Certain foot deformities, reduced skin oxygenation and foot perfusion, poor vision, greater body mass, and both sensory and autonomic neuropathy independently influence foot ulcer risk, thereby providing support for a multifactorial etiology for diabetic foot ulceration.

Both neuropathy and vasculopathy are strong independent risk factors for the development of diabetic foot ulcers. In our model, the strongest risk factor is impaired cutaneous oxygenation. However, in the clinical setting, sensory examination with a 5.07 monofilament probably remains the single most practical measure of risk assessment.

Poorer glycemic control increases the risk of neuropathy and is amenable to intervention. Height and age directly increase risk of neuropathy and may help identify patients at risk. A proportion of neuropathy in diabetic veterans is probably due to or worsened by alcohol ingestion. Neuropathy was less common in current smokers than subjects not currently smoking.

The natural history of tissue repair and the critical determinants of faulty healing of diabetic ulcers remain obscure despite recent advances in our knowledge of the cellular physiology of normal cutaneous healing. To characterize the chronology and identify important factors affecting healing, we applied an objective method to quantify the rate of wound healing of full-thickness lower-extremity ulcers in 46 diabetic outpatients who received local wound care under a standardized clinical protocol. The initial ulcer healing rate, eventual status of tissue repair, and definitive clinical outcome were not significantly associated with age; diabetes type, duration, or treatment; level or change in glycosylated hemoglobin; current smoking; presence of sensory neuropathy; ulcer location or class; initial infection; or frequency of recurrent infections. However, direct measures of local cutaneous perfusion, estimated by periwound measurements of transcutaneous O2 tension (TcPo2) and transcutaneous CO2 tension (TcPco2), were significantly associated with the initial rate of tissue repair (P = 0.003 and 0.005, respectively). The strong prediction of early healing by these parameters of local skin perfusion was independent from the effects of segmental Doppler arterial blood pressure at the dorsalis pedis, although eventual ulcer reepithelialization was significantly related to foot blood pressure and periwound TcPo2 and TcPco2. We conclude that periwound cutaneous perfusion is the critical physiological determinant of diabetic ulcer healing, indicating a 39-fold increased risk of early healing failure when the average periwound TcPo2 is less than 20 mmHg.

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Los autores declaran no tener ningún tipo de interés económico o comercial. RESUMEN Objteivo:Valorar si existe relación entre el aumento de temperatura en el pie y la neuropatía diabética periférica. Métodos: La muestra fueron 27 pacientes diabéticos a que se le realizó una exploración neurológica y vascular, además, haciendo uso de un termómetro infrarrojo medimos la temperatura en distintos puntos anatómicos de la planta del pie. Resultados: La temperatura es mayor los pacientes con neuropatía con una diferencia de 2,24ºC (p=0,454) en el pie derecho y 0,86ºC (p=0,589) en el pie izquierdo. Conclusión: Los resultados sugieren que la automonitorización de la temperatura del pie por parte del paciente diabético podría ayudar a reducir la alta incidencia de complicaciones en el pie diabético. Palabras clave: Diabetes; neuropatía diabética periférica; monitorización de la temperatura. ABSTRACT Objective:To evaluate the existence of correlation between a higher foot temperature and diabetic peripheral neuropathy. Methods: 27 diabetic patients that we do a neurological and vascular exploration, and we used an infrared skin thermometer to measure temperatures on different sole foot sites. Resultados: Patients with diabetic neuropathy had a higher foot temperature, 2, 24ºhigher on right foot (p=0,454). In the same way, left foot temperature it´s higher too in patients with diabetic neuropathy, although this result it´s less significant (0,86ºC)(p =0,589) Conclusions: these results suggest that at home patient self-monitoring foot temperatures may be an effective tool to prevent foot complications in individuals with high risk diabetic foot. Key words: Diabetes; diabetic peripheral neuropathy; temperature-monitoring.Referencia normalizada: Chicharro-Luna, E., Portabales Botana, I., Ramírez Monreal, L., Torrent Ivorra, E. Monitorización de la temperatura del pie como herramienta en la neuropatía diabética. Rev. Int. Cienc. Podol. 2016; 10(1): 9-16. Sumario: 1. Introducción. 2. Material y método. 3. Resultados. 4. Discusión y conclusión. Bibliografía.

We examined neuropathy, ankle pressure index (API), and other factors as predictors of transcutaneous oxygen (TcPO2) in the lower limbs of 657 diabetic subjects. Eligible subjects underwent a clinical assessment that included three standard measures of autonomic neuropathy. TcPO2 measurements were performed at 37 °C and 44 °C at four lower limb locations. Associations between potential predictors and TcPO2 were tested using univariate and multivariate statistics. Mean TcPO2 at any site did not differ by presence of autonomic neuropathy at either temperature, except for a significantly lower value at 44 °C below the knee (56.5 versus 59.2 mmHg, p = 0.021). In multivariate analysis, autonomic neuropathy was significantly and independently related to leg 44 °C TcPO2 only (coefficient = −2.6734, p= 0.0182). Much stronger associations were seen between TcPO2 and age, ankle blood pressure, and relative body weight on the plantar foot; and between API, glycosylated haemoglobin, ankle blood pressure, and pedal oedema on the dorsal foot and leg. We conclude that factors related to lower limb TcPO2 vary depending on measurement site. Autonomic neuropathy is not an important determinant of TcPO2 in the feet of diabetic subjects. Although several predictors of TcPO2 were identified, most of the variance of this measurement remains unexplained.

We previously reported an unexpected statistically significant decline in the mean transcutaneous partial pressure of oxygen (TcPO2) with cutaneous warming from 37 degrees C to 44 degrees C on the plantar diabetic foot, as opposed to the expected increase seen at the dorsal sites. To elucidate this relationship we compared changes with cutaneous warming in TcPO2 and skin circulation measured by laser Doppler flowmetry on the right plantar foot surface of 20 consecutive subjects. Neuropathy by monofilament testing was present in 55% of the cases. Right dorsal foot TcPO2 increased with cutaneous warming from 37 degrees C to 44 degrees by a mean change of +43.6+/-20.7 mmHg (+/- standard deviation) in 95% of the cases. In 42% of cases right plantar first metatarsal head TcPO2 fell with warming from 37 degrees C to 44 degrees C by a mean change of -10.7+/-7.6 mmHg. In the remaining 58% of cases right plantar first metatarsal head TcPO2 rose by 6.8+/-6.3 mmHg. In 95% of cases right plantar great toe laser Doppler perfusion units (LDPU) increased with warming from 36 degrees C to 44 degrees C by a mean change of +50.4+/-37.1. Blood flow measured by laser Doppler flowmetry increased in 95% of the subjects with heating. The finding that blood flow was increased with warming contradicts the hypothesis that arterioles in the plantar great toe cannot vasodilate in response to thermal stimuli. This finding supports the hypothesis that the decline in TcPO2 with warming might be due to an increase in epidermal oxygen consumption that exceeds the increase in oxygen delivery due to increased blood flow. The pathological mechanisms behind microvascular dysfunction in skin microcirculation in the diabetic foot need further investigation.