Charcot neuroarthropathy is a rare but serious complication of diabetes, causing progressive destruction of the bones and joints of the foot leading to deformity, altered biomechanics and an increased risk of ulceration. Management is complicated by a lack of consensus on diagnostic criteria and an incomplete understanding of the pathogenesis. In this review, we consider recent insights into the development of Charcot neuroarthropathy. It is likely to be dependent on several interrelated factors which may include a genetic pre-disposition in combination with diabetic neuropathy. This leads to decreased neuropeptides (nitric oxide and calcitonin gene-related peptide), which may affect the normal coupling of bone formation and resorption, and increased levels of Receptor activator of nuclear factor kappa-B ligand, potentiating osteoclastogenesis. Repetitive unrecognized trauma due to neuropathy increases levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6, tumour necrosis factor α) which could also contribute to increased bone resorption, in combination with a pre-inflammatory state, with increased autoimmune reactivity and a profile of monocytes primed to transform into osteoclasts - cluster of differentiation 14 (CD14). Increased blood glucose and loss of circulating Receptor for Advanced Glycation End-Products (AGLEPs), leading to increased non-enzymatic glycation of collagen and accumulation of AGLEPs in the tissues of the foot, may also contribute to the pathological process. An understanding of the relative contributions of each of these mechanisms and a final common pathway for the development of Charcot neuroarthropathy are still lacking.
Neuropathic changes in the foot are common with
a prevalence of approximately 1%. The diagnosis of neuropathic arthropathy
is often delayed in diabetic patients with harmful consequences
including amputation. The appropriate diagnosis and treatment can
avoid an extensive programme of treatment with significant morbidity
for the patient, high costs and delayed surgery. The pathogenesis
of a Charcot foot involves repetitive micro-trauma in a foot with impaired
sensation and neurovascular changes caused by pathological innervation
of the blood vessels. In most cases, changes are due to a combination
of both pathophysiological factors. The Charcot foot is triggered
by a combination of mechanical, vascular and biological factors
which can lead to late diagnosis and incorrect treatment and eventually
to destruction of the foot. This review aims to raise awareness of the diagnosis of the Charcot
foot (diabetic neuropathic osteoarthropathy and the differential
diagnosis, erysipelas, peripheral arterial occlusive disease) and
describe the ways in which the diagnosis may be made. The clinical
diagnostic pathways based on different classifications are presented. Cite this article:
Charcot neuro-osteoarthropathy (CN) of the midfoot
presents a major reconstructive challenge for the foot and ankle
surgeon. The Synthes 6 mm Midfoot Fusion Bolt is both designed and
recommended for patients who have a deformity of the medial column
of the foot due to CN. We present the results from the first nine
patients (ten feet) on which we attempted to perform fusion of the
medial column using this bolt. Six feet had concurrent hindfoot fusion
using a retrograde nail. Satisfactory correction of deformity of
the medial column was achieved in all patients. The mean correction
of calcaneal pitch was from 6°
(-15° to +18°) pre-operatively to 16° (7° to 23°) post-operatively;
the mean Meary angle from 26° (3° to 46°) to 1° (1° to 2°); and
the mean talometatarsal angle on dorsoplantar radiographs from 27°
(1° to 48°) to 1° (1° to 3°). However, in all but two feet, at least one joint failed to fuse.
The bolt migrated in six feet, all of which showed progressive radiographic
osteolysis, which was considered to indicate loosening. Four of
these feet have undergone a revision procedure, with good radiological
evidence of fusion. The medial column bolt provided satisfactory correction
of the deformity but failed to provide adequate fixation for fusion
in CN deformities in the foot. In its present form, we cannot recommend the routine use of this
bolt. Cite this article:
Limited forefoot amputation in diabetic patients
with osteomyelitis is frequently required. We retrospectively reviewed
diabetic patients with osteomyelitis, an unhealed ulcer and blood
pressure in the toe of >
45 mmHg who underwent limited amputation
of the foot with primary wound closure. Between 2006 and 2012, 74
consecutive patients with a mean age of 67 years (29 to 93), and
a median follow-up of 31 months, were included. All the wounds healed
primarily at a median of 37 days (13 to 210; mean 48). At a median
of 6 months (1.5 to 18; mean 353 days), 23 patients (31%) suffered
a further ulceration. Of these, 12 patients (16% of the total) required
a further amputation. We conclude that primary wound closure following limited amputation
of the foot in patients with diabetes is a safe and effective technique
when associated with appropriate antibiotic treatment. Cite this article:
