Progressive pain, foot deformity present in patient with type 2 diabetes, good glycemic control

A 56-year-old woman with a 17-year history of type 2 diabetes complicated by diabetic retinopathy, nephropathy and neuropathy was seen in the diabetes clinic for a follow-up visit. Her past medical history includes morbid obesity with a BMI of 48, hypertension, dyslipidemia, primary hypothyroidism, vitamin D deficiency and osteoporosis with multiple compression vertebral fractures.

Before the institution of insulin therapy seven years ago, she had poor glycemic control with an HbA1c of 11% to 14% (reference range 4% to 6%). Insulin therapy was started after a referral to the endocrine clinic that resulted in excellent glycemic control with HbA1c in the range of 5.5% to 7%. She is currently using basal insulin and rapid-acting insulin analogue with each meal and has been compliant with a regimen of glucose self-monitoring three to four times per day. In the past, proliferative diabetic retinopathy has led to episodes of retinal hemorrhages requiring photocoagulation. The patient has chronic kidney disease stage III with serum creatinine of 1.6 mg/dL to 2 mg/dL and glomerular filtration rate of 30 mL/min to 40 mL/min as a result of diabetic nephropathy.

Seven years ago, when the patient first presented to the endocrine clinic, she complained of right foot pain. Dislocation of the right talonavicular joint was confirmed by radiography, and the diagnosis of Charcot’s arthropathy of the right midfoot was made (see figures 1 and 2). The patient was managed conservatively by orthopedic and podiatry specialists with avoidance of weight-bearing and use of orthotics.

In 2004, the patient suffered from a chronic ulcer at the plantar surface of her right foot. The ulcer failed to heal after three to four months of repeated wound debridement and courses of oral antibiotics. The patient underwent excision of the foot ulcer and underlying bony prominence by her podiatrist. She recovered well from surgery without recurrence of the foot ulcer.

Pornpoj Pramyothin, MD

Stephanie L. Lee

The patient currently complains of numbness but denies painful or tingling sensation in her feet. She has been able to ambulate with some difficulty, requiring occasional use of a cane. She has been compliant with use of surgical shoes and custom inlay. She lives independently and works full-time as a senior secretary.

‘Rocker-bottom’ deformity

Examination of her feet revealed absent vibratory and proprioceptive sensation in both feet that were warm to touch. Ankle reflexes were absent bilaterally. Dorsalis pedis pulses were strong and present in both feet, and symmetric. Pes planus deformity with instability of the right forefoot and a well-healed surgical scar at the plantar surface of her right foot were noted.

Plain films of the right foot from seven, five and two years ago demonstrate typical radiographic changes of diabetic Charcot’s arthropathy (figures 1 and 2). In the oblique films of the right foot (figure 1), progressive resorption and sclerotic changes of the small bones of the midfoot (cuboid, cuneiforms and navicular) and progressive dislocation of the navicular bone with compression deformity caused by the anterior end of the talus are noted. Osseous fragments are noted throughout the mid- and hindfoot. Lateral films of the right foot again demonstrate the dislocation of the navicular bone, and subluxation of the cuboid and cuneiforms above the talus, resulting in direct articulation between the talus and fourth and fifth metatarsals (figure 2). There is progressive loss of the foot arch (pes planus deformity), resulting in the classic “rocker-bottom” deformity (figure 2).

Charcot’s arthropathy (diabetic neuropathic arthropathy/diabetic osteoarthropathy) is defined as a progressive deformity of the foot caused by joint dislocation, pathological fractures and severe destruction of the foot architecture in association with peripheral neuropathy. It was first described by Charcot in 1868 in patients with peripheral neuropathy due to tabes dorsalis. Diabetes has surpassed tertiary syphilis as the leading cause of this condition in the contemporary era.

Charcot’s arthropathy in diabetes most commonly affects the foot and ankle, usually in a neuropathic limb with good vascular perfusion. This condition should always be considered in a unilateral, warm and swollen foot in a patient with neuropathy. Early disease may have a normal bone appearance, but the bone injury can be detected with a technetium diphosphonate bone or MRI scan. It is thought that this condition is caused by diabetic neuropathy that results in a loss of protective sensation and increased peripheral blood flow due to autonomic dysfunction.

Figure 1: Oblique images of the right foot show the radiographic changes over time of diabetic Charcot’s arthropathy. Photos courtesy of: Stephanie L. Lee

Figure 2: Lateral radiographs of the right foot show pes planus deformity.

Eight to 12 weeks of treatment

The lack of proprioception leads to repetitive damage to the joint by minor trauma, with resultant microfracture, ligamentous laxity, joint subluxation and instability. Further destruction of the joints occurs with continued weight-bearing. Autonomic neuropathy leads to impairment of vascular smooth muscle tone and vasodilatation, which causes hyperemic bone resorption. It has also been proposed that cytokines from local inflammation may be responsible for the increase in osteoclastic activity and bone remodeling. Fracture, trauma and orthopedic procedures such as amputation are known associated factors of Charcot’s arthropathy, as these conditions lead to mechanical imbalance, abnormal joint pressures and enhanced local inflammation.

Treatment of Charcot’s arthropathy involves eight to 12 weeks of nonweight-bearing, with transition to partial and full weight-bearing on the affected limb over three to six months. Compressive dressings, removable cast walker, pneumatic walking brace, total contact cast and simple assistive devices such as crutches, wheelchair or walker have been used successfully to immobilize and off-load affected joints. Early studies have suggested beneficial roles of bisphosphonates (intravenous pamidronate and oral alendronate) and intranasal calcitonin in reducing pain, markers of bone turnover and loss of foot bone density in patients with Charcot’s arthropathy when used as an adjunct to conventional measures.

Surgery is best avoided in most cases but may be offered to patients with joint instability, deformity and progressive destruction despite immobilization. Arthrodesis may provide relief of pain attributable to chronic instability. Recurrent ulcers with underlying bony prominences may require partial ostectomy to allow proper wound healing. Major foot reconstructions and arthrodeses are reserved for younger patients with limited medical comorbidities. Glycemic control and involvement of a multidisciplinary team of endocrinologists, orthopedists and podiatrists remain the cornerstone in the prevention of morbidity and loss of limb due to Charcot’s arthropathy.

Pornpoj Pramyothin, MD, is a Fellow in the Section of Endocrinology, Diabetes and Nutrition, and Stephanie L. Lee, MD, PhD, is Associate Chief in the Section of Endocrinology, Diabetes and Nutrition, and Associate Professor of Medicine, both at Boston University Medical Center.

For more information:

• Bem R. Diabetes Care. 2006;29:1392-1394.
• Frykberg RG. Charcot arthropathy in the diabetic foot. In: Veves A, Giurini JM, LoGerfo FW, eds. The Diabetic Foot. 2nd ed. Totowa, NJ: Humana Press; 2006:269-298.
• Jeffcoate WJ. Lancet. 2005;366:2058-2061.
• Pitocco D. Diabetes Care. 2005;28:1214-1215.