A patient with longstanding type 1 diabetes and a swollen, warm, and red footBMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e7760 (Published 16 November 2012) Cite this as: BMJ 2012;345:e7760
- Nicholas Tentolouris, assistant professor of internal medicine 1,
- Frank L Bowling, podiatrist2,
- Edward B Jude, consultant diabetologist3
- 1Athens University Medical School, Athens, Greece
- 2Central Manchester University Hospitals and University of Manchester, Manchester, UK
- 3Tameside Hospital NHS Foundation Trust and University of Manchester, UK
- Correspondence to: E B Jude, Tameside Hospital NHS Foundation Trust, Ashton under Lyne, OL6 9RW, UK
A 54 year old man with type 1 diabetes since the age of 13 years was referred to the diabetic foot clinic with a warm swollen right foot of seven days duration. Over the past four years he had had acceptable diabetes control and an average glycated haemoglobin of 57 mmol/mol (7.4%). He had a history of hypertension, microalbuminuria, and background diabetic retinopathy. He did not remember any trauma to his foot, had only mild pain in the affected area, and had no signs or symptoms of systemic infection.
On examination, his right foot was swollen and erythematous over the dorsal aspect. No active foot ulceration or cracked skin was present. He had symmetrical peripheral sensorimotor neuropathy, with loss of protective sensation (inability to feel the 10 g Semmes-Weinstein monofilament, also known as 5.07 gauge monofilament nylon fibre) and intact circulation in both feet.
1 What is the diagnosis?
2 How would you confirm the diagnosis?
3 How would you manage this patient?
What is the diagnosis?
Acute Charcot neuropathic osteoarthropathy (or acute Charcot foot) should always be considered when a person with diabetes and peripheral neuropathy develops unexplained inflammation in the foot. Refer the patient for urgent diagnosis or exclusion by an expert team. Meanwhile, urge the patient to limit weight bearing on the affected foot until he or she has been assessed.1 2
Acute Charcot neuropathic osteoarthropathy (or acute Charcot foot) should always be considered when a person with diabetes complicated by peripheral neuropathy develops unexplained inflammation in the foot. Refer the patient for urgent diagnosis or exclusion by an expert team.1 2 Meanwhile, urge the patient to limit weight bearing on the affected foot until he or she has been assessed. Other potential diagnoses include sprain, cellulitis, deep venous thrombosis, and gout.1 2 3
The classic description of this condition by Jean-Martin Charcot in 1883 was in patients with tabes dorsalis.1 With the decline of tertiary syphilis, diabetes mellitus is now the main cause of Charcot foot. A minor trauma, often unrecognised by the patient, may initiate the process of joint and bone destruction.1 3 4 The mean age of presentation is during the sixth decade, and most patients have had diabetes for more than 15 years.1 3 Rarely, it can be a presenting feature of type 2 diabetes.
Foot trauma, even minor, has been associated with development of the condition in about half of cases. Other triggers are soft tissue or bone infections, ulceration, and foot surgery.1 3 5 Pain is less than would be expected on the basis of the severity of the underlying destructive process. Because a history of joint trauma cannot always be established, a diagnosis of acute Charcot foot should be considered in anybody with longstanding diabetes who has a swollen warm foot. Patients usually have some degree of peripheral sensory neuropathy. Occasionally, patients have only small fibre neuropathy, which can be detected with specific tests.1 Blood supply to the feet is normal, and many patients have pedal pulses that are characteristically bounding unless obscured by concurrent oedema.1 2
Usually only one area, often the tarsometatarsal joint (70% of cases), is affected.1 5 6 Most patients have had poor diabetes control for many years, and neuropathy is the essential predisposing condition for the development of Charcot foot. However, no data are available on the association between the degree of glycaemia and outcome in these patients.1
In January 2011 an international task force of experts was convened by the American Diabetes Association and the American Podiatric Medical Association to summarise available evidence on the pathophysiology, natural course, presentation, and treatment recommendations for this entity.1 It concluded that four criteria were necessary for a diagnosis of Charcot foot in people with diabetes: a markedly swollen, warm, and often erythematous foot with only mild to modest pain or discomfort; presence of peripheral sensory neuropathy; normal or even exaggerated arterial blood flow in the foot; and bone or articular (or both) involvement on imaging, such as plain radiography, nuclear imaging, or magnetic resonance imaging (MRI).1
Soft tissue infections can mimic Charcot foot. Cellulitis is a common infection of the dermis and subcutaneous tissue that results in pain, erythema, oedema, and warmth of the affected area; fever may be present.1 5
Deep vein thrombosis (DVT) usually presents with a cramping pain in the lower calf that persists for several days and becomes more uncomfortable as time progresses. Physical findings, if present, may consist of mild discomfort on palpation of the lower calf and swelling in the leg. Fever and chills usually herald cellulitis rather than deep vein thrombosis.1
Gout, or crystal induced arthritis, tends to occur first in the great toe or foot (podagra), but it can occur in other joints of the lower extremities, such as the ankle and knee. The articular surfaces are affected and are swollen, warm, red, tender, and sensitive to light touch of the skin. Plasma uric acid concentrations are often raised.1 4 5
2 How would you confirm the diagnosis?
The diagnosis of acute Charcot foot is mainly based on history and clinical findings but should be confirmed by imaging. The initial imaging modality should be plain radiography. Look for subtle fractures or subluxations if no obvious disease is visible. MRI or nuclear imaging can confirm the clinical diagnosis if radiographs seem to be normal.1
A high index of suspicion is essential to make a diagnosis of Charcot foot. Diagnosis is based mainly on history and clinical findings but should be confirmed by imaging.1 The initial imaging modality should be plain radiography. MRI or nuclear imaging can confirm the diagnosis if radiographs seem to be normal.1 Determining the white blood cell count (with a differential count), erythrocyte sedimentation rate, C reactive protein concentration, and serum uric acid concentration can help exclude cellulitis or gout. Doppler imaging of the calf veins can confirm or exclude deep vein thrombosis.5
In the early acute stage, a plain radiograph may or may not document evidence of fracture or dislocation—a negative result does not confirm the lack of Charcot foot because radiographs may be negative for a few days up to three weeks.1 6
MRI or nuclear imaging shows active bone disease in the early stages of this condition when radiographs are normal.1 6 On MRI, prominent oedema of the marrow bones is seen as increased signal intensity on STIR (short TI inversion recovery) or T2 weighted imaging and decreased T1 weighted signal intensity.6 Three-phase bone scans based on technetium-99m (99mTc) are highly sensitive for active bone disease.1 2 3 5 However, neither MRI nor bone scans can safely discriminate acute Charcot foot from osteomyelitis. More specific tests, such as indium-111 (111In) labelled leucocytes, a combined 99mTc and 111In bone scan, or 99mTc sulphur colloid scan, may be needed.1
Patients with diabetes and foot infections often (but not always) have an increased white blood cell count with left shift and increased C reactive protein. Patients with active Charcot foot not complicated by infection have a normal white blood cell count, whereas the erythrocyte sedimentation rate and C reactive protein can be mildly increased (20-40 mm/hour and 30 mg/L (1 mg/L=9.52 nmol/L), respectively).1 4
In our patient, a plain foot radiograph showed marked deformity in the distal tarsus and at the base of the metatarsals, especially the hallux metatarsal and the cuneiform bone, features suggestive of developing acute Charcot foot (fig 1⇓). A three-phase bone scan based on 99mTc showed areas of increased bone turnover in the “bone phase” in the affected foot, findings consistent with the presence of acute Charcot foot (fig 2⇓).
3 How would you manage this patient?
Patients with acute Charcot foot should be managed in specialised diabetic foot clinics. In the acute phase, disease activity is most effectively reduced by offloading the affected foot by using a non-removable fibreglass cast until inflammation completely resolves. This approach prevents foot ulceration, which occurs in 20-25% of patients in the active phase of the disease, and severe foot deformity. In the long term, regular foot care and use of custom made moulded shoes with insoles to accommodate any residual foot deformity and to reduce increased plantar pressures are mandatory to prevent the development of late foot ulceration.1
Patients with active Charcot foot should be managed in specialised diabetic foot clinics.1 According to recent guidelines, offloading of the affected foot by using a non-removable fibreglass cast is the best way to reduce disease activity and local inflammation. This approach also prevents foot ulceration, which occurs in 20-25% of patients in the active phase of the disease, as well as the development of severe foot deformity, such as midfoot collapse (also described as a “rocker bottom” foot), which is the hallmark late deformity associated with Charcot foot.1 3 7 8
Casting of the acute (active) Charcot foot can prevent further trauma and disruption of the vicious cycle of inflammatory bone resorption. In addition, immobilisation of the foot alleviates symptoms greatly, and patients do not need analgesics.1 The first cast is changed after three days and checked each week because restricted weight bearing and use of the cast rapidly reduce oedema. The cast should then be changed frequently to avoid “pistoning” as the oedema subsides.1 If possible, the patient should use crutches or a wheelchair and should be encouraged to avoid weight bearing on the affected side. The cast should be kept on until the swelling has resolved and skin temperature is within 2°C of the contralateral foot. At this time, custom moulded shoes with appropriate insoles are indicated; this stage usually takes four to six months.1 2 7 8 In addition, after the initial radiographs, surveillance films should be taken at four to six week intervals for follow-up of the bone and articular changes.
In the long term, regular foot care and use of custom made moulded shoes and insoles to accommodate any residual foot deformity and to reduce increased plantar pressures are mandatory for preventing the development of late foot ulceration.1 Because 25% of patients ultimately develop acute Charcot foot on the contralateral site, any minor injury, infection, foot surgery, or ulceration requires careful observation.1
Small randomised double blind controlled trials have shown that treatment with bisphosphonates or calcitonin may retard activity in the early stages of the disease. However, there is little evidence currently to support the use of these drugs for the management of acute Charcot foot.9 10
A non-removable total contact fibreglass cast was applied and the patient was followed up at the diabetic foot clinic. The first cast was changed after three days. He then attended the foot clinic on a weekly basis for the next month. The swelling improved after two weeks, but a difference in temperature of 3°C between the feet persisted at five months. At six months, no temperature difference was found and the cast was removed. A minor foot deformity had developed. Custom made moulded shoes with appropriate insoles were prescribed. The patient still attends the diabetic foot clinic; no further foot deformity or ulceration has developed.
Cite this as: BMJ 2012;345:e7760
Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.
Provenance and peer review: Not commissioned; externally peer reviewed.
Patient consent obtained.