Even though the foot and ankle are ideal locations to exploit the benefits of iontophoresis treatment due to the superficial nature of the pathology, it has demonstrated several positive clinical outcomes with treating Achilles tendinitis, rheumatoid arthritic knees, carpal tunnel syndrome, infrapatellar tendinitis, plantar fasciitis, lateral epicondylitis, and temporomandibular joint dysfunction when using dexamethasone sodium phosphate (DEX-P) (Curney & Wascher, 2008). According to Anderson (2003) and colleagues DEX-P via iontophoresis delivery can penetrate up to 17 mm and theoretically 8 to 10 mm at pharmacologic concentrations, so most structures of the foot and ankle can be reached in this way. They also provided evidence which suggested that comparable iontophoretic doses delivered at low currents over several hours are more effective than those delivered by higher currents over 10 to 30 minutes in the creation of a localized physiologic effect for DEX-P, based on the magnitude and duration of local cutaneous vasoconstriction. In my personal experience, treating the above conditions using DEX-P has led me to discover what a potent modality iontophoresis is. I have been using it to reduce patients’ pain and inflammation, improving scar flexibility, control symptoms of Morton’s neuroma, decrease calcifications in tendons, bursa, and muscles.
Iontophoresis is the introduction of ion compounds into the skin by means of direct current predominantly (alternating current can be used too, but with less effect therefore I will not discuss it). One electrode is always positive (anode) and the other is always negative (cathode). The ionic compound usually consists of charged molecules, which are placed under one or both electrodes such that electrorepulsive forces drive the drug molecules away from the electrodes, into the skin, though the pores of the skin and sweat glands in the skin in particular. In this way, the rate of penetration of charged drugs through the relatively impermeable stratum corneum is greatly enhanced compared to passive diffusion. The typical setup is schematically depicted in Figure 2 (see attached) (Tesselaar & Sjoberg, 2011). I use the Empi Dupel Iontophoresis unit and 80 mA.min dosages at a frequency of three times per week for two -three weeks and then two times per week for additional two weeks, similar to the regimen described by Costa & Dyson (2007). Before each treatment, I clean skin of the localized most painful points with an isopropyl alcohol (70% by volume) swab, in accordance with electrode manufacturer recommendations. I consider contraindications for iontophoresis in patients with higher susceptibility to applied currents. It is difficult at times to determine. Usually I check the site of the administration frequently during of the first treatment. Others are patients carrying electrically-sensitive implanted devices such as cardiac pace makers or patients with damages skin.
My concern always has been with the fact that the injected forms of steroid medication are known to cause soft tissue atrophy of the tendons, ligaments, or fat pads due to abandon amount of the drug on the systemic level. This can lead to tissue rupture (Halpern, Horowitz & Nagel, 1977). In delivering steroids via iontophoresis there is no detectable blood level of the drug. I always educate patients and give them hand out on this treatment I am proposing as some of them have a healthy fear of steroids. Once a patient discovers how much relief they obtain from this modality, they start to ask me to use it on the myriad of their aches and pains. I noticed that with slow delivery the results are noticeable sometimes within minutes or hours and last for 30 to 48 hours after the session. It takes up to 6 to 12 sessions to completely resolve the issue. Sometimes I skip the session and ask patient if they noticed the difference as it is difficult at times to stop therapy for some patients who found salvation from pain with this therapy. Another consideration is the level of skin sensitivity among patients. Some can report poor tolerance and no skin irritation. On the other hand some can tolerate treatment well and blister. I ask if the burning sensation is over the entire surface of the pad or it is over the pinpoint (more likely will have a problem with blistering). In any case, I explain to my patient that if mild blistering occurs it will be resolved in a few hours. I use the Milk of Magnesia (magnesium hydroxide 400mg) over the irritated skin to restore the pH level after the treatment.
I use iontophoresis with ultrasound, stretching, manual techniques, and nerve glide. Administering iontophoresis with DEX-P, followed up by 2 MHz, 1.0 W/cm2, 50% pulsed ultrasound for 15-20 min over the inflamed nerve root which is compressed by herniated disc, causes pain to decrease. This allows me to initiate a stabilization exercise regimen with the patient sooner. In the suggested reading for this week, I came across an article by Costa & Dyson (2007), who presented a case of administering ultrasound over the heel of a 15-year-old female soccer player. The growing plates of teenagers of this age may not be closed as of yet. One consideration of mine is application of ultrasound in the area of the epiphyseal plate (please refer to fig.1) as it pertains to growing children. The ultrasound should be administered at a low intensity of
DEX-P is the drugs of choice when I deal with acute inflammation and pain. (I usually avoid using Lidocaine 4% for pain as I noticed that patients complain of the rebound effect of this medication). I prefer using, acetic acid when a patient presents with calcific tenosynovitis and chronic pain. Other drugs worth considering are Ketoprofen 10%, a non-steroidal anti-inflammatory drug (NSAID). Gabapentin 6% is used to treat neuropathy. Potassium Iodide 10% is useful for softening scars and tendon adhesions. Acetic Acid 4% is commonly used for calcifications (heel spurs, calcific tendonitis). Table 1 (see attached) summarizes the common drugs used in a physical therapy setting (Aiken Compounding Pharmacy, n.d.). I generate the letter of medical necessity to the patient’s referring physician with the request of the drug I plan to use for the diagnosed condition. The Drug Information Handbook states that contraindication for use of DEX-P is hypersensitivity to drug, systemic fungal infection, and cerebral malaria. The medication is introduced locally with avoidance of the systemic distribution through the blood stream which makes side-effects to be abolished. The synthetic glucocorticoid DEX-P is not present in the body at any level but acts as one. It blocks prostaglandin biosynthesis via inhibition of phosphate enzyme activity and suppresses fibroblast deoxyribonucleic acid (DNA), ribonucleic acid (RNA), protein synthesis, and synthesis of collagen. It is said that chronic excess (6.25 mg/kg of cortisone acetate, for example, for 30 days) can impair wound healing by inhibition of epithelization and wound contracture (Gurney & Wascher, 2008). The arachidonic acid then cannot be released from the cell membrane phospholipids (NSADs, in contrast, prevents prostaglandin production via inhibition of the cyclooxygenase enzymes). DEX-P ionizes into a negatively charged compound and therefore, when used for iontophoresis, is placed under the cathode. According to Anderson (2003) and his colleagues, DEX-P is uncharged and has a poor solubility in aqueous solutions, the water-soluble DEX-P is generally used in iontophoretic applications. I found it is difficult for patients to find the appropriate form of DEX-P. The injectable form is not acceptable and therefore DEX-P needs to be compounded in the pharmacy which is familiar with preparation of the DEX-P for use in iontophoresis. In Vitro study by Sylvestre (2008) and colleagues pointed out that -not all commercially available Dex-Phos solutions are equivalent for iontophoresis. The ideal donor solution contains no background electrolyte to compete with the drug to carry a charge across the skin- (p.1183). Some patients in my practice used to bring the prescribed by MD injectable form of DEX-P for treatment. I contacted a few pharmacies and found out that most of them were not aware of the differences between topical and injectable form of the drug. Finally, I was able to get information from the local compounding pharmacy owner, Peter Fallon (2000, personal conversation), who told me that the injectable form contains competitive ions from the preservatives they put into the drug. It is sterilized which makes the drug more expensive for the user, and some people can have an allergic reaction to the preservative, while the topical DEX-P solution they make has just aqueous ionic DEX-P solution.
Even though many studies suggest the use of the iotophoretic delivery of drugs such as DEX-P, there are clinical trials that have indicated a lack of clinical efficacy of iontophoresis. The fact that the drug dose in the tissue during iontophoresis is unknown, regardless of the delivery regime, is perhaps the major limitation of the method in comparison with in-vitro methodology. A better understanding of the local drug kinetics and response dynamics during iontophoresis of vasoactive drugs is needed to enable more accurate dose response analysis (Tesselaar & Sjoberg, 2011). In addition, several studies were not randomized and some had no control group. According to Curney and Wascher (2008) the iontophoretic transmission of DEX-P through living human skin with absorption of DEX into dense connective tissue is unknown.
This may be the reason why iontophoresis is not approved by insurances carriers for coverage. The method of iontophoresis was first described by Pivati in 1747; in 1900 Leduc introduced the term iontotherapy and formulated the laws for this process (Gazelius, n.d.). According to Gurney and Wascher (2008) iontophoresis has been used clinically for 62 years! One might think that over this period of time and rise of a technological world, we find ways to overcome these limitations. Personally, I believe that iontophoresis is an underestimated modality, and remains expensive due to being an uncovered service. The treatment cost is approximately $35 (cost of electrodes and drug per one site of treatment), not to include the labor time and effort, but it makes the experience of rehabilitation less painful for my patients. When they finish the treatment and continue with their lives feeling better than when they started therapy, it improves compliance. Lastly, what I gain from using iontophoresis in my clinic is that patients come back asking for more of -that magic-. I don’t know about you, but I love it when my patients refer to my hands as magic.
Given last week’s discussion on drug reviews and we were talking about not even recommending the use of OTC medications, how comfortable are you administering this treatment? One of my patient used GlucoWatch to monitor the plasma glucose concentration. It is based on the reversed iontophoresis techniques (Nair, Goel, Prakash & Kumar, 2012, Figure 3). Has anyone used reversed iontophoresis system for non-invasive therapeutic drug monitoring?