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Year : 2004  |  Volume : 14  |  Issue : 2  |  Page : 181-184
Pictorial essay : Radiographic changes in diabetic foot


Radio Diagnosis, IGMC and Mayo Hospital Nagpur Amarjyoti X-ray and Sonographic Clinic, Wardha Road, Dhantoli Nagpur-440012, India

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Keywords: Diabetic foot, neuropathic joint

How to cite this article:
Phatak S V, Kolwadkar P K, Phatak M S. Pictorial essay : Radiographic changes in diabetic foot. Indian J Radiol Imaging 2004;14:181-4

How to cite this URL:
Phatak S V, Kolwadkar P K, Phatak M S. Pictorial essay : Radiographic changes in diabetic foot. Indian J Radiol Imaging [serial online] 2004 [cited 2019 Aug 22];14:181-4. Available from: http://www.ijri.org/text.asp?2004/14/2/181/28582

   Introduction Top


The human foot is a mechanical marvel. It consists of 26 bones, 29 joints, 42 muscles and innumerable tendons and ligaments. The interplay among these bones, tendons and ligaments cushions the body, allowing the foot to adapt to uneven surfaces. It provides traction for movement, awareness of joint and body position for balance and leverage for propulsion. Diabetics are especially highly vulnerable for foot problems because of increased plantar pressure, arteriosclerotic obliterans and peripheral neuropathy. The combination of these factors compounded by infection can lead to a gangrene and amputation[1].


   Discussion Top


Changes in skeletal system in Diabetic Patients include osteomyelitis secondary to overlying skin necrosis, gas may be seen in soft tissues, Charcot's joints or neuropathic foot, calcification, resorption of terminal tufts of terminal phalanges, localized osteoporosis and subluxations. Pathological changes in diabetic foot result from neuropathy, infection or combination of the two. Although diabetic angiopathy may cause overall ischemia, autonomic neural impairment results in loss of vasoconstriction in smaller vessels causing hyperemia and osteoporosis. Chronic hyperglycemia also causes damage to vasa nervorum of peripheral nerves resulting in glove and stocking anesthesia of peripheral neuropathy. The foot consequently provides fertile ground for spread of infection to bone from penetrating ulcers and local cellulites. Because of difficulty in distinguishing the coincidental effects of ischemia, neuropathy and infection the blanket term osteopathy is generally used. Radiological diagnosis of acute osteomyelitis on radiographs takes 8-10 days after onset but clue to underlying process may be gained by soft tissue radiograph showing displaced fascial planes and disappearance of fat shadow as a result of edema fluid. Osteoporosis is present. In chronic osteomyelitis plain film typically show ill-defined areas of bone destruction with adjacent areas of remodeling and local cortical thickening [2],[3]. Pathogenesis of Arteriosclerosis in Diabetes Mellitus has been reviewed by Colwell et al. The deposits of lipids, cholesterol, calcium, smooth muscle cells and platelets in plaque are qualitatively same but much greater in quantity in diabetics. There is often multisegmental involvement, collateral involvement, and involvement of both tibial and peroneal vessels. [1] Charcot's joint is an extreme progression of degenerative osteoarthritis following a loss of proprioceptive or pain sensation [4]. The normal protective reaction are not involved. Relaxation of supportive structures leads to joint instability. Radiologically two forms are known. Atrophic and hypertrophic. Atrophic is seen in upper limb while other form in lower limbs. Spine shows only hypertrophy changes. The underlying disease does not determine which form predominates. Atrophic type is seen as resorption of ends of bone, osteoporosis, no osteophytes or sclerosis, fragmentation or soft tissue debris seen. Hypertrophic arthropathy is also initiated by effusion. Narrowing of joint space, marked bony sclerosis occurs. Fracture and fragmentation of articular surface follow.

Periosteal new bone formation may occur. Subluxations and dislocation proceed to destruction, to mal alignment of articular surface and finally to total disorganization of joint.[5] Radiographic pattern of deossification common to many diseases are best explained by topographic and anatomic relationships of circulatory system of bone. These patterns of local and regional osteoporosis seem to be a function of a disturbance of nutritional circulatory fields in a particular anatomic site rather than a result of direct effect of disease on cellular activity. Five such patterns are identified based on nutritional circulatory fields associated with Hunters circulus articuli vasculosus. Metaphyseal bands, metaphyseal cutbacks, epiphyseal subarticular deossification, combination of these patterns and acute diffuse osteoporosis. Different combinations of these patterns may correlate with combined nutritional circulatory field. One of the particular interest is epi-metaphyseal pencil sharpener, which results from combination of metaphyseal cutback and epiphyseal subarticular deossification occurring in circumferential manner. This produces a pencil point appearance at the end of a bone or several bones. If the metaphyseal band deossification is added to metaphyseal cutback and epiphyseal subarticular deossification the appearance of surgical resection may be produced. This pattern is present in many neuropathic joints. Combination patterns are quite frequent. They may occur with Charcot's joints of syphilis, spinal cord injuries, aseptic necrosis, and arthritis mutilans from leprosy, sarcoidosis, Diabetes, psoriasis, and rheumatoid arthropathy. Acute diffuse osteoporosis may be seen with burns, frost bite, electroshock infection, rheumatoid arthritis, shoulder hand syndrome, trauma with or without fracture, Burgers disease, Raynaud's phenomenon and Diabetics as mottled or spotty osteoporosis may be observed through a large portion of bone or involving many bones of a part. This occurs predominantly in tarsal and carpal bones. Several circulatory fields are involved. Radiographs are characterized by a decreased and mottled density of bone in cortical and cancellous bone [6].

 
   References Top

1.Marvin E. Levin diabetic foot lesions: In Jess R. Young, Jeffy W. Olin, and John R. Bartholomew Peripheral Vascular Diseases second edition Mosby 1996;696   Back to cited text no. 1    
2.Grainger & Allison's Diagnostic Radiology A Text book of Medical imaging, third edition, Churchill Livingstone 1997;1313, 1739, 1874, 1815, 1801-02.  Back to cited text no. 2    
3.Mevin E Clouse, Herbert F. Gramm, Merle legg & Thomas Flood Diabetic osteoarthropathy clinical and roentgenographic observations in 90 cases AJR may 1974 vol. 121, no. 1: 22-34.  Back to cited text no. 3    
4.Cavanaugh PR, Young MJ, Adams JE, Vicker K, Boulton AJM Radiogrpahic abnormalities in the feet of patients with diabetic neuropathy Diabetes care 1994;17:201-209.  Back to cited text no. 4    
5.George B. Greenfield Radiology of bone diseases: Neurotrophic arthropathy 4th edition JB Lippincott company, Philadelphia 1986;857-858.  Back to cited text no. 5    
6.Robert M Allman and Anne C Brower circulatory pattern of deossification RCNA vol. 119, No.4, December 1981:553-569.  Back to cited text no. 6    

Top
Correspondence Address:
S V Phatak
Radio Diagnosis, IGMC and Mayo Hospital Nagpur Amarjyoti X-ray and Sonographic Clinic, Wardha Road, Dhantoli Nagpur-440012
India
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Source of Support: None, Conflict of Interest: None


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    Figures

[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11], [Figure - 12], [Figure - 13], [Figure - 14], [Figure - 15], [Figure - 16]

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