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. 2019 May 13;12(5):e228597. doi: 10.1136/bcr-2018-228597

Acute hot foot: Charcot neuroarthropathy or osteomyelitis? Untangling a diagnostic web

Louise Goldsmith 1, Matthew Barlow 2, Paul Jeffrey Evans 3, Upendram Srinivas-Shankar 2
PMCID: PMC6536222  PMID: 31088814

Abstract

A 55-year-old man with poorly controlled type 1 diabetes with microvascular and macrovascular complications presented with a 1-week history of painful erythematous swelling on the dorsum of the left foot with two areas of foot ulceration. Inflammatory markers were raised. MRI of the left foot revealed a soft tissue swelling on the dorsum of the left foot, marrow oedema and destruction of several small joints of the foot, indicating osteomyelitis and Charcot neuroarthropathy (CN). The soft tissue swelling on the dorsum of the left foot was debrided; per-operatively bone destruction of base of the fifth metatarsal was found. The patient received intravenous antibiotics for 6 weeks. The clinical features of CN including erythema, oedema and elevated temperature of the left foot settled with off-loading the foot in an air cast walker after 6 months. Our case highlights the need to recognise CN in an acutely inflamed foot of diabetic patients with neuropathy, even when other conditions like soft tissue infection and osteomyelitis can explain the clinical features.

Keywords: diabetes, bone and joint infections, peripheral nerve disease, orthopaedics

Background

Diabetes is a common risk factor for foot ulceration, soft tissue infection and osteomyelitis. While ulceration and osteomyelitis are common complications, CN is rare but potentially devastating complication.

This case highlights the importance of considering Charcot neuroarthropathy (CN) in patients with diabetic neuropathy even if there are other reasons for a warm swollen foot. The management of CN differs from the management of soft tissue infection and osteomyelitis. CN requires early diagnosis, offloading of the joint and immobilisation with total contact casting, to prevent further joint destruction and amputation.

Case presentation

Our patient was a 55-year-old man with poorly controlled type 1 diabetes, hypertension, laser-treated retinopathy, maculopathy, peripheral neuropathy, chronic kidney disease (stage 4) and ulcerative colitis. He previously underwent right first and left fifth partial ray amputation for osteomyelitis and soft tissue infection, following foot ulceration. He worked as a chef, never smoked and occasionally consumed alcohol.

The patient attended the accident and emergency department with a 1-week history of pain and swelling to the dorsum of his left foot. A few weeks previously he developed ulceration on the dorsum and lateral border of the left foot due to trivial trauma. Clinical examination revealed an erythematous left foot with a soft tissue swelling on the dorsum (figure 1). There was collapse of the left midfoot and peripheral neuropathy. The patient had features of sensory neuropathy with diminished pin prick to the mid-shin bilaterally and impaired monofilament sensation in the foot. Dorsalis pedis and posterior tibial pulses were palpable.

Figure 1.

Figure 1

Photograph of left foot, erythematous foot with a soft tissue infection and ulceration.

Investigations

Admission bloods tests: white cell count 14.1×109/L (nr 4.0–11.0×109/L), C reactive protein 176 mg/dL (<3 mg/dL).

Tissue culture: Staphylococcus aureus and Klebsiella pneumoniae.

Left foot radiograph: Bone destruction of the second, third, fourth and remnant of the fifth metatarsal bases (figure 2).

Figure 2.

Figure 2

Dorsoplantar radiograph left foot, bone destruction of the second, third and fourth metatarsal bases and remnant of the fifth metatarsal. Soft tissue swelling of lateral midfoot.

MRI left foot (non-contrast): soft tissue abscess involving the lateral and dorsal aspect of the midfoot and forefoot. Extensive marrow oedema in second, third and fourth metatarsals, cuboid and lateral middle cuneiform and to a lesser extent the medial cuneiform and the navicular bone. Destruction of the base of the fifth metatarsal, cuboid and lateral cuneiform was noted. Several small joint effusions in the midfoot joints and in the tibiotalar joint (figure 3).

Figure 3.

Figure 3

MRI left foot, sagittal view, soft tissue abscess involving the lateral and dorsal aspect of the midfoot and forefoot. Extensive marrow oedema in second, third and fourth metatarsals. Destruction of the base of the fifth metatarsal. Several small joint effusions in the midfoot. Abscess circled.

Differential diagnosis

The initial impression of soft tissue infection of the left foot complicated by osteomyelitis, was corroborated by radiological findings. Per-operative features including bony destruction described in the treatment section were consistent with osteomyelitis. CN was diagnosed by persistent erythema, and warmth of the left foot, which did not settle despite 6 weeks’ treatment with intravenous antibiotics and return to baseline of inflammatory markers. Features suggesting CN in our patient include foot deformity, involvement of several bones and joints, periarticular and subchondral oedema on MRI imaging. The X-ray and MRI foot images confirmed features consistent with both osteomyelitis and CN.

The final diagnosis was foot ulceration with abscess complicated by osteomyelitis and active CN in a patient with diabetic neuropathy.

Treatment

Our patient underwent wound debridement (figure 4). Per-operatively, there was destruction of the base of the left fifth metatarsal with communication inferio-medially into the foot and with the soft tissue infection on the dorsum of the foot. Absorbable calcium sulfate pellets with vancomycin and gentamicin were instilled into the infected bone.

Figure 4.

Figure 4

Photograph of left foot, after surgical debridement to healthy tissue.

The patient received a 6-week course of intravenous antibiotics (vancomycin and later ceftriaxone). Offloading of the foot was provided by an air cast walker with a bespoke total contact insole. The patient was advised to keep weight-bearing to a minimum, till the active stage of CN settled.

Outcome and follow-up

The foot ulceration and surgical wound healed in 6 weeks. With effective offloading and limited weight-bearing, oedema, warmth and erythema on the dorsum of the left foot settled in 6 months (figure 5). The patient was provided with bespoke foot wear, after he came off the air cast walker.

Figure 5.

Figure 5

Photograph of left foot after the surgical wound healed and Charcot neuroarthropathy.

Discussion

Our patient had suboptimal glycaemic control with microvascular complications including neuropathy, that increased the risk of foot ulceration. Infected foot ulceration led to cellulitis, abscess and osteomyelitis. Osteomyelitis is a common complication of diabetic foot ulceration with inflammation of the bone marrow,1 presenting with erythema and oedema of the affected part. The diagnosis of osteomyelitis is frequently based on clinical features as the initial radiographs have low sensitivity and specificity for detecting acute osteomyelitis.1 Up to 80% of patients who present in the first 2 weeks of infection onset may have a normal radiograph.2

CN is an uncommon complication (<0.3 %/year) of diabetes.3 Although the presentation of CN is variable, the most common presentation is sudden onset of unilateral warmth, erythema and oedema of the foot, often with a history of minor trauma, or ulceration as in our patient.4 There is progressive degeneration, with bony destruction, bone resorption and eventual deformity in an insensate foot with autonomic neuropathy. This may lead to plantar ulceration and superimposed osteomyelitis, and the need for amputation. Therefore, early identification of this condition is vital to avoid significant morbidity.

CN should be considered in the differential diagnosis of foot after more common conditions like fractures, cellulitis, gout and osteomyelitis are quickly excluded in a patient with diabetes and neuropathy. The treatment of CN requires immediate off-loading and non-weight bearing to halt potentially catastrophic joint destruction and hence the importance of making a prompt diagnosis.5

CN is easier to diagnose in patients without foot ulceration and soft tissue infection. In the presence of soft tissue infection, foot ulceration and osteomyelitis as in our patient, CN may not be considered. Diagnosing both osteomyelitis and CN is crucial as management is different, and failure to consider both conditions may result in severe bone and joint destruction and lead to a major amputation. Berli et al reported that osteomyelitis within the Charcot site is associated with a higher level of amputation and longer duration of antibiotic therapy and immobilisation, compared with osteomyelitis without CN.6

A detailed history and thorough clinical examination with MRI findings help differentiate osteomyelitis from CN and the coexistence of both the conditions as in our patient.7

Patient’s perspective.

Having diabetes for so many years can make it very difficult to keep on top of everything. The reduced sensation in the feet has caused a lot of problems to my feet. I was not aware of this condition called Charcot neuroarthropathy and it was difficult to limit weight-bearing and use the diabetes walker. I am glad that the foot has settled eventually.

Learning points.

  • Consider the diagnosis of Charcot neuroarthropathy (CN) in a patient with diabetes with neuropathy, in any situation with an erythematous, swollen foot, after excluding common conditions like cellulitis, gout, fracture and osteomyelitis.

  • The mainstay of treatment for CN involves early offloading of the foot in specialist multidisciplinary diabetes foot clinics.

  • CN may be precipitated by foot ulceration and can coexist with osteomyelitis.

  • Distinguishing osteomyelitis from CN, often a diagnostic challenge is important and is based on history, clinical features and radiological findings.

  • X-ray of the foot and ankle may be normal in early CN. MRI imaging has high sensitivity and specificity for making a diagnosis of CN.

Acknowledgments

Dr Paul Evans, contributing author has no personal relationship to the patient. The names being the same is simply a coincidence.

Footnotes

Contributors: All authors substantially contributed to the data gathering, interpretation formation and final review of the manuscript. And assisted in the literature review. LG specifically compiled the initial and final drafts. MB contributed to the initial concept, data gathering and processing. PJE specifically assisted in selection, editing and labelling of images. US-S assisted in conceiving the idea, formulating the manuscript plan, editing and literature review.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent for publication: Obtained.

References

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