JBJS | Elevated Peak Plantar Pressures in Patients Who Have Charcot Arthropathy*

The Journal of Bone & Joint Surgery, Volume 80, Issue 3

Articles | March 01, 1998

Elevated Peak Plantar Pressures in Patients Who Have Charcot Arthropathy*

DAVID G. ARMSTRONG, D.P.M.†; LAWRENCE A. LAVERY, D.P.M., M.P.H.†, SAN ANTONIO, TEXAS

Investigation performed at the Department of Orthopaedics, The University of Texas Health Science Center at San Antonio, and The Diabetic Foot Research Group, San Antonio

The Journal of Bone & Joint Surgery. 1998; 80:365-9

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Abstract

Although diabetes and peripheral neuropathy are perhaps the most important risk factors for neuropathic osteoarthropathy, we hypothesized that peak plantar pressures may also be higher in patients who have this condition. We are unaware of any reports in the medical literature that have specifically addressed this hypothesis.We obtained data from the medical records of 164 diabetic patients who had been managed in a multidisciplinary tertiary-care diabetic foot-specialty clinic. We then divided the patients into four groups: those who had acute Charcot arthropathy, those who had neuropathic ulceration, those who had neuropathy without ulceration, and those who had neither neuropathy nor ulceration. The peak plantar pressures were significantly higher in the patients who had acute Charcot arthropathy and those who had a neuropathic ulcer (p < 0.001 for both) compared with the pressures in those who had no history of arthropathy and those who had neuropathy without ulceration. With the numbers available, we could not detect a significant difference in the peak pressure between the affected and the unaffected foot in the patients who had Charcot arthropathy (mean [and standard deviation], 100 ± 8.5 compared with 101 ± 9.6 newtons per square centimeter; p > 0.05). However, the mean peak pressure was significantly higher on the ulcerated side than on the contralateral side in the patients who had a neuropathic ulcer (90 ± 18.8 compared with 86 ± 20.7 newtons per square centimeter; p < 0.02). Although the midfoot was the site of maximum involvement in all patients who had Charcot arthropathy, the peak plantar pressure was on the forefoot, suggesting that the forefoot may function as a lever, forcing collapse in the midfoot.

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Introduction

Introduction | Materials and Methods | Results | Discussion | References

A Charcot joint (neuropathic osteoarthropathy) is a progressive condition affecting the musculoskeletal system and characterized by pathological fracture, dislocation of the joint, and often debilitating deformity⁸. In developed nations, the condition is most commonly encountered in diabetic individuals. The prevalence of this sequela in diabetics is variable, ranging from 0.16 per cent (101 of 63,125)²⁴ of all diabetic patients to as high as 13 per cent (fifty-five of 423) of high-risk patients⁸. It appears that this condition is being diagnosed more frequently as a result of increased awareness of its signs and symptoms.

Although the arthropathy was first described¹⁷ as early as 1703, Charcot provided the first concise description of the neuropathic component of the disease in 1868; he linked the degenerative condition to syphilis, then a common malady. Syphilis was the disease most commonly associated with the arthropathy for several decades, until Jordan linked the arthropathy to diabetes mellitus in 1936. Since the first descriptions of neuropathic arthropathy nearly three centuries ago, numerous theories have been postulated in an attempt to explain the etiology of the condition^11,14,18.

Currently, the prevailing theory suggests that, following the development of autonomic neuropathy, there is an increased blood flow to the extremity, resulting in osteopenia. Subsequently, motor neuropathies result in muscle imbalance, placing abnormal stress on the affected extremity, while sensory neuropathies render the patient unaware of the often profound osseous destruction taking place over time during walking^10,12,15. Although diabetes and peripheral neuropathy are perhaps the most important risk factors for neuropathic osteoarthropathy, we believe that higher peak plantar pressures may also be associated with this condition. We are unaware of any reports in the medical literature confirming this belief. Therefore, the purpose of the current study was to compare peak plantar pressures between patients who had acute Charcot arthropathy and those who had a neuropathic ulcer, those who had neuropathy but no history of ulceration, and those who had no neuropathy and no history of ulceration.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

†Department of Orthopaedics, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78284-7776. E-mail address for Dr. Armstong: armstrong@usa.net.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

†Department of Orthopaedics, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78284-7776. E-mail address for Dr. Armstong: armstrong@usa.net.

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TABLE I DATA ON THE FOUR GROUPS OF PATIENTS

*The values are given as the mean and standard deviation.†p < 0.05 compared with the other groups.

	Charcot Arthropathy	No Neuropathy or Ulcer	Neuropathy without Ulcer	Neuropathic Ulcer
No. of patients	21	61	21	61
Age* (yrs.)	58.1 ± 8.96	50.2 ± 9.68	57.8 ± 10.61	52.5 ± 10.52
Male gender (no. of patients)	10 (48%)	22 (36%)	10 (48%)	45 (74%)†
Duration of diabetes* (yrs.)	16.8 ± 6.2	6.8 ± 4.2†	16.2 ± 12.7	16.0 ± 4.6

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TABLE I DATA ON THE FOUR GROUPS OF PATIENTS

*The values are given as the mean and standard deviation.†p < 0.05 compared with the other groups.

	Charcot Arthropathy	No Neuropathy or Ulcer	Neuropathy without Ulcer	Neuropathic Ulcer
No. of patients	21	61	21	61
Age* (yrs.)	58.1 ± 8.96	50.2 ± 9.68	57.8 ± 10.61	52.5 ± 10.52
Male gender (no. of patients)	10 (48%)	22 (36%)	10 (48%)	45 (74%)†
Duration of diabetes* (yrs.)	16.8 ± 6.2	6.8 ± 4.2†	16.2 ± 12.7	16.0 ± 4.6

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Fig. 1 Distribution of the sixty-one lesions in the group that had a neuropathic ulcer.

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Fig. 2 Graph showing the mean peak plantar pressures in the four groups. The pressures in the patients who had acute Charcot arthropathy and in those who had a neuropathic ulcer were significantly higher than those in the patients who had no history of neuropathy and those in the patients who had neuropathy without ulceration (p < 0.001). The I-bars represent the standard deviation.

Materials and Methods

Introduction | Materials and Methods | Results | Discussion | References

Data were obtained from the medical records of 164 patients who had been managed in a multidisciplinary tertiary-care diabetic foot-specialty clinic between February 1, 1991, and July 1, 1994. These patients were subsequently divided into four groups (Table I).

The first group included twenty-one patients who had acute Charcot arthropathy and no concurrent ulceration. We classified Charcot arthropathy into two treatment-oriented phases, acute and post-acute, on the basis of radiographic¹³, dermal thermometric^2,6, and clinical signs³. As has been described previously⁸, the initial diagnosis of acute Charcot arthropathy was based on profound swelling, locally increased skin temperature, erythema, joint effusion, and bone resorption in an insensate foot. Only patients who had acute Charcot arthropathy were selected for inclusion in the group. Eighteen patients who had been clinically and histologically diagnosed or managed before being seen at our facility were excluded from the analysis. No patient who had concomitant ulceration and Charcot arthropathy was selected for the study. In order to standardize measurements of plantar pressure on the basis of deformity, we enrolled only patients who had Sanders pattern-II Charcot arthropathy, which is arthropathy involving the tarsometatarsal joint²³. This is the most common presenting site; in a previous study, 48 per cent (thirty-one) of sixty-four neuropathic arthropathies within the foot involved the tarsometatarsal joint⁸.

The second group included sixty-one patients who had a single neuropathic plantar ulcer of the forefoot. According to the wound-classification system of The University of Texas²⁰, all ulcers were grade 1A, meaning that they were non-infected, non-ischemic, full-thickness lesions through the epidermis and dermis that did not involve tendon, capsule, or bone. Twenty-six lesions were located plantar to the first metatarsal head; thirteen, plantar to the great toe; eight, plantar to the fifth metatarsal head; and seven, four, and three, plantar to the second, third, and fourth metatarsal heads, respectively (Fig. 1).

The third group comprised twenty-one patients who had neuropathy (loss of protective sensation according to criteria described previously⁷)) but no history of ulceration.

The fourth group consisted of sixty-one subjects who had never had an ulcer of the foot and had intact protective sensation (foot-category 0 according to the diabetic foot-classification system of The University of Texas^5,21).

The patients who had Charcot arthropathy, a neuropathic ulcer, or neuropathy only had clinical loss of protective sensation to the ten-gram Semmes-Weinstein monofilament wire when they were examined with the method and criteria described previously⁷. All subjects were diagnosed as having diabetes mellitus on the basis of the criteria of the World Health Organization, which include treatment with insulin or oral administration of a hypoglycemic agent, two random glucose measurements of more than 200 milligrams per deciliter (11.1 millimoles per liter), or a fasting glucose level of more than 140 milligrams per deciliter (7.8 millimoles per liter). All subjects had palpable pedal pulses on initial evaluation.

We used the EMED pressure platform system (Novel, Dusseldorf, Germany) to evaluate dynamic barefoot pressures on the sole of the foot for all subjects. Pressures were measured in newtons per square centimeter. A mean of the peak pressures from three mid-gait steps was used for purposes of analysis. We performed an analysis of variance to identify differences among the four study groups. If a significant difference was identified between groups, we used the Tukey studentized range test for simultaneous multiple comparisons to determine which treatments were and were not significantly different²². We used a chi-square test to compare the prevalence of gender according to group, and we used a Student t test for matched pairs to compare differences in peak pressure between the affected and the contralateral foot. For all analyses, we used a significance (alpha) level¹⁹ of 0.05.

Results

Introduction | Materials and Methods | Results | Discussion | References

With the number of patients available for study, we could not detect a significant difference between the mean peak plantar pressures (with standard deviation) at the affected site and the contralateral extremity in the patients who had acute Charcot arthropathy (100 ± 8.5 compared with 101 ± 9.6 newtons per square centimeter), in those who had neuropathy only (65 ± 25.6 compared with 67 ± 23.5 newtons per square centimeter), or in those who had no neuropathy or history of ulcer (45 ± 8.0 compared with 47 ± 9.7 newtons per square centimeter). However, the group that had a neuropathic ulcer had a significantly higher mean peak plantar pressure on the ulcerated side than on the non-ulcerated side (90 ± 18.8 compared with 86 ± 20.7 newtons per square centimeter; p < 0.02). In all groups, including the one with Charcot arthropathy, the peak plantar pressure was noted at the level of the metatarsal heads or distally. The peak plantar pressure was at the site of the neuropathic ulcer in all patients who had such a lesion.

The mean peak plantar pressure differed significantly between the group that had Charcot arthropathy (100 ± 8.5 newtons per square centimeter) and the group that had no neuropathy or ulcer (45 ± 8.0 newtons per square centimeter) as well as the group that had neuropathy only (65 ± 25.6 newtons per square centimeter) (p < 0.001 for both comparisons). However, we could detect no significant difference in the mean peak plantar pressure between the group that had Charcot arthropathy and the group that had a neuropathic ulcer (90 ± 18.8 newtons per square centimeter) (Fig. 2). The group that had no neuropathy or ulcer had a significantly lower mean peak plantar pressure than the other three groups (p < 0.01 for all three comparisons).

Although we could not detect a significant difference in gender between the group that had Charcot arthropathy and either the group that had no neuropathy or ulcer or the group that had neuropathy only (Table I), there was a significantly higher proportion of men (74 per cent) in the group that had a neuropathic ulcer than in the group that had Charcot arthropathy (p < 0.04), the group that had neuropathy only (p < 0.04), and the group that had no neuropathy or ulcer (p < 0.0001) (Table I). The patients who had Charcot arthropathy were significantly older than those who had a neuropathic ulcer (p <0.04) and those who had no neuropathy or ulceration (p < 0.003). There was also a significant age difference between the group that had a neuropathic ulcer and the group that had no neuropathy or ulceration (p <0.005).

Discussion

Introduction | Materials and Methods | Results | Discussion | References

High peak plantar pressures have been identified as a risk factor for ulceration and prolonged healing in patients who have diabetes^4,8. It has long been thought that neuropathy, high peak plantar pressures, and repetitive stress may play a pivotal role in the development of Charcot arthropathy, much as they do in the development of neuropathic ulcers⁸. The current etiological theory suggests that, following the development of autonomic neuropathy, there is an increased blood flow to the extremity, resulting in osteopenia. Motor neuropathies subsequently lead to muscle imbalance that places abnormal stress on the affected extremity. Finally, sensory neuropathy renders the patient unaware of the profound osseous destruction that takes place in the Charcot fracture process^{9,10,12,15,25}. The data in the current study lend at least partial support to this conclusion. The patients who had Charcot arthropathy and those who had a neuropathic ulcer had significantly higher peak plantar pressures than their diabetic counterparts who had no history of neuropathy and those who had neuropathy without ulceration (p < 0.001). It is unclear why the patients who had acute Charcot arthropathy did not have a higher peak plantar pressure on the contralateral (unaffected) side. Additional studies are needed to determine why Charcot arthropathy develops in one limb but not the other (in the absence of a clear history of trauma). In a previous, longitudinal study of Charcot arthropathy, we found that forty-one (75 per cent) of fifty-five subjects could not identify a specific episode of trauma⁸.

Interestingly, all sites of peak plantar pressure were in the forefoot, even in the group that had a Charcot joint, although the primary site of the Charcot arthropathy was the tarsometatarsal (Lisfranc) joint complex. The tarsometatarsal joint has been reported to be the most common site of neuroarthropathic collapse in diabetic patients⁸, and this area may be consistently involved because it becomes the focus of forces between the forefoot and the hindfoot. The Achilles tendon pulls the hindfoot into plantar flexion, causing the forefoot to bear a considerably increased load; this forces the central aspect of the foot (the bones in the region of the tarsometatarsal joint) to fracture and collapse. Ultimately, this type of fracture can progress to a deformity in which the medial longitudinal arch collapses, concentrating the bulk of plantar pressures on the midfoot. However, this was not the case in our patients who had Charcot arthropathy because the signs and symptoms of acute Charcot arthropathy were identified early, before profound destruction took place. High peak pressure and sensory neuropathy in the forefoot coupled with a relative equinus deformity in the hindfoot before arthropathy develops may predispose patients to this cascade of events. One limitation of the current study was that we could not clearly demonstrate a cause-and-effect relationship between increased peak plantar pressure in the forefoot and Charcot arthropathy. Although we believe that such increased pressure in the forefoot may trigger an event in the midfoot, we cannot rule out the converse.

Abnormal pressures on the sole of the foot have previously been linked to the development of neuropathic foot ulcers in diabetic patients⁴. Furthermore, increased peak plantar pressures of more than sixty-five newtons per square centimeter have been associated with an increased risk of diabetic ulceration of the foot²¹. Screening to identify patients who have both sensory peripheral neuropathy and high plantar pressures should be used to identify diabetic patients who are at high risk for the development of ulcers of the foot and Charcot arthropathy. These patients should be referred to specialty clinics, intensively educated, evaluated on a regular basis for precursors of lesions of the foot, and provided with therapeutic footwear and insoles to reduce pressures on the foot and to protect it from incidental trauma.

Screening may be as simple as inspection of the foot for deformity or callus. Young et al. demonstrated that pressures on the foot increased significantly when callus formed on the sole of the foot (p < 0.001). Débridement of callus and the use of therapeutic stockings, insoles, and shoes have all been shown to decrease abnormal pressures on the foot²⁷. In addition, relatively inexpensive force-plate systems can be used to quantify abnormal pressures. Because many patients may not have callus as a precursor to ulceration or Charcot arthropathy, force-plates can provide reproducible, objective data concerning the magnitude and location of forces in the sole of the foot. In a health-care environment with dwindling resources, it becomes increasingly important to use selection criteria to stratify patients and to allocate appropriate resources. We believe that the measurement of plantar pressures coupled with a specific evaluation of protective sensation may be an effective means of screening a large number of patients within a relatively short period.

References

Introduction | Materials and Methods | Results | Discussion | References

Armstrong, D. G., and Lavery, L. A.: Monitoring neuropathic ulcer healing with infrared dermal thermometry. J. Foot and Ankle Surg.,35: 335-338, 1996.35335 1996

Armstrong, D. G., and Lavery, L. A.: Monitoring healing of acute Charcot's arthropathy with infrared dermal thermometry. J. Rehab. Res. and Devel.,34: 317-321, 1997.34317 1997

Armstrong, D. G., and Lavery, L. A.: Acute Charcot arthropathy of the foot and ankle. Phys. Ther.,78: 74-80, 1998.7874 1998 [PubMed]

Armstrong, D. G.; Lavery, L. A.; and Bushman, T. R.: Peak foot pressures influence healing time of diabetic ulcers treated with total contact casting. J. Rehab. Res. and Devel.,35: 1-5, 1998.351 1998

Armstrong, D. G.; Lavery, L. A.; and Harkless, L. B.: Treatment-based classification system for assessment and care of diabetic feet. J. Am. Podiat. Med. Assn.,86: 311-316, 1996.86311 1996

Armstrong, D. G.; Lavery, L. .; Liswood, P. L.; Todd, W. F.; and Tredwell, J. A.: Infrared dermal thermometry for the high-risk diabetic foot. Phys. Ther.,77: 169-177, 1997.77169 1997 [PubMed]

Armstrong, D. G.; Lavery, L. A.; Vela, S. A.; Quebedeaux, T. L.; and Fleischli, J. G.: Choosing a practical screening instrument to identify patients at risk for diabetic foot ulceration. Arch. Intern. Med.,158: 289, 1998.158289 1998 [PubMed]

Armstrong, D. G.; Todd, W. F.; Lavery, L. A.; Harkless, L. B.; and Bushman, T. R.: The natural history of acute Charcot's arthropathy in a diabetic foot specialty clinic. Diabetic Med.,14: 357-363, 1997.14357 1997 [PubMed]

Banks, A. S., and McGlamry, E. D.: Charcot foot. J. Am. Podiat. Med. Assn.,79: 213-235, 1989.79213 1989

Brower, A. C., and Allman, R. M.: The neuropathic joint: a neurovascular bone disorder. Radiol. Clin. North America,19: 571-580, 1981.19571 1981

Charcot, J.-M.: Sur quelques arthropathies. Qui paraissent dépendre d'une lésion. Du cerveau ou de la moelle épinière. Arch. physiol. norm. pathol.,1: 161-178, 1868.1161 1868

Edmonds, M. E.; Clarke, M. B.; Newton, S.; Barrett, J.; and Watkins, P. J.: Increased uptake of bone radiopharmaceutical in diabetic neuropathy. Quart. J. Med.,57: 843-855, 1985.57843 1985 [PubMed]

Eichenholtz, S. N.: Charcot Joints. Springfield, Illinois, Charles C Thomas, 1966.

Eloesser, L.: On the nature of neuropathic affections of the joints. Ann. Surg.,66: 201-207, 1917.66201 1917 [PubMed]

Finsterbush, A., and Friedman, B.: The effect of sensory denervation on rabbits' knee joints. A light and electron microscopic study. J. Bone and Joint Surg.,57-A: 949-956, Oct. 1975.57-A949 1975

Jordan, W. R.: Neuritic manifestations in diabetes mellitus. Arch. Intern. Med.,57: 307-366, 1936.57307 1936

Kelly, M.: De arthritide symptomatica of William Musgrave (1657-1721): his description of neuropathic arthritis. Bull. Hist. Med.,37: 372-377, 1963.37372 1963 [PubMed]

Kelly, M.: John Kearsley Mitchell (1793—1858) and the neurogenic theory of arthritis. A reappraisal. J. Hist. Med.,20: 151-156, 1965.20151 1965

Kirkwood, B. R.: Essentials of Medical Statistics, pp. 87-117. Oxford, Blackwell Scientific, 1988.

Lavery, L. A.; Armstrong, D. G.; and Harkless, L. B.: Classification of diabetic foot wounds. J. Foot and Ankle Surg.,35: 528-531, 1996.35528 1996

Lavery, L. A.; Armstrong, D. G.; Vela, S. A.; Quebedeaux, T. L.; and Fleischli, J. G.: Practical criteria for screening patients at high risk for diabetic foot ulceration. Arch. Intern. Med.,158: 158-162, 1998.158158 1998

Neter, J.; Wasserman, W.; and Kutner, M. H.: Applied Linear Statistical Models, edited by J. Neter. Ed. 3, pp. 580-585. Boston, Irwin Publishing, 1990.

Sanders, L., and Mrdjenovich, D.: Anatomical patterns of bone and joint destruction in neuropathic diabetics [abstract].. Diabetes,40 (Supplement 1): 529A, 1991.40 (Supplement 1)529 1991

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Fig. 1 Distribution of the sixty-one lesions in the group that had a neuropathic ulcer.

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TABLE I DATA ON THE FOUR GROUPS OF PATIENTS

*The values are given as the mean and standard deviation.†p < 0.05 compared with the other groups.

	Charcot Arthropathy	No Neuropathy or Ulcer	Neuropathy without Ulcer	Neuropathic Ulcer
No. of patients	21	61	21	61
Age* (yrs.)	58.1 ± 8.96	50.2 ± 9.68	57.8 ± 10.61	52.5 ± 10.52
Male gender (no. of patients)	10 (48%)	22 (36%)	10 (48%)	45 (74%)†
Duration of diabetes* (yrs.)	16.8 ± 6.2	6.8 ± 4.2†	16.2 ± 12.7	16.0 ± 4.6

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TABLE I DATA ON THE FOUR GROUPS OF PATIENTS

*The values are given as the mean and standard deviation.†p < 0.05 compared with the other groups.

	Charcot Arthropathy	No Neuropathy or Ulcer	Neuropathy without Ulcer	Neuropathic Ulcer
No. of patients	21	61	21	61
Age* (yrs.)	58.1 ± 8.96	50.2 ± 9.68	57.8 ± 10.61	52.5 ± 10.52
Male gender (no. of patients)	10 (48%)	22 (36%)	10 (48%)	45 (74%)†
Duration of diabetes* (yrs.)	16.8 ± 6.2	6.8 ± 4.2†	16.2 ± 12.7	16.0 ± 4.6