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Although diabetes mellitus is a biochemical disease, it has biomechanical consequences for the lower extremity. Numerous alterations occur in the function of the foot and lower extremity in people with diabetes. This article evaluates biomechanical alterations of the foot in the presence of neuropathy in patients with diabetes in the context of several theoretical concepts. Further study of these hypotheses will result in a better understanding of how diabetes causes elevated plantar pressures and the potential of strategies to prevent these changes so that the burden of diabetic foot disease can be reduced.
Emergency department visits for lower extremity complications of diabetes are extremely common throughout the world. Surprisingly, recent data suggest that such visits generate an 81.2% hospital admission rate with an annual bill of at least $1.2 billion in the United States alone. The likelihood of amputation and other subsequent adverse outcomes is strongly associated with three factors: 1) wound severity (degree of tissue loss), 2) ischemia, and 3) foot infection. Using these factors, this article outlines the basic principles needed to create an evidence-based, rapid foot assessment for diabetic foot ulcers presenting to the emergency department, and suggests the establishment of a “hot foot line” for an organized, expeditious response from limb salvage team members. We present a nearly immediate assessment and referral system for patients with atraumatic tissue loss below the knee that has the potential to vastly expedite lower extremity triage in the emergency room setting through greater collaboration and organization.
This report presents the results of analyses of statistical data from 3,368 members of the American Podiatric Medical Association (APMA) who responded to the 1997 Diabetes Survey, conducted from February through March 1997. The purpose of the survey was to determine the extent and methods of treatment of patients with diabetes by doctors of podiatric medicine.
Background: There is limited evidence on the biomechanical effects of type 1 diabetes mellitus (T1DM) on children’s feet. This study aimed to determine whether children living with T1DM aged 10 to 16 years have altered foot structure and gait parameters compared with same-aged children without medical conditions.
Methods: A nonexperimental, case-control study was conducted. Thirty-four healthy children and children living with T1DM were recruited. Participants underwent a clinical biomechanical examination followed by instrumented gait analysis using the Oxford Foot Model to investigate foot segment motion.
Results: Children with T1DM demonstrated more dermatologic lesions and structural foot abnormalities, including claw toes (33.3%), hammertoes (22.2%), and hallux abducto valgus (11.1%), than their healthy counterparts. Gait analysis results indicate a significant difference between the two groups at the hindfoot-to-tibia angle at heel strike and toe-off, suggesting limited ankle joint motion.
Conclusions: Children with T1DM demonstrated a higher frequency of structural foot pathologies than did healthy children possibly associated with limited ankle sagittal plane movement. Screening is warranted to identify and manage these conditions early to reduce their risk of more significant foot problems associated with DM in adulthood.
Background: Proprioceptive disorders may occur when thick fibers are affected in diabetic neuropathy. This can lead to impaired joint stabilization and increased risk of falls and fractures. We evaluated joint position sense (JPS) in diabetic patients to detect those at risk for neuropathy earlier.
Methods: Sixty diabetic patients and 30 healthy individuals aged 30 to 60 years were included in the study and divided into three groups: 30 diabetic patients with peripheral neuropathy, 30 diabetic patients without peripheral neuropathy, and 30 nondiabetic control patients. Presence of neuropathy was determined electrophysiologically. Passive ankle JPS was evaluated by an isokinetic system in all three groups. Both 10° and 30° plantarflexion and 10° dorsiflexion were determined as target angles. The mean absolute angular error (MAAE) values for three trials with each angle were assessed by Kruskal-Wallis and Mann-Whitney U tests.
Results: The MAAEs with all of the angles were significantly higher in diabetic patients with peripheral neuropathy compared with diabetic patients without peripheral neuropathy and the control group (P < .001 for all of the comparisons). The MAAEs with right ankle 10° plantarflexion (P = .004) and 10° dorsiflexion (P = .007) and left ankle 10° plantarflexion (P = .008) were significantly higher in diabetic patients without peripheral neuropathy than in the control group.
Conclusions: According to these results, ankle JPS may be deteriorated before determination of neuropathy electrophysiologically.Therefore, we believe that prophylactic programs in terms of the risk of falls and fractures by evaluating JPS need to be developed in the early stages of diabetes.
Throughout our medical training, we are taught how to manage patients who present with symptoms: perform a clinical examination, make a diagnosis, and develop a management plan. However, virtually no time is spent on teaching us how to manage patients who have no symptoms because they have lost the ability to feel pain, that is, patients with peripheral neuropathy. The lifetime incidence of foot ulceration in people with diabetes has been estimated to be as high as 25%, and a variety of contributory factors result in a foot being at risk for ulceration. Most important among these factors is peripheral neuropathy, or the loss of the ability to feel pain, temperature, or pressure sensation in the feet and lower legs. Up to 50% of older type 2 diabetic patients have evidence of sensory loss, putting them at risk for foot ulceration. If we are to succeed in reducing the high incidence of foot ulcers, regular screening for peripheral neuropathy is vital in all patients with diabetes. Those found to have any risk factors for foot ulceration require special education and more frequent review, particularly by podiatric physicians. The key message is, therefore, that neuropathic symptoms correlate poorly with sensory loss and that their absence must never be equated with lack of risk of foot ulceration. If we are to succeed in reducing the high incidence of foot ulceration and particularly recurrent ulceration, we must realize that with loss of pain there is also diminished motivation in the healing and prevention of injury. (J Am Podiatr Med Assoc 100(5): 349–352, 2010)
Diabetes mellitus is a disease in which the capillary basement membranes are substantially altered. This diabetic microangiopathy is characterized by a thickening of the basement membrane and changes in its permeability characteristic due to a disturbance in the production and distribution of its functional components. Glucose metabolism and insulin imbalance have been implicated in these basement membrane modifications. The authors describe normal capillary basement membrane architecture and then discuss how pathologic changes caused by diabetes mellitus are related to diabetic foot pathology.
The authors attempt to assess the relationship between exercise, diabetes, and bone metabolism. An animal model system was developed to study the relationship. Animals given streptozotocin to induce a type I diabetic state show elevated plasma glucose and triglyceride levels and a decrease in body weight. Analysis of femurs revealed alterations in copper, phosphorus, and zinc levels in animals with diabetes compared with controls. Mineral analysis of femurs from diabetic animals placed on an exercise regimen revealed values closer to control levels.
Understanding the factors associated with pedal ulceration in patients with diabetes mellitus will increase the successful management of the high-risk diabetic foot and decrease the occurrence of ulcerative events. The authors review the associative factors that have been shown to be involved with pedal ulceration.
