APLEY BAB VI - Osteonecrosis and Osteochondritis.pptx

Osteonecrosis and Osteochondritis

1. Osteonecrosis and Osteochondritis Orthopaedi And Traumatology Departement Dr. Soetomo General Academic Hospital, Medical Faculty of Universitas Airlangga

2. Osteonecrosis

3. Introduction Avascular necrosis (AVN) has long been recognized as a complication of femoral neck fractures, the usual explanation being traumatic disruption of the blood supply to the femoral head. Osteonecrosis also appears as a distinctive feature in a number of non-traumatic disorders So, Osteonecrosis, based on its cause, can be categorized into 2 : Traumatic Osteonecrosis Non-traumatic Osteonecrosis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

4. Aetiology and Pathogenesis Certain sites are peculiarly susceptible to ischaemic necrosis including : The femoral head , the femoral condyles , the head of the humerus , the capitulum and the proximal parts of the scaphoid and talus . These subarticular regions : Lie at the most distant parts of the bone’s vascular territory Largely enclosed by cartilage, giving restricted access to local blood vessels The subchondral trabeculae are further compromised in that they are sustained largely by a system of end arterioles with limited collateral connections. Vascular sinusoid have no adventitial layer, so their patency is determined by the volume and pressure of the surrounding marrow tissue Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

5. Aetiology and Pathogenesis The process can be initiated in at least four different ways: Disruption of the local blood supply Venous stasis and retrograde arteriolar stoppage Intravascular thrombosis Compression of capillaries and sinusoids by marrow swelling. Ischaemia, in the majority of cases, is due to a combination of several of these factors. Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

6. Aetiology and Pathogenesis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

7. TRAUMATIC OSTEONECROSIS The vascular anatomy is particularly important. For example, in fractures and dislocations of the hip The retinacular vessels supplying the femoral head are easily torn. If, in addition, there is damage to or thrombosis of the ligamentum teres , osteonecrosis is inevitable. Displaced fractures of the femoral neck are complicated by osteonecrosis in over 20% of cases . Undisplaced fractures also sometimes result in subchondral necrosis ; this may be due to thrombosis of intraosseous capillaries or sinusoidal occlusion due to marrow oedema. Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

8. TRAUMATIC OSTEONECROSIS Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

9. TRAUMATIC OSTEONECROSIS Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

10. TRAUMATIC OSTEONECROSIS Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

11. NON-TRAUMATIC OSTEONECROSIS The mechanisms here are more complex and may involve several pathways to intravascular stasis or thrombosis, as well as extravascular swelling and capillary compression. Aliran darah terhambat karena adanya thrombus (intravascular) Aliran darah terhambat karena adanya penekanan dari jaringan sekitar (extravascular) Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

12. NON-TRAUMATIC OSTEONECROSIS Intravascular thrombosis Over 80% of cases are associated with high-dosage corticosteroid medication and/or alcohol abuse. These conditions give rise to : Hyperlipidaemia Fatty degeneration of the liver. Fat embolism plays a part, giving rise to capillary endothelial damage, platelet aggregation and thrombosis. Thrombophilia and hypofibrinolysis are important aetiological factors in both adult osteonecrosis and Perthes’ disease. Other coagulopathies have been implicated, including Antiphospholipid deficiency in SLE Enhanced coagulability in sickle-cell disease. It seems likely that coagulation abnormalities play a contributory role in some of the disorders associated with non-traumatic osteonecrosis. Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

13. NON-TRAUMATIC OSTEONECROSIS Extravascular marrow swelling High-dosage corticosteroid administration and alcohol overuse  Fat cell swelling in the marrow Increase in marrow fat volume in the femoral head  Sinusoidal compression  Venous stasis  Retrograde ischaemia  Trabecular bone death; in other words, the establishment of a compartment syndrome. Both intravascular and extravascular factors come into play at a fairly early stage and each enhances the effect of the other (see Figures 6.2 and 6.3). Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

14. NON-TRAUMATIC OSTEONECROSIS Alcohol and high-dosage corticosteroid Hyperlipidemia  Fat embolism Sickle-cell Disease Tendency of the sickle-shaped cell to clump  Capillary flow ↓ + Intracapillary thrombosis Caisson Disease Under increased air pressure, blood and other tissues (especially fat) become supersaturated with nitrogen  If decompression os too rapid, the gas is released as bubbles  Local tissue damage + Generalized embolic phenomena + Intracapillary coagulation Gaucher Disease Accumulation of Gaucher’s cells (macrophages with glycosylceramide accumulation) in bone marrow  Increased medullary volume + Sinusoidal compression + Abnormal cell emboli Radiation Necrosis Damage to small blood vessels, marrow cells and bone cells Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

15. Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

16. Pathology and natural history Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Bone cells die after 12–48 hours of anoxia In the marrow : loss of fat cell outlines, inflammatory cell infiltration, marrow oedema, the appearance of tissue histiocytes, and eventual replacement of necrotic marrow by undifferentiated mesenchymal tissue. The tendency to bone repair , and within a few weeks one may see new blood vessels and osteoblastic proliferation at the interface between ischaemic and live bone  Increase in mineral mass  Sclerosis Reparative new bone formation proceeds slowly and probably does not advance for more than 8–10 mm into the necrotic zone  Structural failure begins to occur in the most heavily loaded part of the necrotic segment. Usually this takes the form of a linear tangential fracture close to the articular surface, possibly due to shearing stress  The crack may break through the articular cartilage and at operation it may be possible to lift the ‘lid’ off the necrotic segment like the cracked shell of a hard-boiled egg.

17. Pathology and natural history Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

18. Clinical Features Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t The earliest stage of bone death is asymptomatic ; by the time the patient presents, the lesion is usually advanced. Pain is a common complaint. It is felt in or near a joint, and perhaps only with certain movements. ‘Click’ in the joint, probably due to snapping or catching of a loose articular fragment. Stiffness in later stages. Local tenderness may be present Swelling if a superficial bone is affected. Movements may be restricted Fixed deformities in advanced case

19. X-Ray Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t The early signs of ischaemia are confined to the bone marrow and cannot be detected by plain X-ray examination. X-ray changes, when they appear (seldom before 3 months after the onset of ischaemia), are due to (1) reactive new bone formation at the boundary of the ischaemic area, (2) trabecular failure in the necrotic segment. An area of increased radiographic density appears in the subchondral bone; soon afterwards, suitable views may show a thin tangential fracture line just below the articular surface – the ‘crescent sign’ . In the late stages there is distortion of the articular surface and more intense ‘sclerosis’, now partly due to bone compression in a collapsed segment.

20. X-Ray Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t With all the changes described here (and this is the cardinal feature distinguishing primary avascular necrosis from the sclerotic and destructive forms of osteoarthritis) the ‘joint space’ retains its normal width because the articular cartilage is not destroyed until very late

21. X-Ray Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

22. MRI Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t MRI is the most reliable way of diagnosing marrow changes and bone ischaemia at a comparatively early stage The first sign is a band-like low-intensity signal on the T1 weighted spin echo (SE) image (and a similar but high-intensity signal on the short-tau inversion recovery (STIR) image), corresponding to the interface between ischaemic and normal bone.

23. CT-Scan Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t CT involves considerable radiation exposure and it is not very useful for diagnosing osteonecrosis. However, it does show the area of bone destruction very clearly and it may be useful in planning surgery.

24. Staging – Ficat Arlet Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t In 1980 Ficat and Arlet introduced the concept of radiographic staging for osteonecrosis of the hip. The system has since been updated to account for imaging modalities such as MRI. Stage 0 Preclinical and preradiological and AVN can be suggested only if it is has been diagnosed in, for example, the opposite hip. Stage 1 The early resorptive phase. The plain X-rays are normal but changes become visible on MRI or bone scintigraphy. Stage 2 The reparative stage where the femoral head contour is still normal but there are early signs of reactive change in the subchondral area. Stage 3 Early collapse of the femoral head. There are clear-cut X-ray signs of osteonecrosis with evidence of structural damage and distortion of the bone outline. Stage 4 Collapse of the articular surface and signs of secondary OA.

25. Staging – Ficat Arlet Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Stage 0 Preclinical and preradiological and AVN can be suggested only if it is has been diagnosed in, for example, the opposite hip. Stage 1 The early resorptive phase. The plain X-rays are normal but changes become visible on MRI or bone scintigraphy. Stage 2 The reparative stage where the femoral head contour is still normal but there are early signs of reactive change in the subchondral area. Stage 3 Early collapse of the femoral head. There are clear-cut X-ray signs of osteonecrosis with evidence of structural damage and distortion of the bone outline. Stage 4 Collapse of the articular surface and signs of secondary OA.

26. Staging – ARCO (Association Research Circulation Osseous – ARCO) which applies mainly to femoral head necrosis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Stage 0 Patient asymptomatic and all clinical investigations ‘normal’ Biopsy shows osteonecrosis Stage 1 X-rays normal MRI or radionuclide scan shows osteonecrosis Stage 2 X-rays and/or MRI show early signs of osteonecrosis but no distortion of bone shape or subchondral ‘crescent sign’ Sub-classification by area of articular surface involved: A = less than 15% B = 15–30% C = more than 30% Stage 3 X-ray shows ‘crescent sign’ but femoral head still spherical Sub-classification by length of ‘crescent’/articular surface: A = less than 15% B = 15–30% C = more than 30% Stage 4 Signs of flattening or collapse of femoral head: A = less than 15% of articular surface B = 15–30% of articular surface C = more than 30% of articular surface Stage 5 Changes as above plus loss of ‘joint space’ (secondary OA) Stage 6 Changes as above plus marked destruction of articular surfaces

27. Treatment – Early Stage Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Some lesions heal spontaneously and with minimal deformity; this is seen especially in areas which are not heavily loaded There is low-level evidence that drug therapy (such as bisphosphonates , statins and low molecular weight heparin ) may have some efficacy in early stages Lesions in heavily loaded joints have a poor prognosis and will probably end in structural failure if left untreated Simple measures to reduce loading of weight-bearing joints may help. If the bone contour is still intact, an ‘unloading’ osteotomy will help Medullary decompression and bone grafting may have a place in ARCO stage 1 and 2 osteonecrosis of the femoral head Rates of femoral head collapse can be reduced through augmentation with mesenchymal stem cells.

28. Treatment – Intermediate Stage Osteonecrosis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Once there is structural damage and distortion of the articular surface, conservative operations are inappropriate. However, the joint may still be salvageable and in this situation realignment osteotomy – either alone or combined with curettage and bone grafting of the necrotic segment – has a role. If mobility can be sacrificed without severe loss of function (e.g. in the ankle or wrist), arthrodesis will relieve pain and restore stability.

29. Treatment – Late Stage Osteonecrosis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Destruction of the articular surface may give rise to pain and severe loss of function. Three options are available: Non-operative management , concentrating on pain control, modification of daily activities and, where appropriate, splintage of the joint Arthrodesis of the joint (e.g. the ankle or wrist) Partial or total joint replacement , the preferred option for the shoulder, hip and knee

30. Treatment – Late Stage Osteonecrosis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

31. Osteochondritis

32. Introduction Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t The terms ‘osteochondrosis’ or ‘osteochondritis’ have for many years been applied to a group of conditions in which there is demarcation, and sometimes separation and necrosis, of a small segment of articular cartilage and bone. The affected area shows many of the features of ischaemic necrosis , including death of bone cells in the osteoarticular fragment and reactive vascularity and osteogenesis in the surrounding bone. The disorder occurs mainly in adolescents and young adults, often during phases of increased physical activity, and it may be initiated by trauma or repetitive stress.

33. Pathogenesis Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t The pathogenesis of these lesions is still not completely understood. Impact injuries can cause oedema or bleeding in the subarticular bone, resulting in capillary compression or thrombosis and localized ischaemia. The critical event may well be a small osteochondral fracture, too faint to show up on plain X-ray examination but often visible on MRI. If the crack fails to unite, the isolated fragment may lose its blood supply and become necrotic. Traction injuries may similarly damage the blood supply to an apophysis. However, it is thought that there must be other predisposing factors, for the condition is sometimes multifocal and sometimes runs in families.

34. Clinical Presentation Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t The classic example of this disorder is the condition known as osteochondritis dissecans. This occurs typically in young adults, usually men, Affects particular sites: the inner (medial) surface of the medial femoral condyle in the knee, the anteromedial corner of the talus in the ankle, the superomedial part of the femoral head, the humeral capitulum and the head of the second metatarsal bone. (Note that these are all slightly bulbous areas with convex articular surfaces.) The patient usually complains of intermittent pain ; sometimes there is swelling and a small effusion in the joint . If the necrotic fragment becomes completely detached, it may cause locking of the joint or unexpected episodes of ‘ giving way ’ in the knee or ankle.

35. Imaging Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t X-rays must be taken with the joint in the appropriate position to show the affected part of the articular surface in tangential projection. The dissecting fragment is defined by a radiolucent line of demarcation. When it separates, the resulting loose body or donor site may be obvious. The early changes are better shown by MRI

36. Imaging Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t

37. Treatment Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t Treatment in the early stage consists of load reduction and restriction of activity. In young people complete healing may occur, though it can take up to 2 years. For a large joint such as the knee, it is generally recommended that partially detached fragments be pinned back in position after roughening of the base, while completely detached fragments should be pinned back only if they are fairly large and completely preserved. These procedures may be carried out by arthroscopy. If the fragment becomes detached and causes symptoms, it should be fixed back in position or else completely removed.

38. References Blom, A., Warwick, D., & Whitehouse, M. (Eds.). (2017). Apley & Solomon's System of Orthopaedics and Trauma (10th ed.). CRC Press. https://doi.org/10.4324/9781315118192t