Biomedical subjects
Publications and source records attributed to R G Frykberg.
Acute and chronic Charcot's foot deformity is a progressive, disabling and disfiguring condition that is prone to ulceration and infection. If conservative treatment is ineffective, bone and soft-tissue reconstruction is a viable option.
The purpose of this manuscript was to describe a classification of diabetic foot surgery performed in the absence of critical limb ischaemia. The basis of this classification is centered on three fundamental variables which are present in the assessment of risk and indication: 1) the presence or absence of neuropathy (loss of protective sensation); 2) the presence or absence of an open wound; 3) the presence or absence of acute, limb-threatening infection. The conceptual framework for this classification is to define distinct classes of surgery in an order of theoretically increasing risk for high-level amputation. These classes include: Class I: Elective Diabetic Foot Surgery (procedures performed to treat a painful deformity in a patient without loss of protective sensation); Class II: Prophylactic (Procedure performed to reduce risk of ulceration or reulceration in person with loss of protective sensation but without open wound); Class III: Curative (Procedure performed to assist in healing open wound) and Class IV: Emergent (Procedure performed to limit progression of acute infection). The presence of critical ischaemia in any of these classes of surgery should prompt a vascular evaluation to consider a) the urgency of the procedure being considered and b) possible revascularization prior or temporally concomitant with the procedure. It is our hope that this system begins a dialogue amongst physicians and surgeons which can ultimately facilitate communication, enhance perspective, and improve care.
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Foot ulcerations, infections, and Charcot neuropathic osteoarthropathy are three serious foot complications of diabetes mellitus that can too frequently lead to gangrene and lower limb amputation. Consequently, foot disorders are one of the leading causes of hospitalization for persons with diabetes and can account for expenditures in the billions of dollars annually in the U.S. alone. Although not all foot complications can be prevented, dramatic reductions in their frequency have been obtained through the implementation of a multidisciplinary team approach to patient management. Using this concept, the authors present a Clinical Practice Guideline for diabetic foot disorders based on currently available evidence. The underlying pathophysiology and treatment of diabetic foot ulcers, infections, and the diabetic Charcot foot are thoroughly reviewed. Although these guidelines cannot and should not dictate the standard of care for all affected patients, they are intended to provide evidence-based guidance for general patterns of practice. The goal of a major reduction in diabetic limb amputations is certainly possible if these concepts are embraced and incorporated into patient management protocols.
Foot ulcerations, infections, and Charcot neuropathic osteoarthropathy are three serious foot complications of diabetes mellitus that can too frequently lead to gangrene and lower limb amputation. Consequently, foot disorders are one of the leading causes of hospitalization for persons with diabetes and can account for expenditures in the billions of dollars annually in the U.S. alone. Although not all foot complications can be prevented, dramatic reductions in their frequency have been obtained through the implementation of a multidisciplinary team approach to patient management. Using this concept, the authors present a Clinical Practice Guideline for diabetic foot disorders based on currently available evidence. The underlying pathophysiology and treatment of diabetic foot ulcers, infections, and the diabetic Charcot foot are thoroughly reviewed. Although these guidelines cannot and should not dictate the standard of care for all affected patients, they are intended to provide evidence-based guidance for general patterns of practice. The goal of a major reduction in diabetic limb amputations is certainly possible if these concepts are embraced and incorporated into patient management protocols.
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OBJECTIVE: High plantar foot pressures in association with peripheral neuropathy have been ascertained to be important risk factors for ulceration in the diabetic foot. Most studies investigating these parameters have been limited by their size and the homogeneity of study subjects. The objective of this study was therefore to ascertain the risk of ulceration associated with high foot pressures and peripheral neuropathy in a large and diverse diabetic population. RESEARCH DESIGN AND METHODS: We studied a cross-sectional group of 251 diabetic patients of Caucasian (group C) (n=121), black (group B) (n=36), and Hispanic (group H) (n=94) racial origins with an overall age of 58.5+/-12.5 years (range 20-83). There was an equal distribution of men and women across the entire study population. All patients underwent a complete medical history and lower extremity evaluation for neuropathy and foot pressures. Neuropathic parameters were dichotomized (0/1) into two high-risk variables: patients with a vibration perception threshold (VPT) > or =25 V were categorized as HiVPT (n=132) and those with Semmes-Weinstein monofilament tests > or =5.07 were classified as HiSWF (n=190). The mean dynamic foot pressures of three footsteps were measured using the F-scan mat system with patients walking without shoes. Maximum plantar pressures were dichotomized into a high-pressure variable (Pmax6) indicating those subjects with pressures > or =6 kg/cm2 (n=96). A total of 99 patients had a current or prior history of ulceration at baseline. RESULTS: Joint mobility was significantly greater in the Hispanic cohort compared with the other groups at the first metatarsal-phalangeal joint (C 67+/-23 degrees, B 69+/-23 degrees, H 82+/-23 degrees, P=0.000), while the subtalar joint mobility was reduced in the Caucasian group (C 21+/-8 degrees, B 26+/-7 degrees, H 27+/-11 degrees, P=0.000). Maximum plantar foot pressures were significantly higher in the Caucasian group (C 6.7+/-2.9 kg/cm2, B 5.7+/-2.8 kg/cm2, H 4.4+/-1.9 kg/cm2, P=0.000). Univariate logistic regression for Pmax6 on the history of ulceration yielded an odds ratio (OR) of 3.9 (P=0.000). For HiVPT, the OR was 11.7 (P=0.000), and for HiSWF the OR was 9.6 (P=0.000). Controlling for age, diabetes duration, sex, and race (all P < 0.05), multivariate logistic regression yielded the following significant associations with ulceration: Pmax6 (OR=2.1, P=0.002), HiVPT (OR=4.4, P=0.000), and HiSWF (OR=4.1, P=0.000). CONCLUSIONS: We conclude that both high foot pressures (> or =6 kg/cm2) and neuropathy are independently associated with ulceration in a diverse diabetic population, with the latter having the greater magnitude of effect. In black and Hispanic diabetic patients especially, joint mobility and plantar pressures are less predictive of ulceration than in Caucasians.
OBJECTIVE: We have compared the hyperemic response to heat and the endothelium-dependent and endothelium-independent vasodilatation between the dorsum of the foot and the forearm in diabetic neuropathic and non-neuropathic patients and healthy control subjects. RESEARCH DESIGN AND METHODS: We studied the cutaneous microcirculation in the forearm and foot in 15 diabetic patients with neuropathy, in 14 diabetic patients without neuropathy, and in 15 control subjects matched for age, sex, BMI, and in the case of diabetic patients, for the duration of diabetes. Patients with peripheral vascular disease and/or renal impairment were excluded. The cutaneous microcirculation of the dorsum of the foot and the flexor aspect of the forearm was tested in all subjects. Single-point laser Doppler was employed to measure the maximal hyperemic response to heating of the skin to 44 degrees C and laser Doppler imaging scanner was used to evaluate the response to iontophoresis of 1% acetylcholine chloride (Ach) (endothelium-dependent response) and 1% sodium nitroprusside (NaNP) (endothelium-independent response). RESULTS: The transcutaneous oxygen tension was lower in the neuropathic group at both foot and forearm level, while the maximal hyperemic response to heat was similar at the foot and forearm level in all three groups. The endothelium-dependent vasodilation (percent increase over baseline) was lower in the foot compared to the forearm in the neuropathic group (23 +/- 4 vs. 55 +/- 10 [mean +/- SEM]; P < 0.01)], the non-neuropathic group (33 +/- 6 vs. 88 +/- 14; P < 0.01), and the control subjects (43 +/- 6 vs. 93 +/- 13; P < 0.001). Similar results were observed during the iontophoresis of NaNP (P < 0.05). No differences were found among the three groups when the ratio of the forearm:foot response was calculated for both the endothelium-dependent (neuropathic group, 2.25 +/- 0.24; non-neuropathic group, 2.55 +/- 0.35; and control subjects, 2.11 +/- 0.26; P = NS) and endothelium-independent vasodilation (neuropathic group, 1.54 +/- 0.27; non-neuropathic group, 2.08 +/- 0.33; and control subjects, 2.77 +/- 1.03; P = NS). The vasodilatory response, which is related to the C nociceptive fiber action, was reduced at the foot level during iontophoresis of Ach in the neuropathic group. In contrast, no difference was found during the iontophoresis of NaNP at the foot and forearm level and of Ach at the forearm level among all three groups. CONCLUSIONS: In healthy subjects, the endothelial-dependent and endothelial-independent vasodilatation is lower at the foot level when compared to the forearm, and a generalized impairment of the microcirculation in diabetic patients with neuropathy preserves this forearm-foot gradient. These changes may be a contributing factor for the early involvement of the foot with neuropathy when compared to the forearm.
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Primary care of the diabetic patient with foot ulcer can be provided by medically or surgically trained practitioners. We have prospectively followed 90 sequential patients with newly developed foot ulcers from two major centers. One in the USA where the primary doctor was a podiatrist and one in Europe with a diabetologist. Thirty-four patients from Boston and 56 from Pisa (mean age, 55.6; range, 26-75 years; vs. 66.5; range, 35-94; P < 0.001), matched for sex, weight, type, duration of diabetes, renal impairment and retinopathy took part. Boston patients had more severe neuropathy, assessed with clinical examination utilizing a neuropathy disability score (NDS) (16 +/- 6 vs. 6 +/- 3 (mean +/- S.D.) P < 0.001) and vibration perception threshold (46 +/- 8 vs. 35 +/- 12 V: P < 0.001) while no difference existed in the number of patients with clinical infection, a history of lower extremity by-pass operation (6 (18%) vs. 3 (5%); P = NS) and in the size and the severity of the ulcer, according to the Wagner classification. Initial treatment was similar in both centers with emphasis on outpatient ulcer debridement, pressure relieving foot-wear and topical wound care. Hospitalization was needed in five (15%) Boston and 12 (21%) Pisa patients (P = NS) while surgery was performed on five (15%) Boston and 16 (29%) Pisa patients (P = NS). The in-hospital stay was similar in both centers (1.4 +/- 4.4 vs. 2.1 +/- 5.9 days; P = NS). The most common operations in both centers were incision, drainage and bone debridement. Ulcers healed in all patients but the amount of healing time was shorter in Boston patients (6.7 +/- 4.2 vs. 10.5 +/- 6.5 weeks; P < 0.02). We conclude that despite the differences in the two systems similar success rates were achieved in the two centers while a more surgically oriented strategy may have resulted in a slightly shorter healing time.
Through a discussion of the etiology and pathology of diabetic foot lesions with particular emphasis on ulceration and osteoarthropathy, the author will develop a plan for treatment and prevention using a multidisciplinary approach to such problems. Underlying risk factors including neuropathy, ischemia, infection, and, especially high pressures must be evaluated and appropriately ameliorated in order to promote resolution and avoidance of recidivism. Accordingly, conservative management with pressure-relieving devices, topical therapies, and prophylactic surgery on structural deformities plays an integral part in the overall podiatric management of the high-risk foot in diabetes mellitus.
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Diabetic osteoarthropathy, once considered a rare disorder, is becoming a more frequent finding in the growing diabetic population. However, the diagnosis is often not made during the critical early stages owing to a lack of familiarity with the disorder by the medical community. This article highlights the characteristics of the diabetic Charcot foot including cause and effect and treatment rationale.
The laser is a new therapeutic modality that is both applauded by its advocates and condemned by its critics. Its high cost is usually offset by high-volume use, leading to questions of ethics and overuse. This article addresses the controversy surrounding the laser and provides the reader with a basic understanding of its technology and its value in podiatry.
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Neuropathic arthropathy (Charcot's joint) is a relatively painless, progressive and degenerative condition due to underlying neurologic deficits. Although a variety of neurologic disorders may produce this arthropathy, diabetes mellitus has become the most common cause. In diabetes, the foot and ankle are the sites most often involved, particularly the tarsometatarsal and tarsal joints. In addition to neuropathy, trauma is an essential factor in producing the arthropathy.
The diabetic Charcot foot is a major limb-threatening complication of long-term diabetes mellitus and neuropathy. Although first described over 100 years ago, we are still lacking definitive studies regarding its prevalence in this population, precise etiology, or most effective treatments. Trauma in the presence of peripheral sensory neuropathy and abundant arterial perfusion seem to be the primary causal factors leading to this severe foot deformity. Misdiagnosis or delayed diagnosis of osteoarthropathy allows the destructive phase of this disorder to continue with resultant further destruction of the foot architecture. The authors discuss the natural history of this entity as well as potential treatment options and recommendations. Through a better understanding of the underlying pathogenesis, Charcot arthropathy can be more effectively managed and thereby limit the development of severe deformity, ulceration, infection and limb loss.