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Current Insights On Treating Charcot Arthropathy And Related Complications
These authors discuss the treatment of Charcot foot in a Native American man complicated by hardware failure, nonunion, a second incidence of Charcot, patient non-adherence and osteomyelitis.
Charcot arthropathy is a non-infectious, destructive joint disease most commonly affecting the foot and ankle. Although initially described by Jean M. Charcot, MD, in 1868 in conjunction with tabes dorsalis resulting from tertiary syphilis, it wasn’t until 1936 that Jordan noted the relationship of Charcot with diabetes.1,2 The connection between Charcot and diabetes is widely recognized.3
The national average prevalence of diabetes is 9.3 percent among adults age 20 or older. The diabetes prevalence of 16 percent among Native American adults age 20 or older is significantly higher than the national average.4 With a higher rate of diabetes, Charcot events naturally occur in greater frequency and severity amid the Native American population.
Due to the rapidly destructive nature of Charcot arthropathy, one should treat every case as an emergency. Many factors affect patient outcome following a Charcot event. These factors may include choice of treatment, patient adherence and overlying infection or other complicating events.
The following case report outlines the management and treatment of Charcot arthropathy in the foot of a Native American man with diabetes. The treatment process was complicated by hardware failure, non-union, a second Charcot event, patient non-adherence and osteomyelitis.
What You Should Know About The Initial Patient Presentation And Surgery
A 55-year-old Navajo man presented to the emergency room with a chief complaint of a red, hot, swollen right foot. The patient’s heart rate, respiratory rate and temperature were all within normal limits. Physicians suspected Charcot and ordered plain radiographs.5 Figure 1 demonstrates osteolysis with diffuse soft tissue edema and partial collapse of the midfoot, all indications of Charcot.5
The patient’s leg was immobilized with a total contact cast for a period of four weeks. The foot subsequently demonstrated signs of coalescence and the inflammation subsided. The attending physician performed a tibiotalocalcaneal arthrodesis and utilized an intramedullary nail in conjunction with an external fixation device to stabilize the foot. We placed a 0.062 K-wire through the anterior aspect of the now partially dislocated medial column and extended it through the navicular into the talar head (see Figures 2-9). The patient was non-weightbearing during the 12-week post-op recovery.
We removed the external fixation device 12 weeks post-surgery. While the intramedullary nail fixation remained in place, we still noted significant soft tissue edema. The K-wire through the midfoot is beginning to back out of the talar head, indicating initial hardware failure (see Figures 10-12). We removed the medial column pin in the clinic after the pin backed out through the skin one month after the first tibiotalocalcaneal fusion.
Addressing The Patient’s Post-Op Complications
The patient began cautious weightbearing but experienced pain and discomfort in his ankle during gait. The patient expressed this continued pain and discomfort at his two-week follow-up appointment. In addition, the patient again experienced inflammation, edema, erythema and heat in the right foot. Plain radiographs demonstrated both a nonunion at the attempted tibiotalocalcaneal arthrodesis and a second midfoot Charcot event within the fragmentation phase (see Figures 13-17).6 The patient was again immobile per the recommended protocol.5
Three weeks after the second Charcot event, radiographs demonstrated that the nonunion at the tibiotalar joint was unchanged (see Figures 18-20). Against the attending physician’s recommendation, the patient left the hospital to attend to personal affairs.
The patient presented to the emergency room three weeks after leaving the hospital with a red, hot, swollen foot and ankle, and no palpable adenopathy. The hardware, however, was exposed, with the calcaneal screw having penetrated and exited the skin of the posterior calcaneus. Emergency room physicians removed the screw as it was completely loose. Radiographic imaging indicated no gas was present within the tissue (see Figures 21-22). The patient was readmitted and put on IV vancomycin and piperacillin/tazobactam. Although signs of infection were prevalent and the patient had a history of exposed hardware, the patient declined surgery as he was not mentally prepared. He was offered a psych consult but declined.
The patient agreed to surgery one week following his presentation with exposed hardware at the ER. We removed the intramedullary nail due to the risk of contamination. Upon exposure of the ankle joint, the bone in both the distal tibia and dorsal talus showed signs of osteomyelitis. The patient had ankle joint resection with copious irrigation. We obtained multiple deep bone biopsies to avoid a sampling error. We sized an antibiotic spacer and placed it in the ankle joint to aid in treatment of the osteomyelitis. The patient had external fixation with placement of smooth pins away from the infection site (see Figures 23-25).
A Closer Look At The Post-Op Course
The external fixation remained in place for eight weeks. We removed antibiotic spacers and performed copious irrigation (see Figures 26-28). We obtained clean bone biopsies from multiple sites. The pathology report returned with clean biopsies.
The patient has remained in the hospital for the course of his treatment due to difficult social circumstances. He is currently awaiting further treatment with the current plan to attempt another tibiotalocalcaneal arthrodesis.
Dr. Bland is in private practice at the New Mexico Bone and Joint Institute.
Dr. Anderson is in private practice at the New Mexico Bone and Joint Institute.
Mr. Simmons is a fourth-year student at the Midwestern University School of Podiatric Medicine.
References
1. Charcot JM. On some arthropathies which seem to depend on a lesion of the brain or spinal cord (in French). Arch Physiol Norm Pathol. 1868;1:161–178.
2. Jordan WR. Neuritic manifestations in diabetes mellitus. Arch Intern Med. 1936;57:307–366.
3. Rogers LC, Frykberg RG, Armstrong DG, et al. The Charcot foot in diabetes. Diabetes Care. 2011;34(9):2123–2129.
4. Schiller JS, Ward BW, Freeman G, Peregoy JA. Early release of selected estimates based on data from the 2012 National Health Interview Survey. National Center for Health Statistics. June 2013. Available from: https://www.cdc.gov/nchs/nhis.htm .
5. Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders: a clinical practice guideline (2006 revision). J Foot Ankle Surg. 2006; 45(Suppl 5):S1-66.
6. Rosenbaum AJ, DiPreta JA. Classifications in brief: Eichenholtz classification of Charcot arthropathy. Clin Orthop Rel Res. 2004; 473(3):1168–1171.
