Treatment of a large infected thoracic spine wound using high voltage pulsed monophasic current.

Electrical stimulation has long been recommended as an adjunct treatment for wound healing. Some investigators[1-4] described the use of low intensity direct currents for wound healing. These treatments were believed to enhance wound healing by stimulating growth of granulation tissuel[1-4] and by producing bactericidal effects.[5,6]

High voltage monophasic pulsed current (HVPC) has been used to accelerate wound healing in pressure ulcers[7,8] and diabetic ulcers.[9,10] Kloth and Feedar[7] reported 100% healing of wounds over a mean period of 8 weeks in patients who received HVPC, compared with a 29% increase in wound size during a similar time period for a control group of patients. Griffin et al[8] reported a significant reduction in the size of pressure ulcers at 5, 15, and 20 days after initiation of treatment in patients with spinal cord injury who received HVPC compared with patients who received a placebo.

Thurman and Christian,[9]in an attempt to promote wound healing of an infected diabetic ulcer, used HVPC combined with induction of muscle contraction to improve circulation in the area of the wound. Alon et al,[10] in a pilot study, used a protocol with HVPC intensities below that at which muscle contraction is induced for healing diabetic ulcers. A total of 12 out of 15 subjects' wounds were completely healed after 2 1/2 months of treatment.

Bactericidal effects may also be achieved with HVPC. Kincaid and Lavoie[11] found that the growth of Stapbylococcus aureus, Escberichia coli, and Pseudomonas aeruginosa was inhibited in culture with HVPC. The effectiveness of HVPC for killing

This article was submitted April 27, 1992, and was accepted JAnuary 29, 1993. GK Fitzgerald, PT, OCS, is Assistant Professor, Department of Orthopedic Surgery and Rehabilitation, Program in Physical Therapy, Hahnemann University, MS 502, Broad and Vine Sts, Philadelphia, PA 19102 (USA). Address all correspondence to Mr Fitzgerald. D Newsome, PT, is Staff Physical Therapist, Children's Rehabilitation Hospital, 3905 Ford Rd, Philad PA 19131.

bacteria in human wounds has not been well established.

The purpose of this case report is to describe how HVPC was used as a treatment adjunct for wound healing in a patient with a large, infected wound following surgical debridement.

Patient Description

The patient was a 21-year-old man with spastic quadriplegic cerebral palsy and severe mental retardation, secondary to congenital toxoplasmosis. He was dependent for mobility and all self-care, and feeding was accomplished via a gastrointestinal tube (G-tube).

Luque rods had been surgically implanted in 1988 for stabilization of a scoliotic spine. The patient had a recurrent history of infection from the Luque rods, which resulted in multiple, chronic, infected wounds over the thoracic spine. The patient's physician decided that it would be necessary to remove the Luque rods to resolve the infection and allow the wounds to heal. On July 16, 1991, these rods were surgically removed, and necrotic tissue was debrided from the affected area.

Postoperatively, the patient had a large wound over the area of the thoracic spine from approximately T-1 to T-8 that involved several tissue layers. Portions of the thoracic vertebrae were exposed and could be seen. The wound was infected with Stapbylococcus aureus. Because the patient had a history of poor wound healing prior to surgery, the surgeon believed that hospitalization for aggressive wound care was necessary postoperatively. The patient was admitted to Children's Rehabilitation Hospital, Philadelphia, Pa, on July 22, 1991, for wound care and intravenous antibiotic treatments.

Initial wound care consisted of packing the wound with sterile gauze bandages soaked in 25% Dakin's solution (25 cc of Clorox(*) per 1,000 cc of sterile water) and covering the wound with four abdominal pads. Dressings were changed twice daily. A Hickman catheter([dagger]) was inserted and used to deliver an antibiotic (Ancefs[R],([double dagger])50 mg, every 8 hours) to the patient. Intravenous antibiotic treatment was continued for 6 weeks. Isocal HN([sections]) (70 cc/h) was administered through the G-tube for feeding. Iron sulfate (325 mg, twice daily) was administered with the G-tube feedings.

The patient's primary care physician believed that because of the large size of the wound and the patient's history of poor wound healing, the use of electrical stimulation would be a useful adjunct to the other aggressive wound care treatment. He therefore requested electrical stimulation treatment for wound healing on July 24, 1991. The physician's order was not received by physical therapy until July 26, 1991. There was also a 4-day delay in receiving the electrical stimulation device from a medical equipment vendor. Therefore, treatment was not initiated until July 30, 1991, 14 days after removal of the rods and the debridement procedure.

Wound size measurements at the time of the initial physical therapy evaluation were as follows: length=17 cm, top width (the widest portion in the top one third of the wound)=7.5 cm, middle width (the widest portion in the middle one third of the wound) = 5.5 cm, bottom width (the widest portion in the bottom one third of the wound)=2 cm, and depth (the deepest portion of the wound) 5 cm. Wound measurements were taken directly from the wound. We did not test the reliability of our measurements. Similar methods for measuring the length and width of wounds have been found to yield reliable measurements.12

Electrical Stimulation Treatment

The PGS 2000 Pulsed Galvanic Stimulator, ([parallel]) a portable device powered by four 9-V batteries, was the instrument used for treatment. The waveform produced by the stimulator was pulsed monophasic exponential spikes, delivered in pairs with a fixed interpulse interval of 100 microseconds (Fig. 1).

The dispersive electrode was placed on the patient's abdomen. The terminal ends of the two active electrode lead wires were wrapped in sterile gauze pads soaked in saline solution and were then placed inside the wound. Electrode placement sites within the wound were located at the top and bottom thirds of the wound length.

A treatment protocol suggested by Newton[13] was used as a guideline to select stimulus parameters. The stimulus pulse rate was set between 80 and 100 pulses per second. We did not use higher pulse rates because 100 pulses per second was the maximum pulse rate provided by our instrument. The stimulus intensity was set at the highest level that did not induce muscle contraction. This level of stimulus intensity varied between 100 and 120 V from treatment to treatment. The duration of treatment was 60 minutes. Negative polarity was used for the first 20 minutes of treatment, followed by 40 minutes of treatment with positive polarity. The initial frequency of treatment was one session per day, 5 days per week (Monday through Friday).

Course of Treatment

Figure 2 is a graphic representation of wound size measurement data recorded throughout the course of treatment. Photographs of the wound at various stages of healing are presented in Figures 3 through 5. After 2 weeks of daily electrical stimulation treatment August 15, 1991), the width and depth of the wound were reduced by approximately 1 cm. Wound care with Dakin's solution was discontinued at this time and was replaced by packing the wound with sterile gauze bandages soaked in saline solution. The electrical stimulation was increased to twice daily. Because progress was observed in wound healing, we believed that increasing the use of electrical stimulation might further enhance the healing process. The patient had not exhibited adverse reactions to electrical stimulation at this point, so there was no reason to believe increasing the treatment frequency would be harmful. Wound dressings were changed after each electrical stimulation treatment.

The Hickman catheter was removed on September 13, 1991 (approximately 6 weeks after the initiation of electrical stimulation treatment), and intravenous antibiotic treatment was discontinued. Wound size measurements at this time indicated that the length of the wound was reduced from 17 cm to 10 cm, the top width was reduced from 7.5 cm to 1 cm, the middle width was reduced from 5.5 cm to 1 cm, and the depth was reduced from 5 cm to 1 cm. Electrical stimulation was continued twice daily in conjunction with the sterile saline bandage dressings. The size of the wound was too small for both electrodes to be placed inside the wound at this time. Therefore, one electrode was placed in the center of the wound area, and the second electrode placed on the patient's skin, proximal to the open wound.

The patient's wound was completely closed on October 8, 1991. Electrical stimulation treatment was discontinued at this time, and the area of the wound was covered with a synthetic transparent covering# to provide added protection against shear forces that may be applied to the newly healed wound. The time from the start of electrical stimulation treatment until the wound was completely closed was 10 weeks.

Discussion

Researchers[7,14] have reported that electrical stimulation with pulsed monophasic current can accelerate the rate of wound healing in patients with chronic decubitus ulcers. Kloth and Feedar[7] reported an average weekly healing rate of 44%, with 100% healing in an average of 7.3 weeks when stage IV decubitus ulcers were treated with HVPC. The wounds in the control group of their study increased in size at a rate of 11.6% per week. Feedar et all reported an average weekly healing rate of 14%, with 67% healing after 4 weeks of electrical stimulation with pulsed monophasic current in patients with stage 11, 111, and IV decubitus ulcers. The control group in this study demonstrated an average weekly healing rate of 8.25%, with 44% healing after 4 weeks. There was no indication that infection was present in any of the wounds examined in these studies. The results of these studies suggest that HVPC and pulsed monophasic current may accelerate healing of noninfected decubitus ulcers.

The patient in this case report was treated for 10 weeks with HVPC combined with other wound care interventions, resulting in 100% healing. The average weekly healing rate for this patient would be difficult to compare with those of other studies because wound size measurement methods were different. From our measurements, it appears that the average weekly healing rate (determined by combining the average weekly reduction in length, width, and depth of the wound) was approximately 20%. The rate of healing and the extent of healing in our patient's wound appear to be similar to those of wounds treated with pulsed monophasic current in the previously mentioned studies.

Thurman and Christian9 described the use of HVPC as an adjunct treatment for wound healing in a patient with diabetes who had an infected wound between the first and second toes of the left foot. Because circulation in the area of the wound was compromised, HVPC treatment was administered to enhance circulation by inducing left lower-extremity muscle contraction. The intensity of the stimulation was great enough to induce muscle contraction, and the pulse rate was reported as 5 pulses per minute for a duration of 20 minutes. The patient received 2 months of inpatient treatment and 4 months of outpatient treatment until the wound eventually healed.

Thurman and Christian's patient had compromised circulation in the area of the wound.9 We do not believe that this was true for our patient. After surgical debridement of the necrotic tissue associated with the wound, there was no evidence of poor circulation in the area of the wound. The stimulus intensity we used for treatment differed from that of Thurman and Christian's protocol because we did not attempt to stimulate muscle contraction to improve wound circulation. We chose to keep the intensity of the stimulation below the threshold for muscle contraction because we believed that [1] this manner of stimulation would ensure patient comfort and [2] potential interference with tissue healing that may result from forces applied to the tissues by muscle contraction may be avoided.

Limitations

A number of factors may have influenced the rate of wound healing for the patient in this report. The high degree of skin mobility in the area of the wound may have facilitated skin contraction.15 Surgical debridement of necrotic tissue from the wound may have enhanced the growth of healthier tissues in the area of the wound. Aggressive antibiotic treatment to control the infection probably enhanced the rate of tissue healing. The patient's nutritional status was closely monitored to ensure that nutrition would be adequate for tissue healing during the course of treatment. Therefore, the role of HVPC stimulation in accelerating the wound healing rate in our patient needs to be considered with respect to these other factors.

We indicated that the polarity of the treatment electrodes was changed during the course of each treatment. Our rationale for doing this, at the time this patient was treated, was to use negative polarity for bactericidal effects and positive polarity for stimulating granulation tissue growth.

There is some evidence to suggest that polarity may not be a dependent factor for bactericidal effects of HVPC. Kincaid and Lavoie[11] found that the growth of Stapbylococcus aureus could be inhibited in vitro under both the cathode and anode during HVPC electrical stimulation.

We are unable to determine whether HVPC induced a bactericidal effect in our patient. The patient was receiving aggressive antibiotic treatment for more than half the course of electrical stimulation treatment. Cultures of the wound were not taken during the course of treatment to monitor any bactericidal effect that may have been present. When antibiotic treatment was discontinued, there was no indication of infection, based on daily inspection of wound drainage color and odor, or of elevation of the patient's body temperature.

The duration of treatment may not have been long enough to induce bactercidal effects. Guffy and Asmussen[16] were unable to induce bactericidal effects in vitro when using negative-polarity HVPC for 30 minutes. Kincaid and Lavoie[11] induced bactericidal effects in vitro using HVPC with a treatment duration of 2 hours. Because our treatment duration was a total of 60 minutes, including 20 minutes of electrical stimulation with negative polarity, the duration of treatment may not have been enough to induce a bactericidal effect.

This case report illustrates how HVPC stimulation was used as an adjunct to treatment of a large, infected wound involving multiple tissues. Our treatment approach was based on information obtained from the literature. We believe that HVPC stimulation may have been helpful in accelerating wound healing for this patient. Other factors, however, such as antibiotic treatment, nutritional supplements, and nursing care were also used. This prevents us from clearly defining the role of HVPC. We are currently continuing our use of HVPC as described in this case report as an adjunct treatment for wound healing. Further experimental studies using a control group and large numbers of subjects are needed to examine the effectiveness of HVPC in accelerating the healing of infected wounds.

Acknowledgments

We thank Susan L Michlovitz, PT, CHT, and Philip McClure, PT, OCS, for their editorial assistance in preparing this report. (*) Clorox Co, 7901 Oakport St, Oakland, CA 94621. ([dagger]) Bard Access Systems, 5425 W Amelia Earhart Dr, Salt Lake City, UT 84116. ([double dagger]) Smith, Kline & French Laboratories, 1500 Spring Garden St, PO Box 7929, Philadelph ([sections]) Isocal HN, Meade-Johnson Nutritional Group, 2400 W Lloyd Expressway, Evansville, IN 477 ([parallel]) Universal Technology Systems, PO Box 7908, Jacksonville, FL 32238-0908.

References

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