The Charcot Foot in Diabetes

Reviews/Commentaries/ADA Statements CONSENSUS REPORT The Charcot Foot in Diabetes 1 8 LEE C. ROGERS, DPM ALEXANDRA JIRKOVSKA, MD associated with this condition is midfoot 2 4 ROBERT G. FRYKBERG, DPM, MPH EDWARD JUDE, MD “ ” 3 9 collapse, described as a rocker-bottom DAVID G. ARMSTRONG, DPM, PHD STEPHAN MORBACH, MD 4 10 foot (Fig. 1), although the condition ap- ANDREW J.M. BOULTON, MD WILLIAM B. MORRISON, MD 5 11 pears in other joints and with other pre- MICHAEL EDMONDS, MD MICHAEL PINZUR, MD 6 12 sentations. Pain or discomfort may be a GEORGES HA VAN, MD DARIO PITOCCO, MD 6 13 AGNES HARTEMANN, MD LEE SANDERS, DPM feature of this disorder at the active 7 14 FRANCES GAME, MD DANE K. WUKICH, MD (acute) stage, but the level of pain may 7 15 fi WILLIAM JEFFCOATE, MD LUIGI UCCIOLI, MD be signi cantly diminished when com- pared with individuals with normal sensation and equivalent degrees of injury. The diabetic Charcot foot syndrome is a serious and potentially limb-threatening lower-extremity The set of signs and symptoms that complication of diabetes. First described in 1883, this enigmatic condition continues to chal- occur together with CN qualifies this lenge even the most experienced practitioners. Now considered an inflammatory syndrome, the condition as a syndrome, the “Charcot diabetic Charcot foot is characterized by varying degrees of bone and joint disorganization foot syndrome.” secondary to underlying neuropathy, trauma, and perturbations of bone metabolism. An international task force of experts was convened by the American Diabetes Association and the Definition and classification American Podiatric Medical Association in January 2011 to summarize available evidence on the pathophysiology, natural history, presentations, and treatment recommendations for this entity. recommendations c Nomenclature should be standardized Diabetes Care 34:2123–2129, 2011 to CN or the Charcot foot. c Existing classifications do not provide prognostic value or direct treatment. he Charcot foot in diabetes poses DEFINITION—Charcot neuropathic Active or inactive should be used to many clinical challenges in its di- osteoarthropathy (CN), commonly re- T describe an inflamed or stable CN, re- agnosis and management. Despite ferred to as the Charcot foot, is a condi- spectively. Acute and chronic can also the time that has passed since the first tion affecting the bones, joints, and soft be used in this regard, but there is publication on pedal osteoarthropathy in tissues of the foot and ankle, character- no accepted measure that defines the 1883, we have much to learn about the ized by inflammation in the earliest phase. transition point. pathophysiology, and little evidence ex- The Charcot foot has been documented to ists on treatments of this disorder. The occur as a consequence of various periph- PATHOGENESIS—There is no sin- international task force was convened in eral neuropathies; however, diabetic neu- gular cause for the development of the January 2011 at the Salpêtrière Hospital ropathy has become the most common Charcot foot, but there are factors that in Paris, France, to review the literature etiology. The interaction of several com- predispose to its development, as well as and report on the definition, pathogene- ponent factors (diabetes, sensory-motor a number of likely precipitating events. sis, diagnosis, and treatment of the dia- neuropathy, autonomic neuropathy, The current belief is that once the disease betic Charcot foot. Recommendations in trauma, and metabolic abnormalities of is triggered in a susceptible individual, this report are solely the opinions of the bone) results in an acute localized in- it is mediated through a process of un- authors and do not represent the official flammatory condition that may lead to controlled inflammation in the foot. This positions of the American Diabetes Asso- varying degrees and patterns of bone inflammation leads to osteolysis and is ciation or the American Podiatric Medical destruction, subluxation, dislocation, indirectly responsible for the progressive Association. and deformity. The hallmark deformity fracture and dislocation that characterizes ccccccccccccccccccccccccccccccccccccccccccccccccc its presentation (1). The evidence to sup- 1 2 port this hypothesis is largely circumstan- From the Amputation Prevention Center at Valley Presbyterian Hospital, Los Angeles, California; the Carl T. fl Hayden Veterans Affairs Medical Center, Phoenix, Arizona; the 3Southern Arizona Limb Salvage Alli- tial. A neurally mediated vascular re ex ance (SALSA), University of Arizona College of Medicine, Tucson, Arizona; the 4Department of Medicine, leading to increased peripheral blood University of Manchester, Manchester, U.K.; the 5Diabetic Foot Clinic, King’s College Hospital, London, flow and active bone resorption has 6 U.K.; the Diabetes and Metabolic Diseases Department, Pitié-Salpêtrière University Hospital, Paris, France; been proposed as an etiological factor in the 7Department of Diabetes and Endocrinology, Nottingham University Hospitals NHS Trust, Nottingham, U.K.; the 8Institute for Clinical and Experimental Medicine, Diabetes Centre, Prague, Czech Republic; the the development of bone and joint de- 9Department of Diabetes and Angiology, Marienkrankenhaus, Soest, Germany; the 10Department of Radiology, struction in neuropathic patients. How- Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; the 11Department of Orthopedic Surgery, ever, the relationship between increased Loyola University Health System, Maywood, Illinois; the 12Diabetes Center and Foot Care Unit A, Gemelli fl 13 blood ow to bone and active bone resorp- Hospital, Catholic University, Rome, Italy; the Podiatry Service, Veterans Affairs Medical Center, Lebanon, tion has not been conclusively defined. Pennsylvania; the 14Department of Orthopedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; and the 15Department of Internal Medicine, University of Rome Tor Vergata, Rome, Italy. Corresponding author: Lee C. Rogers, [email protected]. Uncontrolled inflammation DOI: 10.2337/dc11-0844 When a bone is fractured, the release of This article is copublished in Diabetes Care and the Journal of the American Podiatric Medical Association, under proinflammatory cytokines including tumor joint copyright. a b © 2011 by the American Diabetes Association and the American Podiatric Medical Association. Readers may necrosis factor- and interleukin-1 leads use this article as long as the work is properly cited, the use is educational and not for profit, and the work is to increased expression of the polypep- not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. tide receptor activator of nuclear factor-kB care.diabetesjournals.org DIABETES CARE, VOLUME 34, SEPTEMBER 2011 2123 Consensus Report Predisposition The researchers also reported an associa- Neuropathy is a universal feature of the tion between BMD and the relative preva- affected limb. Although it has been sug- lence of fracture and of dislocation in the gested that people with a Charcot foot affected foot (11). may have particular patterns of sensory Diabetes may be associated with os- loss reflecting involvement of different teopenia, but the available evidence sug- fibers (5,6), this is not generally accepted. gests that reduction of BMD is a feature of Nevertheless, three groups have shown type 1 diabetes more so than type 2 dia- that people who have had an acute Char- betes (12). Any reduction of BMD in type cot foot exhibit retention of vasodilatory 1 diabetes may relate to loss of islet pep- reflexes in contrast to diabetic individuals tides such as insulin and amylin (IAPP), with distal symmetrical neuropathy with- both of which act as growth factors for out CN (7–9). bone. Despite this, the fracture risk in Despite these observations, it should type 2 diabetes may be no less than in be noted that the syndrome might also type 1 diabetes (12), and this would ex- occur in patients with a spectrum of plain the fact that the presentation does unrelated diseases complicated by nerve not appear to differ between the two types damage. These include distal neuropathies of the disease. Any associated deficiency caused by toxins (ethanol, drug related) of vitamin D—with or without renal failure and infection (leprosy), as well as diseases and secondary hyperparathyroidism— of the spinal cord and nerve roots (tabes would increase the possibility of reduced Figure 1—The typical appearance of a later- dorsalis, trauma, syringomyelia) and a BMD in diabetes. The use of thiazolidine- stage Charcot foot with a rocker-bottom de- number of other conditions (Parkinson’s diones could theoretically increase the like- formity. disease, HIV, sarcoidosis, rheumatoid dis- lihood of an acute Charcot foot through an ease, and psoriasis). Although the neuro- effect on bone density, but this has not yet arthropathy is typically more proximal in been reported. The use of corticosteroids ligand (RANKL) from any of a number of those with disease of the spinal cord, the as immunosuppressants in people with di- local cell types. RANKL triggers the syn- presentation may be otherwise indistin- abetes who have had a renal and/or pan- thesis of the nuclear transcription factor guishable. creatic transplant (13) may explain the nuclear factor-kb (NF-kb), and this in Loss of protective sensation will in- apparent high incidence of the Charcot turn stimulates the maturation of osteo- crease the likelihood of trauma to the foot, foot in this group. clasts

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