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Dysbarism refers to medical conditions resulting from changes in ambient pressure. Various activities are associated with pressure changes. Scuba diving is the most frequently cited example, but pressure changes also affect people who work in pressurized environments (e.g. caisson workers), and people who move between different altitudes. more...

Dandy-Walker syndrome
Darier's disease
Demyelinating disease
Dengue fever
Dental fluorosis
Dentinogenesis imperfecta
Depersonalization disorder
Dermatitis herpetiformis
Dermatographic urticaria
Desmoplastic small round...
Diabetes insipidus
Diabetes mellitus
Diabetes, insulin dependent
Diabetic angiopathy
Diabetic nephropathy
Diabetic neuropathy
Diamond Blackfan disease
Diastrophic dysplasia
Dibasic aminoaciduria 2
DiGeorge syndrome
Dilated cardiomyopathy
Dissociative amnesia
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Double outlet right...
Downs Syndrome
Duane syndrome
Dubin-Johnson syndrome
Dubowitz syndrome
Duchenne muscular dystrophy
Dupuytren's contracture
Dyskeratosis congenita
Dysplastic nevus syndrome

Ambient pressure

Ambient pressure is the pressure in the water around the diver (or the air, with caisson workers etc). As a diver descends, the ambient pressure increases. At 10 meters (33 feet) in salt water, it is twice the normal pressure on land at sea level. At 40 meters (the recommended safety limit for recreational diving) it is 5 times the pressure at sea level.

Pressure decreases as we rise above sea level, but less dramatically. At 3000 feet altitude (almost 1000 meters), the ambient pressure is almost 90% of sea level pressure. Ambient pressure does not drop to 50% of seal level pressure until 20,000 feet or 6,000 meters altitude.

Effects of pressure on the body

Direct effects on tissues

This is not of practical importance, because the body is mostly composed of barely-compressible materials such as water. People often wonder whether scuba divers feel their body being crushed by the pressure. The answer is no. Divers would have to reach depths of thousands of feet before their flesh began to suffer significant compression.

Air spaces

Air is very compressible. Humans have many air spaces: sinuses, middle ears, gas in our bowels, cavities in our teeth, and largest of all, our lungs. On land in our daily lives, the pressure in our air spaces is usually exactly the same as the pressure outside, because our air spaces are connected to the outside world. If there was a pressure difference between the outside world and one of our air spaces, then we experience painful pressure on the walls of that air space, as air “tries” to get from the higher-pressure side to the lower-pressure side. This is why we sometimes get painful ears on air trips.

Dissolved gas

A percentage of the gas we breathe (air) is always dissolved in our blood, like the gas dissolved in a soda bottle with the lid on. If we move to a higher ambient pressure, then the gas we breathe is at a higher pressure, and more of it dissolves in our blood and body tissues. If we move back to a lower pressure, and we move slowly, then the extra gas comes out slowly until we are back to our normal amount of dissolved gas. But if we move quickly to a lower ambient pressure, then the gas comes out of our blood and tissues violently, in large bubbles, like to the difference between slowly opening a bottle of soda (dropping the pressure in the bottle slowly down to sea level), versus ripping the cap off quickly.

Types of dysbarism

Different types of illness result from increases in pressure (e.g. descent during a SCUBA dive, descent during a plane flight), versus decreases in pressure (e.g. coming up from a caisson, or ascending a mountain). Dysbarism comprises several types of illness:


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Early lesions of the labrum and acetabular cartilage in osteonecrosis of the femoral head
From Journal of Bone and Joint Surgery, 1/1/02 by Kloen, P

Osteonecrosis of the femoral head can be caused by a variety of disorders and affects the relatively

young patient. Most studies have concentrated on the femoral changes; the sites of early lesions of the labrum and acetabular cartilage have not been recorded. We studied 17 hips with osteonecrosis and a wide congruent joint space on radiographs and by direct inspection of the femoral head, labrum and acetabular cartilage during surgery. All of the femoral heads had some anterosuperior flattening which reduced the head-neck ratio in this area. A consistent pattern of damage to the labrum and the acetabular cartilage was seen in all hips. Intraoperatively, impingement and the cam-effect with its spatial correlation with lesions of the labrum and acetabular cartilage were observed. These findings could be helpful when undertaking conservative surgery for osteonecrosis, since the recognition of early radiologically undetectable acetabular lesions may require modification of the surgical technique.

J Bone Joint Surg [Br] 2002;84-B:66-9.

Received 15 February 2001; Accepted after revision 11 July 2001

Many aspects of the aetiology, pathogenesis, natural history and treatment of osteonecrosis of the femoral head remain controversial. 1-5 It is a disease which affects the relatively young patient. A multitude of aetiological factors has been described including alcohol abuse, corticosteroids, triglycerides, systemic lupus erythematosus (SLE), trauma, infection, dysbarism and the haemoglobinopathies. The underlying lesion is characterised by necrosis of bone with subsequent deformation of the involved part of the femoral head, leading to a stiff painful hip.

There are many classifications such as those of Ficat,6 Marcus, Enneking and Massam,7 Steinberg, Hayken and Steinbergs and the ARCO.9 The most commonly used is that of Ficat (Table I) in which the stages range from the silent hip (stage 0) to secondary degeneration (stage IV).

The disease primarily affects the anterosuperior portion of the femoral head, and although progressive deformation will lead to incongruency of the joint with consequent acetabular involvement, it has not been noted as to when and where this initially develops. We have therefore documented the presence and site of early acetabular lesions in a group of patients with osteonecrosis in whom plain radiography still showed a well-preserved joint space and who were thus candidates for conservative surgery, such as revascularisation (stage II) or femoral osteotomy (stage III).5,7,10-14

Patients and Methods

We have studied 17 hips in 14 patients (four women, ten men). Their mean age at the time of surgery was 29 years (14 to 46). They were screened for risk factors for osteonecrosis. The radiological classification was undertaken according to Ficat6 (Table I) with anteroposterior (AP) and false-profile and contour views.15 Preoperative evaluation included recording the Kerboul angle12 which consists of the added arcs of surface involvement on AP and lateral radiographs. The surgical approach was by a Gibson (7 hips) or Kocher-Langenbeck (10 his) incision with an osteotomy of the greater trochanter.16 Anterior subluxation or dislocation was carried out to inspect the joint in the course of conservative surgery and to determine more easily the direction and extent of the intertrochanteric osteotomy (ITO) which would be required in order to transfer the load from the affected part of the femoral head. In this approach the tendon of obturator externus is preserved to protect the deep branch of the medial femoral circumflex artery.17 We have not observed any increase in the devascularisation of the femoral head. Using a probe the labrum and acetabular cartilage were tested for stability and lesions. The reduced hip was put through a full range of movement under direct view to record the exact relationship between the proximal femur and the acetabulum. This was documented using a graphic representation of the pathological changes. Based on the site of necrosis, inspection of the joint, evaluation of impingement and the extent of the damage, reconstructive surgery was undertaken.

In order to simplify evaluation, all images were converted to represent right-sided joints. The labrum and acetabulum were divided into four quadrants with clockwise marking, 12 o'clock being the most cephalad position.18 The lesions of the labrum and acetabulum were assigned numbers correlating with their position. Using computerised data analysis, a frequency distribution was calculated for the site of both the acetabular and labral lesions. The femoral deformity was described in extent and localisation, as well as the cephalocervical offset or ratio.


The presumed aetiological factors for the development of osteonecrosis in these patients and their details are shown in Table II. The primary complaint in 15 of 17 hips was pain which was related to activity and most often localised in the groin. Sharp pain on flexion, internal rotation and/or adduction of the hip was observed in eight patients (8 hips). The mean duration of symptoms before surgery was 9.3 months (1 to 26). According to the classification of Ficat two hips were stage II, two were stage II to stage III, 12 were stage III, and one was stage III to stage IV. The Kerboul angles were 200 deg or more in ten hips (i.e., extensive involvement), between 1600 and 2000 (medium involvement) in four, and in three there were insufficient data since only AP radiographs were available. Plain radiographs showed a well-maintained joint space in all patients.

All hips had a similar pattern of damage to the labrum and acetabular cartilage in the anterosuperior region (Fig. 1). Most often there was a tear of the undersurface of the labrum between 12 and 3 o'clock. An acetabular lesion was seen consistently adjacent to the labral damage. Its appearance ranged from superficial roughening to an ulcer extending to subchondral bone with adjacent subchondral delamination. The femoral head showed flattening of the contour even in the two hips graded as Ficat stage II. Flattening was more pronounced in advanced stages with more extensive necrosis. Pressure on this region would create a wave-like deformation or buckling at the periphery, thus leaving the outer margins relatively proud. More significant lesions of the acetabulum and labrum were associated with increasing anterosuperior flattening, but this could not be quantified. No correlation could be found between the Kerboul angles and the extent of acetabular and/or labral damage. Intraoperative movement revealed impingement of the anterolateral flattened aspect of the femoral head and/or the femoral head-neck junction against the anterosuperior aspect of the acetabulum and its rim in all hips during flexion and internal rotation and/or adduction. It seemed that prominent edges of cartilage in stage III-hips enlarged the area of acetabular damage. Reconstructive surgery addressing the osteonecrosis and/or impingement included recontouring of the anterior head-- neck junction (7 hips), cement augmentation of the area of necrosis of the femoral head19 (8 hips), ITO (5 flexion, 2 extension), a vascularised graft from the iliac crest (1 hip), arthroplasty (1 hip) and combinations thereof (Table II).


We suggest that the initial damage to the labrum and acetabular cartilage in osteonecrosis of the femoral head is caused by anterior impingement. Deformation of the involved anterosuperior segment of the femoral head leads to a reduced anterior offset between the head and neck, resulting in impingement in flexion and flexion-internal rotation and adduction at the anterosuperior aspect of the labrum and acetabulum. With increasing pressure in flexion, the high stresses between the flattened anterior contour of the femoral head and the opposing surface of the acetabulum14 will lead to lesions on the undersurface of the labrum and destruction at the adjacent acetabular cartilage. Further degeneration results in reactive bony changes as seen in stage IV. We recently reported a similar appearance in patients with a slipped capital femoral epiphysis in whom impingement by the altered contour of the head-neck junction led to early mechanical damage of labral and acetabular cartilage.20

The implications of these findings are that, despite an acetabulum which appears radiographically normal (Ficat stages II and III), damage to the labrum and adjacent acetabular cartilage should be anticipated and may warrant conservative surgery. With minor acetabular damage operation may consist of re-establishment of a sufficient anterior contour of the head by cement, or the head-neck ratio by resection osteoplasty, or an intertrochanteric flexion osteotomy in order to decrease impingement. The accuracy of MRI for assessment of cartilage and labral damage continues to improve" and it is likely that the results of MRI will correlate with the intraoperative findings (Fig. 2). We usually undertake preoperative MRI, but feel that useful additional information can be obtained at the time of surgery using a capsulotomy. Careful preservation of the tendon of obturator externus will prevent further devascularisation.17 With high-quality MRI and/or arthroscopy, subluxation of the hip at the time of surgery may not always be necessary. However, it is helpful when checking the direction and extent of the required osteotomy. Arthroscopy of the hip also implies the use of an additional procedure.

Many forms of surgical treatment for osteonecrosis have been described including vascularised bone graft, osteotomy, cement augmentation, core decompression, and arthroplasty.5,7,10-14,19,21,22 Despite increased information about the condition, there are still no clear guidelines as to the appropriate treatment. This is reflected in our patients, who underwent a variety of procedures. We usually recommend a revascularisation procedure in stage-II hips, and cement augmentation with or without osteotomy in stageIII. Drilling of the femoral head is done when the necrotic area is a confluence of irregular zones rather than a clearly defined sector. Recontouring of the anterior head-neck junction is undertaken when there is impingement.20 In younger patients, a joint-preserving approach should be pursued, even in the presence of some labral and acetabular pathology. For patients aged over 55 to 60 years it remains unclear as to whether hemiarthroplasty or total hip replacement is the most suitable surgical treatment. Based on our findings, in patients in this age group careful inspection of the joint seems mandatory. When extrapolating from our findings in the younger group we would expect similar or more extensive damage to the labrum and acetabular cartilage which would suggest the requirement of a total hip age which would suggest the requirement of a total hip arthroplasty rather than a hemiarthroplasty. This was also suggested in two recent studies23,24 although these authors did not comment on labral pathology or the specific sites of damage to the acetabular cartilage.

We have documented the consistent early presence and sites of labral and acetabular lesions in patients with necrosis of the femoral head who have a radiologically normal joint space without acetabular changes. A mechanical rationale for these lesions is given. The finding may explain why some patients treated by conservative surgery continue to experience pain although the joint space is maintained rediologically. Acetabular damafe should be assessed when considering conservative or joint-replacement surgery. Our observations suggest that total hip replacement is more suitable than hemiarthroplasty in these patients.

No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.


1. Aaron RK. Osteonecrosis: etiology, pathophysiology and diagnosis. In: Callaghan JJ, Rosenberg AG, Rubasch HE, eds. The adult hip. Philadelphia, Lippincott-Raven Publishers, 1998:451-66.

2. Hungerford DS. Bone marrow pressure, venography and core decompression in ischemic necrosis of the femoral head. In: The hip: proceedings of the seventh open scientific meeting of The Hip Society. St Louis: CV Mosby, 1979:218-37.

3. Hungerford DS, Zizic TM. Pathogenesis of ischemic necrosis of the femoral head. In: Hungerford DS, ed. The hip. Procs of the ]]th meeting of the Hip Society. St. Louis, etc: CV Mosby, 1983:249-62.

4. Mankin HJ. Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med 1991;326:1473-9.

5. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg [Am] 1995;77-A:459-74.

6. Ficat RP. Idiopathic bone necrosis of the femoral head: early diagnosis and treatment. J Bone Joint Surg [Br] 1985;67-B:3-9.

7. Marcus ND, Enneking WF, Massam RA. The silent hip in idiopathic aseptic necrosis: treatment by bone grafting. J Bone Joint Surg [Am] 1973;55-A:1351-66.

8. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg [Br] 1995;77-B:34-41.

9. ARCO Committee on Terminology and Staging. The ARCO perspective for reaching one uniform staging system of osteonecrosis. In: Schoutens A, ed. Bone circulation and vascularization in normal and pathological conditions. New York, Plenum Press, 1993:375-80.

10. Ito H, Kaneda K, Matsuno T. Osteonecrosis of the femoral head: simple varus intertrochanteric osteotomy. J Bone Joint Surg [Br] 1999;81-B:969-74.

11. Kern O, Klockner, Weber U. Femur head preserving therapy, using vascular pedicled iliac bone graft, in segmental femoral head necrosis. Orthopade 1998;27:482-90.

12. Kerboul M, Thomine J, Postel M, Merle d'Aubigne R. The conservative surgical treatment of idiopathic aseptic necrosis of the femoral head. J Bone Joint Surg[Br] 1974;56-B:291-6.

13. Saito S, Ohzono K, Ono K. Joint-preserving operations for idiopathic avascular necrosis of the femoral head: results of core decompression, grafting, and osteotomy. J Bone Joint Surg [Br] 1988;70-B:78-84.

14. Wagner H, Baur W, Wagner M. Joint-preserving osteotomy in segmental femur head necrosis. Orthopade 1990;19:208-18.

15. Schneider R. Die intertrochantere Osteotomie bei Coxarthrose. Berlin, etc: Springer Verlag, 1979.

16. Mercati E, Guary A, Myquel C, Bourgeon A. A postero-external approach to the hip joint: value of the formation of a diagnostic muscle. J Chir (Paris) 1972;103:499-504.

17. Gautier E, Ganz K, Kriigel N, Gill T, Ganz R. Anatomy of the medial femoral circumflex artery and its surgical implications. J Bone Joint Surg 2000;82-B:679-83.

18. Leunig M, Werlen S, Ungersbock A, Ito K, Ganz R. Evaluation of the acetabular labrum by MR arthrography. J Bone Joint Surg [Br] 1997;79-B:230-4.

19. Hernigou P, Bachir D, Galacteros F. Avascular necrosis of the femoral head in sickle-cell disease: treatment of collapse by the injection of acrylic cement. J Bone Joint Surg [BrI 1993;75-B:87580.

20. Leunig M, Casillas MM, Hamlet M, et al. Slipped capital femoral epiphysis: early mechanical damage to the acetabular cartilage by a prominent femoral metaphysis. Acta Orthop Scand 2000;71:370-5.

21. Lachiewicz PF, Desman SM. The bipolar endoprosthesis in avascular necrosis of the femoral head. J Arthroplasty 1988;3:131-8.

22. Urbaniak JR, Harvey EJ. Revascularization of the femoral head in osteonecrosis. J Am Acad Orthop Surg 1998;6:44-54.

23. Steinberg ME, Corces A, Fallon M. Acetabular involvement in osteonecrosis of the femoral head, J Bone Joint Surg [Am] 1999;81-A:60-5.

24. Im G-I, Kim D-Y, Shin J-H, Cho W-H, Lee C-J. Degeneration of the acetabular cartilage in osteonecrosis of the femoral head: histopathologic examination of 15 hips. Acta Orthop Scand 2000;71:28-30.

P. Moen, M. Leunig, R. Ganz

From the University of Berne, Switzerland

P. Kloen, MD, Orthopaedic Surgeon, 1999 M. E. Muller Foundation Fellow

Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA.

M. Leunig, MD, Orthopaedic Surgeon

R. Ganz, MD, Professor and Chairman

Department of Orthopaedic Surgery, University of Berne, Inselspital, Berne, 3010-CH, Switzerland.

Correspondence should be sent to Dr M. Leunig.

Copyright British Editorial Society of Bone & Joint Surgery Jan 2002
Provided by ProQuest Information and Learning Company. All rights Reserved

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