Mr. L, aged 53 years, with a history of recently diagnosed type 2 diabetes, presented to the foot clinic with a 1-month history of left foot swelling, redness and warmth. He was referred by his internist after not responding to various oral antibiotics prescribed for further evaluation and management.

The patient denied any recent or past trauma to his left foot or nausea, vomiting, fever, diaphoresis, chills, palpitations or shortness of breath for the past month. His work requires him to be on his feet most of the time, and Mr. L was anxious for his foot to recover.

The patient’s medical history included class I obesity, hypertension, hyperlipidemia, recently diagnosed type 2 diabetes for 4 years. He had smoked half a pack of cigarettes per day for 15 years. Mr. L attempted unsuccessfully to quit smoking previously without use of smoking cessation medications. He denied any past surgical history.

The patient’s medication profile included amoxicillin and clavulanic acid (Augmentin) 875 mg by mouth twice daily, metformin 500 mg by mouth twice daily, simvastatin 20 mg by mouth twice daily and enalapril 10 mg by mouth twice daily.

Mr. L reported that he did not perform glucose self-monitoring at home and was unaware of his glycemic control. However, he denied symptoms of hyperglycemia including polyuria, polydipsia,and blurred vision.

Labs

Hemoglobin A1C (HbA1c): 7.4%
Basic Metabolic within normal limits (blood urea nitrogen (BUN) 17, creatinine 1, glucose 94)
Complete Blood Count (CBC) with Differential within normal limits (white blood count was 6.5)
Liver function tests within normal limits
Magnetic resonance imaging (MRI)

Left foot dorsal dislocation of the cuneiforms and dorsal and lateral dislocation of the 4^th and 5^th metatarsals with high grade tear of the posterior tendon proximal to the navicular.

Examination

Vital Signs: 130/74, 82, 20, 98.6F
Weight: 235 lb
Height: 6’1”
BMI: 31

A focused examination revealed an obese man without signs of distress. The patient was alert, oriented, and conversant. Bilateral lower extremity with palpable pedal pulses, dorsalis pedis and posterior tibial pulses two plus equally, capillary refill less than 2 seconds, bilateral calf soft and nontender to palpation, bilateral groin nonpalpable lymph nodes.

The patient’s left foot was warm to touch, whereas his right foot had a tactile temperature within normal limits. The skin temperature on his left foot was six degrees Celsius warmer than the right foot. Left foot with two plus nonpitting edema and no erythema. Right foot no edema or erythema. Bilateral foot with skin intact. Absent monofilament forefoot 4/10 bilaterally, indicated diminished sensation.

The patient was diagnosed with acute Charcot arthropathy (CN) of the left foot.

Recommendation

The patient stopped all antibiotics. He was advised to wear a pneumatic short leg boot to left foot at all times that was to be removed only for foot cleansing and assessment.

To maintain nonweight bearing on left lower extremity, the use of crutches or knee walker was recommended. Radiographs of the patient’s left foot and ankle were scheduled for 3 weeks later.

Mr. L underwent smoking cessation counseling, and was e-prescribed a nicotine transdermal patch (NicoDerm CQ). A follow-up was scheduled for 3 weeks later.

Outcome

The patient returned in 3 weeks with persistent left foot edema, unchanged left foot temperature differential and no radiographic sign of bone healing.

Mr. L was recommended to undergo left foot arthrodesis with internal fixation due to refractory CN. The patient was referred back to his internist for preoperative glycemic management prior to surgery given HbA1c above 7%.

Two weeks later, Mr. L underwent ambulatory arthrodesis and was discharged home in a below-the-knee splint with instructions to observe 3 months of strict nonweight bearing.

Within the 3 months, the patient had repeat casting of the left lower extremity. Repeat radiograph indicated proper bone alignment maintained with joint union. The patient was transitioned to specialized foot wear (CROW Walker) and started weight bearing activities.

Discussion

Charcot neuropathic osteoarthropathy, also known as Charcot neuroarthropathy or Charcot foot, is a condition of localized inflammation leading to varying degrees and patterns of bone destruction, subluxation, dislocation and deformity of the foot and ankle.¹

It is named after Jean-Martin Charcot, a French neurologist who first described the condition in 1868 among patients with tertiary syphilis.

CN is a complication that can also be found in various conditions affected by peripheral neuropathy including HIV, leprosy, poliomyelitis, chronic alcoholism, tabes dorsalis, trauma, syringomyelia, Parkinson disease, sarcoidosis, rheumatoid disease and psoriasis. However, diabetic neuropathy remains the most prevalent cause internationally.¹

CN is a rare complication of diabetes, and perhaps the least recognized. The prevalence of CN among patients with diabetes is between 0.08% to 0.40% and as high as 13% in some patients.²

CN affects patient with both type 1 and type 2 diabetes. With 29.1 million people in the U.S. with diabetes, especially when one in 10 primary-care visits involve diabetes, the incidence of Charcot presenting at the primary care setting will inevitably increase.³

The diagnosis of CN is often delayed due to initially being mismanaged as cellulitis, osteomyelitis, acute gout or deep vein thrombosis. The only universal predisposing factor of CN is peripheral neuropathy. Other inconclusive risk factors include osteopenia, localized trauma (often minor), history of ulceration or infection, recent foot surgery including successful revascularization.¹

CN is a syndrome without definitive causation. The prevailing belief is that uncontrolled inflammation in the foot leads to osteolysis with consequent progressive fracture and dislocation. Another theory indicates that a neutrally mediated vascular reflex results in increased peripheral blood circulation and active bone resorption with consequent joint and bone destruction.¹

Typical manifestations of Charcot foot are a markedly edematous, warm (three to six degrees Celsius higher)and often erythematous foot with mild-to-moderate discomfort or pain and bounding pedal pulses, except when concealed by edema.

Chronic CN presents with more obvious musculoskeletal deformity and lower extremity ischemia.¹ X-rays are usually the initial imaging study of choice for diabetic foot disorders.

During the first 3 weeks of acute CN, there are usually no changes seen on foot x-rays. Radiographic evidence of dislocation and fracture appear at later stages.⁴ MRI is the study of choice in the timely diagnosis/confirmation of CN. In cases when MRI is contraindicated, nuclear medicine exams maybe used.¹

The initial management of acute Charcot foot is offloading to arrest the progression or prevention of deformity. Immobilization with repeat application of a total contact case (TCC) is the preferred offloading method.

Another option is to use a prefabricated removable walking cast also known as “instant TCC” (this was initially prescribed to Mr. L). Once healed, as indicated by resolution of acute symptoms, the patient will require protective weight bearing in the form of specialized foot wear to minimize recurrence or ulceration secondary to bony deformities (recommended to Mr. L after postoperative healing).

There is no conclusive evidence in the use of antiresorptive medications such as bisphosphonates in active CN and limited support for use of external bone stimulators in the management of Charcot ankle.¹

Surgical management is often reserved for patients not responding to offloading and immobilization or those with CN and chronic ulceration. There are three common surgical interventions for CN patients: exostectomy, Achilles tendon lengthening and arthrodesis.¹

Exostectomy involves shaving down bony prominences to alleviate bony pressure points which cause ulcerations. Achilles tendon lengthening involves making small cuts into the Achilles tendon to stretch the tendon to reduce forefoot pressure.

Arthrodesis involves permanent fusion of affected joints with the use of instrumentation due to chronic joint nonunion and or instability. Hardware used to stabilize the fusion may be placed internally (will not need to be removed, as in the case of patient Mr. L) or externally (requiring removal after 3 months).

Diabetes and cigarette smoking have been known to result in compromised surgical wound and bone healing. A study of patients who underwent subtalar arthrodesis reported a 3.8 times increase rate of nonunion in smokers compared with nonsmoker and that patients with diabetes were 18.7 times more likely to have a malunion.⁵

Nicotine causes vasoconstriction, increases platelet adhesion, reduces proliferation of red blood cells, fibroblasts and macrophages. Carbon monoxide decreases oxygen transport and metabolism. Hydrogen cyanide interferes with cellular oxidative metabolism and oxygen transport. ⁶

Over 100 physiologic factors have been implicated to cause poor wound healing in individuals with diabetes including decreased or impaired growth factor production, angiogenic response, macrophage function, collagen accumulation, epidermal barrier function, and keratinocyte and fibroblast migration and proliferation.⁶

If a fusion procedure fails, the patient will likely require a limb amputation in the near future. For the above reasons, Mr. L was high risk for poor surgical outcome and was started preoperatively on cigarette cessation therapy.

CN also affects psychological well-being. It is a chronic mobility limiting condition, predisposing patients to the life-long consequences of limb amputations. Although it is well recognized that patients with diabetes are at higher risk for depression than the general population, having diabetes and CN (without active ulcerations or amputations) further increases the level of depression and anxiety compared with those who have only diabetes. Those patients at the highest risk are within the CN-diabetes group are female, unemployed and nonwhite.⁴

In conclusion, clinicians managing patients with diabetes should be aware of CN as a diagnostic differential in individuals presenting with peripheral neuropathy and foot inflammation.

CN is a rare but potentially limb-threatening condition. Prevention is the best way to minimize CN risk for patients with diabetes. Clinicians can increase awareness of lower extremity complications through self-management education regarding complications of diabetic neuropathy and lower extremity issues, the importance of maintaining good glycemic control, and encouraging daily foot self-examination with routine foot assessment at each clinical care visit for early detection.

Patients with diabetes should be referred to a diabetic foot center for an annual comprehensive foot examination as recommend by the American Diabetes Association to detect and manage diabetic neuropathy and other foot complications.⁷

Annie D. Lu, ANP-BC, ADM-BC, practices at the NYULMC-Hospital for Joint Diseases Diabetic Foot and Ankle Center.

References

Rogers, LC et al. 2011; The Charcot Foot in Diabetes. Diabetes Care. 34: 2123-2129
Armstrong, DG, Todd, WF, Lavery, LA, Bushman, TR. 1997; The Natural History of Acute Charcot Arthropathy in a Diabetic Foot Specialty Clinic. Diabetic Medicine. 14 (5): 357-3663
Center for Disease Control and Prevention. 2014; National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States. US Department of Health and Human Services. Retrieved 10/9/14 from http://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes-report-web.pdf
Chapman, Z, Shuttleworth, CMJ, Huber, JW. High Levels of Anxiety and Depression in Diabetic Patients with Charcot Foot. 2014; Journal of Foot and Ankle Research. 7-22
Chahal, J et al. 2006; Factors Associated with Outcomes After Subtalar Arthrodesis. Journal of Orthopaedic Trauma. 20 (8): 555-561
Brem, H, Tomic-Canic, M. 2007; Cellular and Molecular Basics of Wound Healing in Diabetes. The Journal of Clinical Investigation 117 (5): 1219-1222
American Diabetes Association. 2014; Standards of Medical Care in Diabetes 2014. Diabetes Care. 37 (1): 514-577

All electronic resources accessed 12/18/2014.

This article originally appeared on Clinical Advisor

Foot Inflammation in Type 2 Diabetes