An Unexpected Detrimental Effect on the Incidence of Heel Pressure Ulcers After Local 5% DMSO Cream Application: A Randomized, D
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Pressure ulcers (PU) continue to be an enormous healthcare problem that affects large segments of the patient population. A PU is an area of localized damage to the skin and underlying tissues caused by pressure, shear, or friction.1 Apart from relief of tissue loading there are no appropriate therapies for preventing PU.
The complete etiology of PU is not yet fully understood. However, some components of the injury are caused by ischemia followed by reperfusion.2 Ischemia-reperfusion (I-R) injury has been defined as the injury, at the cellular level, resulting from the restoration of blood flow to tissue with previous ischemia. Reoxygenation promotes the generation of various reactive oxygen species (ROS) leading to the uncontrolled oxidation of vital cellular components. The hydroxyl radical (HO•), which is formed during the reaction between superoxide and hydrogen peroxide in the presence of iron, appears to be the critical oxidant and an important initiator of lipid-peroxidation during I-R injury.3,4
Several defense mechanisms are present within tissues and cells for the protection against ROS. In addition, a number of drugs and antioxidants have been shown to prevent or scavenge damaging oxidants and free radicals. Studies in ischemia-reperfusion related PU animal studies showed a decrease of tissue necrosis after treatment with various systemically or locally applied antioxidants.2,5–7
Dimethyl sulfoxide [DMSO (CH3)2SO] has a potentially complex mechanism of action due to its anti-ischemic, anti-inflammatory, and antioxidant properties. DMSO is widely used as antioxidant in both in-vivo and in-vitro I-R models for its ability to scavenge the highly cytotoxic hydroxyl radical and inhibit leukocyte adherence.8,9 Topical application of DMSO, an organic liquid with excellent penetrating properties, has been shown to increase the survival of primarily ischemic island skin flaps.10 As I-R injury plays a role both in ischemic skin flaps and PU, topical DMSO could, likewise, be useful in the prevention of PU development.11 Local therapy to improve the outcome of I-R damage in PU development other than pressure relief may open a new therapeutic window for PU prevention.
Against this background, a double-blinded randomized study with a local antioxidant (DMSO) was conducted. This study is the first part of a more in-depth crossover investigation of the effect of DMSO on the buttocks versus the heel and ankle area.12
The objective of this study was to determine whether topically applied DMSO in a 5% concentration prevents or attenuates PU formation in a population prone to this condition.
Methods
A double blind, randomized, multicenter, placebo-controlled study to investigate the effect of a 5% DMSO cream on 2 separate locations (the buttocks and heel/ankle) in a population prone to PU development was conducted. Both buttocks and heel/ankle area are vulnerable for PU development. The heel and ankle region are particularly susceptible because of their relatively lower resting blood perfusion, higher surface pressure under load, and the extent of subcutaneous tissue covering the heel bone, or malleoli of the fibula and tibia. Due to similarities between heel and ankle they are taken together in the incidence rates.
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