Since 1991 we have treated small-area skin wounds, particularly burns, with hypertonic saline mixed with local anaesthetic. Initially the method was used only to eliminate local oedema and relieve pain. However, in practice we found that not only pain had been greatly relieved but also speed and quality of healing had unexpectedly increased. We termed the method ‘hypertonic saline soaking therapy’ (HSST).
The theory behind HSST can be summarised as follows. The cardinal principle in burn surface treatment is to occlude the surface as soon as possible, and application of an aqueous solution is undoubtedly the simplest, fastest and most convenient method. The aqueous solution may cause infiltrative oedema, but this can be overcome by using hypertonic preparations, and surface anaesthesia can relieve discomfort caused by hypertonicity.
Wound occlusion is crucial in modern wound surface treatment [1]. The substance of traditional exposure therapy is occlusion of the wound surface by drying scab; hot air blowing, infrared radiation or early-phase escharectomy and skin grafting to accelerate the process. However, wet treatment has become more common, and is promising particularly in the acute stage, with the advantage of being simpler and more effective in occluding the wound surface. Wet treatments radically change the therapeutic concept, mobilising fully the organism's self-regenerative repair functions in order to save tissues on the wound surface and heal naturally to the maximum degree.
Wet treatments may be included in traditional therapy but are considered supplementary only, because they can cause infiltrative oedema of the burned surface; many previous studies have shown increased osmotic pressure in burned tissue. Traditional wet treatments administer isotonic saline, which is relatively hypotonic, and continuous application will inevitably result in infiltrative oedema. This can impede drainage, obstruct microcirculation, induce or aggravate infection and damage healing. Thus the theory behind traditional treatment is paradoxical. On one hand, it advocates wet treatment to irrigate the would and provide a moist environment; on the other hand, it shows that moistening the burn surface with isotonic saline encourages bacterial growth. The problem can only be solved by using hypertonic preparations.
HSST applies hypertonic saline not only at the stage of granulation oedema but also at the beginning of the treatment, without causing infiltrative oedema or infection. The concentration of hypertonic saline we used initially ranged from 5% to 10%. With experience, however, the concentration was set at 3%, which has been adequate. Some experts worry that the wet compress of hypertonic saline may cause hypernatraemia and hyperchloraemia but, as 10% sodium chloride is given intravenously in the treatment of cerebral oedema, it should be safe to apply 3% saline externally; electrolyte disorder should be regulated in the course of holistic treatment. Some scholars also suggest that hypertonic wet compresses may worsen dehydration. What we are most concerned about in practice is the drying up of dressings, but hypertonic wet compresses combat this by improving the microcirculation.
We used 0.2% lidocaine hydrochloride on the wound surface to relieve pain, and the overall effect was satisfactory. Lidocaine is a rapidly effective amide topical anaesthetic. It can stabilise the electric potential of cytomembranes, improving cell metabolism; low concentrations of lidocaine are less toxic and can dilate capillaries, improving microcirculation of the wound surface. Therefore, even in the absence of pain we add 10–50
mg/100ml lidocaine to the wet compress solution, because it encourages healing of the wound surface and reduction of the cicatrix.
Medium- and small-area burns are the most common, so these concentrations are suitable in most cases. We have not treated large-area burns by this method, but for such wounds we are considering a reduction in the concentration of sodium chloride to 1–1.5% and a similar reduction in the concentration of lidocaine; in our experience, a dosage of less than 400mg lidocaine is safe for external use.
Following the same principles, we find that HSST can also be applied to other seeping, swollen and painful wound surfaces, such as ulcers of the lower limbs and pressure sores.
To prevent wound surface infection, we tried dissolving 80,000–160,000 units of gentamicin in 500ml wet compress solution, but found that this caused a skin rash. Oral antibiotics were administered in serious cases, but no wound surface became infected with the use of hypertonic wet compresses. Hypertonic sodium chloride solution cannot kill bacteria but is quite effective in inhibiting proliferation by hypertonic dehydration, drainage, improved microcirculation, environmental acidulation and meticulous dressing changes. Scarring is more serious after infection, when growth factors stimulate over-proliferation of fibroblasts and myofibroblasts which secrete excessive extracellular matrix to form abnormal scar. HSST quickly occludes the burned surface, promotes drainage and diminishes inflammation, thus restraining fibroblast and myofibroblast proliferation and activation.
In this letter, we introduce our experience of applying HSST to small-area burn surfaces. We note that the application of hypertonic preparations has the all the advantages of wet therapy and also enhances drainage and improves microcirculation, which is beneficial in preventing infection and promoting coalescence of the wound surface. We hope that our work may inspire more scientific research to confirm the effectiveness and feasibility of HSST.
Conflict of interest statement
Our research is completely voluntary without any financial support, so there is not any conflict of interest. In January 2007, we have been issued a “Certificate of Invention Patent” by the State Intellectual Property Office of the Peoples Republic of China with the certificate number: 302897 and the patent name: the Hypertonic Burn Embrocation. All authors have no other disclosure.
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