unknown because it is used in a relatively young population with a long life expectancy.
Early recompression of experimental limb bends in sheep prevents progression to DON, and this validates the clinical practice of recompression of all cases of DCS to reduce long-term damage.
Early recognition is imperative, and the following investigations are recommended for all professional divers exposed to frequent hyperbaric conditions at depths greater than 15 metres.
Baseline long bone x-ray studies.
MRI examination in doubtful plain x-ray findings or to define extent of lesions.
MRI 3 months after an episode of DCS involving the hips or shoulders.
Image-guided biopsy of suspicious lesions (or even surgical biopsy) may be appropriate in special circumstances.
The disease is rare in recreational scuba divers who follow decompression tables and use only compressed air to depths less than 50 metres. For these groups, unless there is a specific cause for concern, serial radiological investigation is certainly not warranted because of the unnecessary irradiation hazards and expense.
The problem of what to do when confronted with an asymptomatic B lesion is not yet clear. If the B lesion is thought to be provoked by non-adherence to established diving tables, these should clearly be followed in the future. Under these conditions, it is assumed that the B lesion is induced because of excessive provocation. If the diver has adhered to normal decompression tables, then it is presumed that he or she is particularly predisposed to DON, and consideration is given to restricting diving to reduce the risk of further lesions. It is generally accepted that the need for formal decompression staging should be avoided, as should experimental or helium diving. Doubtful cases should be treated as if positive until further radiological assessment clarifies the issue.
If a juxta-articular lesion is present, traditional teaching suggests that all exposure to compression should cease. There is, however, no evidence that this modifies the subsequent course of the problem. Today, a pragmatic approach is more common, with close attention given to the functional capacity of the individual diver along with counselling about avoiding further provocative diving if possible. Annual assessment of these divers will pay close attention to their continued functional capacity.
The value of the plain x-ray examination in early diagnosis is being questioned, and other imaging techniques are being increasingly used. Imaging techniques:
Computed tomography (including single photon emission computed tomography).
Magnetic resonance imaging.
Bone scintigraphy (bone scans)
This investigation had an established role in the early detection of the bony reaction to osteonecrosis, before there are any changes on plain x-ray studies. Use has declined with the greater availability and lower cost of MRI (see later). Any lesion that stimulates bone formation is shown as a ‘hot spot’ by the radioactive bone-seeking tracer, on the scintigram (Figure 14.10). Technetium-99m–labelled methylene diphosphonate (MDP) is the most widely used tracer, but several newer diphosphonate compounds have been introduced that appear to have relatively higher skeletal affinity and may be more sensitive. These agents are injected intravenously, and images taken over time with a gamma camera. Scintigraphy-positive ‘lesions’ can be produced in animals as early as 2 to 3 weeks after decompression and have been shown to involve necrotic bone and osteogenesis at autopsy at 3 months, even though x-ray changes still had not developed in most cases.
Similar findings in humans with biopsy or radiological follow-up indicate that the ‘hot spots’ occur far earlier and are more numerous than the radiological changes. However, these ‘hot spots’ may resolve with no apparent longer-term changes and are therefore insufficient to establish a firm diagnosis. Overall, then, scintigraphy in early lesions is much more sensitive than radiology but has low specificity because any bone reparative reaction will be detected, no matter what the cause is.
Single position emission computed tomography
Single photon emission CT (SPECT) is said to improve specificity, and ‘cold’ areas occurring immediately after occlusion of blood supply may also be detected. Despite its promise, SPECT has not found a routine place in the diagnosis of DON, probably because of the high cost and poor availability of this technology.
CT gives greater definition revealing both structural collapse and areas of new growth. CT scans may help in the diagnosis of early or doubtful changes on plain x-ray films. This imaging technique is essential if some of the surgical techniques, such as rotational osteotomy, are being contemplated.
Magnetic resonance imaging
MRI can detect necrosis of marrow fat within 2 to 4 days of the ischaemic episode and thus offers the best opportunity for early diagnosis. MRI studies may indicate far greater necrosis than conventional plain radiography and can also reveal bone lesions at other sites when a lesion has been detected on plain x-ray films. MRI of the shoulder joint has been suggested as the best surveillance technique for professional divers who are exposed deeper than 15 metres (Figure 14.11). At present, MRI is not routinely used as a screening tool because of the cost of examination.
Invasive investigations have been undertaken to aid in earlier diagnosis and therapeutic intervention. These techniques include arteriography, intraosseous phlebography, intramedullary pressure measurement and core biopsy. The latter three investigations are often combined in a technique described by Ficat in 198511 as functional exploration of bone, but this approach has not been widely adopted.
Two main questions may arise in early or atypical lesions: Is the radiological lesion under examination either a variant of normal bone structure or perhaps a minor dysplasia of bone? Does the osteonecrosis have a cause other than the dysbaric environment?
Early diagnosis is based on minor alterations in the trabecular pattern of bone that result in abnormal densities or lucencies. Early detection of asymptomatic lesions may be verified only by serial radiological examinations, showing the progression of the lesion. Considerable skill is required in these assessments, and this work became the province of highly specialized panels of independent observers. Members compare their independent written reports before coming to a consensus position. In the United Kingdom a central registry for cases and x-ray studies was sponsored by a government body (the Medical Research Council). Lesions are classified as in Table 14.4 (Figures 14.2 through 14.9). This classification is useful to compare results among different studies. For a good review of this area see Williams and associates.
The first decision to make is whether the bone is normal9. Cysts and areas of sclerosis occur sporadically in otherwise normal persons but also in other diseases. Chance cortical bone defects must he eliminated, and the recognition of the normal bone island is essential.
These are dense areas of bone within the cancellous bone structure but that are sharply defined, round or oval, with the long axis running parallel to the long bone. Thought to develop early in life, they have a normal trabecular pattern around them and have no clinical significance.
In our enthusiasm to monitor divers at risk, we must also be aware of the dangers of irradiation – the promotion of malignancy being the most obvious. Even with good equipment and technique, a diver receives one third of the annual maximum recommended dose of body irradiation for one long bone series. Unnecessary irradiation is to be avoided, and readers are advised to seek up-to-date recommendations on the frequency of long bone series in occupational divers. Currently, a common recommendation is a series at employment and then on leaving employment if more than 5 years have elapsed – with the former only required if the latter was not done on leaving the most recent employment. This practice protects both the diver and the employer from misinterpretation of bony changes.
Causes of radiological anomaly that may produce confusion in diagnosis include the following:
Bone islands (see earlier).
Enchondroma and other innocent tumours: These may calcify, causing an osteoclastic appearance in the shaft of the long bone. Medullary osteochondroma may show foci of calcification, which are more circular, whorled and in closer apposition than the foci of calcification of DON.
Normal variants: These include sesamoid bones, the shadow of the linea aspera and its endosteal crest.
Osteoarthritis: Osteoarthritis, not associated with juxta-articular DON, usually causes a reduction of the joint space, with sclerosis of the underlying bone on both sides of the joint. In DON, the cartilage space is not narrowed unless secondary osteoarthritis has occurred.
Other causes of osteonecrosis must be excluded (see Table 14.3). Both the radiological features and medical history are important in establishing the diagnosis. These causes should be rare in a fit, active diving population who have undergone medical assessment (see Chapters 53 and 54). Among the more important are the following:
Trauma: DON has been reported remote from the site of multiple fractures.
Alcohol: A history of heavy consumption or other organ damage may be obtained.
Steroid therapy: The likelihood of osteonecrosis increases with increased dose, the minimum being 10 mg prednisone or its equivalent per day for 30 days. Short courses of high-dose ‘pulse’ therapy have also been incriminated.
Haemoglobinopathies: Sickle-cell anaemia, thalassaemia and other variants may also be causative. Diagnosis is made by haematological investigations and by demonstrating lesions in the spine and skull.
Specific bone necrosis syndromes such as Kienbock’s disease (spontaneous avascular necrosis of the carpal lunate) and Freiberg’s disease (second metatarsal head): The osteochondroses of epiphyseal heads, such as Legg-Calvé-Perthe’s disease (hip) and Kohler’s disease (tarsal scaphoid), have specific age and clinical parameters.
Collagen diseases: Systemic lupus erythematosus and rheumatoid arthritis are associated with a very high incidence of osteonecrosis of the hip, both with and without steroid therapy.
The initial diagnosis of DON must be reasonably certain because it has serious implications for the professional diver. Solitary lesions especially require careful assessment, whereas multiple lesions make the diagnosis easier.
Symptoms and plain x-ray lesions are both relatively late manifestations, with MRI and scintigraphy (the latter now seldom used) both capable of identifying earlier lesions if sought (see later). The first radiological signs may be noted within 3 to 6 months of MRI changes, but they may take much longer – even years. The experienced radiologist looks for an increase in bone density as a result of the reactive changes to the presence of dead tissue, with new bone laid down on the surface of the dead bone.
The pathological lesion may never produce radiological changes. A 10-year radiological follow-up of 15 caisson workers revealed lesions in previously normal areas and worsening of known lesions despite cessation of further hyperbaric exposure10. Autopsy often reveals the pathological areas are far more extensive than the radiological demarcation. Diagnostic radiological parameters include the following:
Juxta-articular lesions (A lesions)
Dense areas with intact cortex (usually humeral head).
Spherical opacities (often segmental in humeral head).
Linear opacities (usually humeral head).
Structural failure showing as translucent subcortical bands (especially in heads of femur and humerus) and often collapse of articular cortex with sequestration.
Secondary degenerative arthritis with osteophyte formation.
There is usually no narrowing of the joint spaces until later stages. These lesions appear to be quite different from those of other causes of avascular necrosis.
Head, neck and shaft lesions (B lesions)
Dense areas, usually multiple and often bilateral, commonly in the neck and proximal shaft of the femur and humerus. These must be distinguished from normal ‘bone islands’.
Irregular calcified areas in the medulla. These are commonly seen in the distal femur, proximal tibia and the proximal humerus. They may be bilateral.
Translucent areas and cysts, best seen in tomograms of the head and neck of the humerus and femur.
Emphasis is on minor variations of trabecular structure, and special radiographic techniques combined with skilled interpretation are required. Cylinder cone and tomography may be used. Computed tomography (CT) or bone scintigraphy may clarify a questionable area.
There may be a history of DCS or repeated inadequate decompression leading to investigation for possible disease. However, a definite connection between the site of DCS and the site of bone lesions has been notoriously difficult to establish. Early lesions are usually completely asymptomatic and may currently be detected only by bone scintigraphy (radioactive isotope scan), magnetic resonance imaging (MRI) or radiological examination. However, there are reports of persistent limb pain, in some cases quite severe, before the development of x-ray changes. Occasional patients have pain in the area of subsequent necrosis dating from the DCS incident. Persistent limb pain may be indicative of a bone compartment syndrome, which may progress to typical DON.
Symptoms of pain and restricted joint movement, usually affecting the hip or shoulder joint, may develop insidiously over months or years and are caused by secondary degenerative osteoarthritic changes.
An increase of 50 per cent in the total mineral content of the bone is necessary before it can be recognized as an area of increased density on the x-ray film, and these changes may take 3 to 6 months from the time of initial insult. MRI and, to a lesser extent, scintigraphy have emerging roles in earlier diagnosis, and reports have even suggested that causative bubbles may be visualized in the fatty marrow7.
X-ray lesions are usually found in the large long bones of the upper and lower limbs. These may be subdivided into juxta-articular (A) or head, neck and shaft (B) lesions.
There are two major sites for the radiological lesions, classified by their prognostic implications. These lesions may be present alone or in combination and are classified as juxta-articular lesions (A lesions) and head, neck and shaft lesions (B lesions).
These are also referred to as joint lesions or A lesions and are potentially disabling. They may eventually result in collapse of the articular surface. The most common sites are the hips and shoulders. The lesions predominate in caisson workers and divers working in undisciplined or experimental conditions. Rare cases have been reported in other joints, e.g. the ankle. It is estimated that about one in five articular lesions will progress to articular surface collapse and up to one in five of these will be treated by arthroplasty or other surgical procedures.
Head, neck and shaft lesions
Lesions away from the articular surface are referred to as medullary or B lesions. They are usually asymptomatic and are seldom of orthopaedic significance. The most common sites are the shafts of the femur and humerus. These lesions do not extend beyond the metaphysis or involve the cortex of the bone. The shaft is not weakened, and pathological fracture is a rare complication. New bone replacement has been observed in these lesions. Their importance lies in that they may demonstrate that people with the lesions are at greater risk of further DON, although this has not been proven statistically.
In assessing the radiological diagnosis of these lesions, it is important to realize that the X-ray will show only a fraction of the total lesion, and that some bone necrosis areas revealed by scintigraphy never become apparent on the x-ray studies.
Symptoms referable to juxta-articular lesions depend on the position and severity of the bone damage. Usually there is pain over the joint. This may be aggravated by movement and may radiate down the limb. There is often some restriction of movement, although a useful range of flexion may remain. In the shoulder, the signs are similar to those of a rotator cuff lesion, i.e. a painful arc from 60 to 180 degrees of abduction with difficulty in maintaining abduction against resistance. Lifting heavy weights may precipitate the onset of pain. Secondary degenerative osteoarthritis follows collapse of the articular cartilage and further reduces joint movement. The site of these lesions is approximately in the ratio of femur to the humerus, 1:2 to 1:3.
Malignant tumours of bone (usually fibrous histiocytoma) have been reported in cases of aseptic necrosis, many of which were asymptomatic. The risk appears greatest with large medullary lesions.
Histologically, the area of necrosis is usually much more widespread than is evident radiologically. Necrosis is first recognized by the absence of osteocytes in the bone lacunae. This probably starts within a few hours of infarction.
Revascularization then commences from areas of viable bone to form an area of vascular granulation tissue that extends into the infarcted area. Necrotic trabeculae are effectively thickened and strengthened by this new growth, and some lesions even disappear. The revascularization may be arrested before all areas of necrosis have been invaded. Continuing formation of new bone forms a zone of thickened trabeculae separated from necrotic bone by a line of dead collagen. This area of increased bone bulk is usually the first detectable radiological sign.
The necrotic trabeculae not strengthened by the revascularization process may eventually collapse under a load. It is at this stage that clinical symptoms, not necessarily temporally related to recent hyperbaric exposure, are noted. With lesions near articular cartilage, there is some flattening of the articular surface, and with further load, stress fractures appear in the subchondral bone. The underlying necrosis causes progressive detachment of the articular surface from its bed. This process resembles that of late segmental collapse, as seen in ischaemic necrosis following fractures of the neck of the femur. Secondary degenerative osteoarthritis often develops in affected joints.
Cases of malignant fibrous histiocytoma, superimposed on DON, may develop in conjunction with the prolonged reparative process set in train by the necrosis.
In terms of clinical pathology, DON is simply one in a long list of causes of aseptic necrosis, but perhaps one of the most fascinating. The most common cause of aseptic necrosis of the femoral head is fracture of the neck of the femur. The necrotic lesions of high-dose steroid therapy, even though multiple and bilateral, often involve the articular surface of the knee and ankle joints, virtually never seen with DON. This variation in distribution suggests that the pathogenesis may be different, even if the pathological features are identical. Osteonecrosis is also frequently reported in association with those diseases in which there is some disturbance of fat metabolism, e.g. diabetes mellitus, pancreatitis, alcoholism and cirrhosis, Gaucher’s disease and hyperlipidaemia. Trauma and steroid administration are the most common associations. Aseptic osteonecrosis may occur without any known risk factors (idiopathic aseptic necrosis). Certain specific isolated-site bone necrosis disorders, such as Legg-Calvé-Perthes disease, may be associated with specific systemic or anatomical abnormalities (Table 14.3).
Table 14.3 Some causes of aseptic necrosis
Decompression sickness or dysbaric exposure.
Trauma (e.g. fractured neck of femur, dislocated hip and unrelated fractures).
Steroids (Cushing’s syndrome and steroid therapy).
Specific bone necrosis disorders (Legg-Calvé-Perthes, Kienbock’s, Freiberg’s and Kohler’s diseases).
It has been postulated that many of these conditions may be associated with fat emboli and these emboli obstruct end arteries in rigid haversian canals of bone, leading to avascular osteonecrosis. These fat emboli may arise from a fatty liver, coalescence of plasma lipoproteins, disruption of bone marrow or other fat tissue or a combination of the foregoing mechanisms. Enhanced coagulability may add to blood vessel obstruction.
The exact mechanism leading to bone necrosis in association with hyperbaric exposure has not been fully elucidated. The most widely held belief is that it results from the decompression phase and represents a delayed or long-term manifestation of DCS (see Chapter 12). There is a definite relationship between DON and exposure to inadequate decompression, experimental diving and clinical DCS.
There are, however, numerous variations on this basic concept. One theory is that the infarction is caused by arterial gas emboli produced during decompression. Certainly, ‘silent’ bubbles can be detected by Doppler techniques during clinically apparently safe decompression schedules. However, several series indicate a relationship with musculoskeletal DCS or total DCS, rather than specifically neurological or serious DCS, and it is the latter that are more likely to be associated with intra-arterial bubbles.
Others propose that the fat in bone marrow takes up large amounts of nitrogen during longer pressure exposures. During or after decompression, gas is liberated from the fat, and expansion with decompression increases intramedullary pressure, thus compromising blood flow within non-compliant bone cavities5. Prompt recompression may prevent later deterioration because there is probably a critical period of bone ischaemia after which pathological changes become irreversible. Osteocytes are known to die after about 4 hours of anoxia. Some affected areas may spontaneously recover, whereas others progress to the typical necrotic lesions.
Bubbles have been found post mortem in the large venous sinusoids in animal experiments with DCS, and they may well have obstructed venous outflow from marrow, leading to areas of infarction. Bubble formation within bony lacunae and subsequent destruction of osteocytes are also possible following decompression.
Changes secondary to intravascular bubbles, whether arterial or venous, such as platelet aggregation and intravascular coagulation, may cause further vascular obstruction (Figure 14.1). Release of fat, thromboplastin and vaso-active substances could also trigger disseminated intravascular coagulation and exacerbate DON2. This model is supported by the post-dive observation of increased platelet adhesiveness and decreased platelet count in volunteers who display higher intravascular bubble counts on Doppler imaging6.
It is possible that a number of factors may combine to produce necrosis in a given situation and that the aetiology is complex and multifactorial. Experimental evidence is available to suggest that both intravascular and extravascular aetiologies are consistent with the bone pathology, but a direct cause-and-effect relationship has not been proven. Asymptomatic or ‘silent’ bubbles during or after decompression are incriminated in those divers who have had neither DCS nor exposure to hazardous diving practices.
All embolism theories (gas, fat or other) do not adequately explain why other tissues do not appear to be embolized and why the femur and upper end of the humerus are particularly affected.
Oxygen toxicity is another possible cause of DON. Several mechanisms have been postulated. One suggests that the local vasospastic reaction to high oxygen pressures leads to ischaemia. High oxygen pressures have been shown to cause swelling of fat cells, which may produce increased intramedullary pressure and ischaemia or, if insufficient to obstruct blood flow completely, could inhibit the clearance of gas from the marrow during decompression. Given the low rates of DON in those who practice oxygen decompression techniques, this seems an unlikely cause of DON.
An osmotic aetiology has also been suggested, incriminating the movement of water into or out of the bone. Rapid pressure changes during compression are associated with large gas gradients because the intravascular partial pressure of all inspired gases is transiently much higher than in the tissues. Thus, a gradient exists across the capillary wall, and water would then move into the vascular compartment. Expansion of the intravascular space within the rigid bone structure may to lead to local bone ischaemia. It has even been suggested that the absolute pressure within the medulla of bone may be transiently lower than that outside the cortex during a rapid compression, and that this alone could promote venous stasis and bone necrosis. It is unclear how this apparent violation of Pascal’s Principle could occur, but such transient differences in pressure have been reported, with no clear explanation.
Dysbaric osteonecrosis is thought to be a long-term effect of inadequate decompression.
Various animal models have been developed to study the aetiology of DON because of the obvious difficulties in early detection and monitoring of such a capricious and chronic disease. Much research thus involves the experimental induction of bone necrosis in animals such as guinea pigs and mice, but it is difficult to be convinced that these lesions are strictly comparable to those of divers and caisson workers. Studies in larger animals such as sheep that have a large fatty marrow compartment in long bones similar to humans have been more successful. These studies in sheep and human post-mortem studies tend to support raised intramedullary pressure combined with hypercoagulability mechanisms.
Any theory must account for the following observations:
Dysbaric osteonecrosis may follow a single exposure to pressure.
Although there appears to be a relationship between DCS and DON, not all divers with DON have a history of DCS.
Not all divers who have DCS develop DON.
Not all divers at high risk develop DON.
The development of effective strategies for prevention and treatment depends on further research elucidating the precise pathophysiological mechanisms involved.
Detailed studies of the incidence of DON were not undertaken until the 1960s. Because the incidence of DON has fallen dramatically since that time, presumably following the advent of strict workplace health and safety rules based on sound decompression practices, most of the clinical and epidemiological work that informs the following discussion dates from the 1970s and 1980s. Figures should be considered cautiously because the radiologists or physicians in each survey may have used different radiological techniques and diagnostic criteria. Other factors influencing the results include the difficulty in obtaining adequate follow-up and the different decompression regimens used.
For example, at the Clyde Tunnel in Glasgow only 241 compressed air workers were surveyed of a total of 1362; 19 per cent of the workers surveyed had lesions, half of which were juxta-articular (next to a joint surface). By 1972, the UK Medical Research Council Decompression Sickness Council Panel had x-ray studies of 1674 workers, of whom 19.7 per cent had positive lesions. Also in 1972, a study by Jones and Behnke on the Bay Area Rapid Transit tunnelling project in San Francisco revealed no clinical or x-ray evidence of necrosis. All prospective workers had pre-employment x-ray studies, and those workers with lesions were excluded. The pressure ranged from 9 to 36 lb/square inch (62 to 248 kPa) gauge, with only one decompression per day. However, the follow-up period was relatively short.
The reported incidence in divers is exceedingly variable, ranging from 2.5 per cent in the US Navy to a doubtful 80 per cent in Chinese commercial divers. Some representative surveys are listed in Table 14.2. The lower incidences are reported in military series and commercial diving operations where strict decompression schedules are adhered to, whereas the incidence is much higher in the self-employed diving fishers of Japan, Hawaii and Australia. The Australian diving fishers undertake relatively deep dives with long bottom times and often inadequate decompression. There is also a higher incidence among divers more than 30 years old, which may reflect increased exposure rather than age itself.
The Medical Research Council Decompression Sickness Central Registry has x-ray studies for nearly 7000 professional divers, and in 1989, Davidson reported there were only 12 cases of subchondral bone collapse, i.e. about 0.2 per cent2. Asymptomatic shaft lesions appeared in about 4 per cent. In 1989, Lowry reported that the prevalence of crippling osteoarthritis leading to total joint replacement had been conservatively estimated at more than 2 per cent in Australian abalone divers1. Most cases in most series involve shaft lesions, which have no long-term significance to health and well-being, except for the rare possibility of malignant change.
Earlier UK studies on professional divers indicated that lesions occurred significantly more commonly among the older men who had longer diving experience and also who had exposures to greater depths. Only 0.4 per cent of the compressed air divers who had never exceeded 50 metres had these lesions. The helium-breathing divers who did not exceed 150 metres had an incidence of 2.7 per cent, which rose to 7.6 per cent if they had been deeper. There was a definite increase in incidence among saturation divers and those with a history of DCS. Approximately one fourth of the lesions were potentially serious, closely associated with joints.
Another UK study of caisson workers, with 2200 subjects, showed an incidence of DON of 17 per cent. The lesions were more often in older men with more exposure to pressure and also correlated significantly with DCS. The incidence rose to 60 per cent for workers who had worked for 15 years in compressed air.
Although rare, several cases have been reported in aviators not exposed to hyperbaric conditions.
Dysbaric osteonecrosis is rare in recreational scuba divers who breathe compressed air at depths of less than 50 metres and who follow the customary decompression tables.
Whether the incidence of bone lesions is related more to the cumulative effects of hyperbaric exposures than to the statistical chance of a single event increasing with multiple exposures is unknown.
The incidence of avascular necrosis of bone, within the general population not exposed to hyperbaric environments, is also not clearly defined.
The disease is rare in sport divers. A few cases (nearly all shoulder disease) have been reported, although it is likely that there are many other unreported sufferers. Gorman and Sandow3 and Wilmhurst and Ross4 published two typical case reports.
Aseptic necrosis of bone has been described in diving lizards (mosasaurs) of the cretaceous period, although the association with human diving may not be entirely germane. In humans, infarction of areas of bone associated with exposure to pressure has been recognized since the turn of the twentieth century. The condition has been reviewed most recently in 20141. Twynam first suggested a causal relationship between bone necrosis and pressure exposure in 1888 in a case report of a caisson worker constructing the Iron Cove Bridge in Sydney, although in retrospect the man appeared to have ‘septic’ necrosis.
In 1912, there were 500 cases of decompression sickness (DCS) reported among the caisson workers on the Elbe tunnel at Hamburg, and 9 had bone changes. Bassoe, in 1913, suggested a relationship between initial joint ‘bends’ and subsequent x-ray evidence of bone atrophy and sclerosis. Taylor, in 1943, noted that several months elapsed between the hyperbaric exposure and the joint symptoms and that shaft lesions are usually asymptomatic. Osteonecrosis has been observed following caisson work at a pressure of 117 kPa (less than 12 metres of sea water equivalent), and also for as short a time as 7 hours, divided into two shifts, at 242 kPa. This disease has gone by many names, but when there is a clear relationship between pressure exposure and the subsequent development of aseptic necrosis, we now use the term ‘dysbaric osteonecrosis’ (DON) (Table 14.1).
DON has been known to develop within 3 months of the presumed causative diving exposure and has occasionally resulted from ‘once only’ exposures. Three of five men who escaped from the submarine Poseidon, in 1931 in the China sea after being at a depth of 38 metres for 2 to 3 hours, subsequently developed osteonecrosis.
The first report of DON in a diver appears to have been by Grutsmacher in the German literature in 1941. The disease affected the shoulder joint. Osteonecrosis affecting hips and shoulders has frequently been reported in commercial diving fishers. It is rare in recreational sport scuba divers.