Menu

 

Recent rapid responses

Rapid responses are electronic letters to the editor. They enable our users to debate issues raised in articles published on bmj.com. Although a selection of rapid responses will be included as edited readers' letters in the weekly print issue of the BMJ, their first appearance online means that they are published articles. If you need the url (web address) of an individual response, perhaps for citation purposes, simply click on the response headline and copy the url from the browser window.

Displaying 1-3 out of 3 published

Acute Charcot’s foot and small vessel vasculitis

24 December 2012

Charcot arthopathy can develop without any history of trauma .In acute phase the foot is warm and swollen. Patient may or may not have pain .The neurovascular and neurotraumatic aetiology explains the pathogenesis of Charcot foot [1]. Although diabetes, alcohol, leprosy are prominent aetiology, but other small vessel vasculopathy are a sinister cause .The other connective tissues involved are: systemic lupus erythematosus, polyarteritis nodosa, sjogren, Churgh Strauss syndrome, CREST syndrome, cryoglobulinemia. Another term is lymphocytoclastic vasculitis (LCV also known as hypersensitive vasculitis and cutaneous necrotising vasculitis).It is a type III injury of vessels. Various triggers has been described. The inflammation of the small blood vessel, most commonly post capillary venules is the cardinal feature of LCV [2].The skin followed by joints [3]are the common organ involved. Histological features of LCV can occur in any vasculitis but also in neurovascular disease such as neutrophillic dermatosis .Immunofluoroscent staining may reveal (immunoglobulin G, M) and complement (C3, C4) deposition on the skin basement membrane suggest Immuno-complex deposition. The treatment involves leg elevation, removal of trigger factor.
Reference:
1. Bomer AC, Allman RM. Pathogenesis of the neuropathic joint: Neurotraumatic vs. Neurovascular. Radiology 1981; 139:349 – 54.
2. Daniel CL. Lymphocytoclastic vasculitis and Henoch-Schonlein purpura .Arthritis and Allied conditions. 15th edition.2005, 86:1793-1797.
3.Martinez-TAbaoda VM,Blanco Garcia –Fuenter M,Rodriguez – Valverda V:Clinical features and outcome of 95 patients with hypersensitive vasculitis. Am J Med 1997, 102:186 -191.

Competing interests: None declared

Kaushik Sanyal, Department of Rheumatology

East Surrey Hospital , Redhill , Surrey ,UK

Click to like:

Re: Acute Charcot foot

31 March 2012

Thanks for the interesting article.
As a general educational point, a bone scan in isolation often adds little to the diagnosis without an accompanying radio-labelled white cell scan or Leukoscan; in combination, the sensitivity/specificity is much nearer the optimistic values quoted for MRI. Either way, this is highly specialised imaging for a condition best managed in specialist centres rather than in primary care.

Competing interests: None declared

Peter Strouhal, Radiologist

Royal Wolverhampton Hospital, Wednesfield Rd, W'ton, WV8 2HW

Click to like:

Re: Acute Charcot foot

22 March 2012

The case report (1) addresses the diagnosis and treatment of acute Charcot foot stage I (positive radiograph, positive MRI (2,3))- however, without mentioning the outcome. If treatment by offloading and immobilisation is commenced already in stage 0, Charcot foot deformity may be avoided(4,5). At this stage, which is characterised by painless swelling from common skeletal trauma (ankle sprain, stress injury (6,7)), bone damage is confined to subcortical, trabecular microfractures (evidenced by MRI rather than x-ray (2)). Offloading is required for about 3 months. If stage 0 remains untreated, continued walking causes progression to stage I (cortical fractures and deformity); treatment of stage I may be required for up to 12 months, depending on the extent of the skeletal destruction (8).

1)Baglioni P, Malik M, Okosieme OE. Acute Charcot foot. BMJ 2012;344:e1397

2)Chantelau E, Poll L. Evaluation of the diabetic Charcot foot by MR imaging or plain radiography- an observational study.
Experimental and Clinical Endocrinology and Diabetes 2006;114:428-431

3)Poll LW, Weber P, Böhm HJ, Ghassem-Zadeh N, Chantelau EA. Sudeck’s disease stage 1, or diabetic Charcot’s foot stage 0 ? Case report and assessment of the diagnostic value of MRI. Diabetology & Metabolic Syndrome 2010;2: 60

4)Kimmerle R, Chantelau E. Weight-bearing intensity produces Charcot deformity in injured neuropathic feet in diabetes. Experimental and Clinical Endocrinology and Diabetes 2007;115: 360-364

5)Perrin BM, Gardner MJ, Suhaimi A, Murphy D. Charcot osteoarthropathy of the foot. Australian Family Physician 2010;38:117-119

6)Chantelau E, Richter A, Schmidt-Grigoriadis P, Scherbaum WA. The diabetic Charcot foot: MRI discloses bone stress injury as trigger mechanism of neuroarthropathy. Experimental and Clinical Endocrinology and Diabetes 2006;114:118-123

7)Chantelau E, Richter A, Ghassem-Zadeh N, Poll L. „Silent“ stress injuries in the feet of diabetic patients with polyneuropathy-a report on 12 cases. Archives of Orthopedic and Trauma Surgery 2007;127:171-177.

8)Zampa V, Bargellini I, Rizzo L, Turini F, Ortori S, Piaggesi A, Bartolozzi C. Role of dynamic MRI in the follow-up of acute Charcot foot in patients with diabetes mellitus. Skeletal Radiol 2011;40:991-999

Competing interests: None declared

Ernst A. Chantelau, Physician

formerly Heinrich-Heine-University, Düsseldorf/Germany, Holthorster Weg 16, 28717 Bremen/Germany

Click to like:

Latest comments and most commented

THIS WEEK'S POLL

Read related article

See previous polls