Vacuum-compression therapy for the treatment of an ischemic ulcer.

Physical therapy intervention in patients with compromised arterial circulation is often sought after other medical and surgical measures have been tried and ischemic ulcerations have developed.[1] The physical therapist's role in the management of such individuals has traditionally consisted of the provision of wound care in conjunction with physical agents and exercise directed at improving peripheral circulation. The success of these conservative measures has often been limited.[2,3]

One of the earliest experiments on the use of a vacuum device to effect circulation was reported by Junod in 1841.[4] He applied large vacuum bells to various body parts to create a negative pressure and cause a severe, localized hyperemia. This was done in an attempt to draw blood away from diseased organs. This technique fell from favor by the turn of the century, and little use of vacuums was noted in the medical literature until the 1950s when a number of investigators became interested in the response of peripheral vessels to various pressure changes.[5,6]

In 1956, Erler and Itting designed a vacuum-compression unit that served as the prototype for a clinical model in use today (Vasotrain 447[R]).[7] The device consists of a plexiglass chamber connected to a compressor. The unit provides a timed alternation of positive and negative pressures at a selectable range of intensities between -0.20 and 0.20 bar (-150 and 150 mm Hg, respectively) (Fig. 1).

The Food and Drug Administration has given an Investigational Device Exemption for the Vasotrain 447[R]. There have not, however, been any reports in the literature of the clinical use of this device in the United States. This case report documents the use of the vacuum-compression device in augmenting the healing of an ischemic ulcer.

Case History of Subject

A 30-year-old woman with a history of hyperlipidemia and severe arteriosclerosis was being seen by the vascular surgery service at the Louisiana State University Medical Center in Shreveport. She was a cigarette smoker and had smoked 1 1/2 packs per day for the previous 15 years. On the day of admission, she was seen in the emergency department with a 3- to 4-day history of pain in the right leg and foot, which had progressed to numbness. One month prior, she had been hospitalized for similar complaints in the left lower extremity. During that hospitalization, the patient underwent emergent fasciotomies of the left leg at the level of the calf medially and laterally and an aortobi-iliac bypass graft. Postoperatively, she was noted to have a foot drop likely secondary to peroneal nerve ischemia, and physical therapy was consulted for range of motion exercises, splinting, and progressive ambulation. At discharge, the fasciotomies on the patient's left leg had been closed secondarily, and, though the foot drop persisted, she was able to ambulate with a walker.

In view of the patient's history, the admitting physician suspected an embolus or thrombus to be present in the popliteal artery. Physical examination revealed strong femoral pulses and weak popliteal pulses bilaterally. Dorsalis pedis and posterior tibial artery pulses were not palpable bilaterally, but could be auscultated on the left with a Doppler stethoscope. The right foot was cool to touch and pale in appearance, and the toes demonstrated a slow capillary refill following release of finger pressure. An arteriogram revealed an occlusion of the right superficial femoral artery at the mid-thigh level with reconstitution of the anterior and posterior tibial arteries distally.

A right popliteal artery embolectomy was performed along with a medial calf fasciotomy. Postoperatively, the fasciotomy wound was dressed three times per day with saline-moistened gauze. These dressing changes were performed by the surgical residents. The patient was discharged on the 12th postoperative day with instructions to continue dressing changes with saline-moistened gauze three times per day.

Four days after discharge, the patient returned to the vascular surgery clinic for follow-up. On this examination by the vascular resident, the fasciotomy wound was noted to be healing poorly. Several necrotic areas had developed, and moderate amounts of serous drainage were present. She was readmitted to the hospital, and begun on antibiotic therapy with Cefadyl[R] [dagger] (1-g intravenous piggyback administered every 6 hours) and treated by the surgical staff with wet-to-dry saline dressings and local debridement. At the time of discharge, the wound had begun to demonstrate the presence of a moderate amount of granulation tissue. The patient was again instructed in home wound care consisting of applications of saline-moistened gauze three times per day.

One month later, the patient was seen in the surgical clinic. The wound measured 7 x 18 cm (Fig. 2). The granulation tissue was judged by the surgeon to be pale and essentially unchanged from the previous admission. In addition, there was evidence of early gangrenous changes in the third toe. The toe was dark in appearance and demonstrated no capillary refill at its most distal aspect. The right dorsalis pedis artery pulse was found to be absent to palpation and to Doppler auscultation. The patient was readmitted to the hospital, and local wound care was performed with saline irrigation and saline-moistened gauze dressings. One week after readmission, the fasciotomy site was covered with a split-thickness skin graft in an attempt to accelerate wound healing. The patient's hospital course was uncomplicated until the sixth postoperative day when a small amount of purulent drainage was noted at the graft site. Cultures revealed the presence of Enterobacter cloacae. The surgeons did not feel that antibiotic therapy was indicated and elected to treat the patient with wet-to-dry dressings with saline-moistened gauze two times per day. Dressing changes were performed by the surgical residents. By the 12th postoperative day, the attending surgeon judged that only 40% of the graft remained viable. The patient was again discharged and instructed in dressing changes utilizing saline-moistened gauze.

Physical Therapy Management

One week following the second hospital stay, the patient was seen by the physical therapist assigned to the vascular clinic. The wound measured 3 x 15.5 cm (46.5 [cm.sup.2]), was hypogranular in appearance, and was covered approximately 50% with necrotic tissue. Hydrocolloid dressings [double dagger] were begun in an effort to promote autolytic debridement of the necrotic tissue. The dressings were changed three times per week, at which time the wound was cleansed via gentle whirlpool irrigation. Whirlpool treatments were for 20 minutes each, and the water temperature was maintained at 38.3 [degrees] C (101 [degrees] F). The whirlpool bath did not contain any additives, with the exception of sodium hypochlorite, which was added to increase the chlorine content to 25 parts per million (14 g [0.5 oz] per 378.54 kg [100 gal] of water). This level of chlorine serves to decrease cross-contamination in tanks. Following 2 weeks of physical therapy management three times per week, the wound began to lose its necrotic appearance. It still demonstrated hypogranulation, however, and its size was unchanged.

At this time, vacuum-compression therapy (VCT) was initiated with the Vasotrain 447 [R]. Following whirlpool cleansing of the wound, the patient's left lower extremity was placed in the Vasotrain 447 [R], and the device was set to deliver - 0.10 bar (- 75 mm Hg) of negative pressure for 90 seconds followed by 0.05 bar (38.5 mm Hg) of positive pressure for 30 seconds. These settings were recommended by the manufacturer and were designed to emphasize the vacuum phase of the cycle in an attempt to increase capillary filling. Within 60 seconds of beginning the vacuum phase of the cycle, visible hyperemia was apparent just distal to the knee and extending to the foot. The patient reported that she felt a tingling sensation in the foot. During the compressive phase, the extremity color would return to baseline (pretreatment color), and the tingling sensation would subside. The patient was treated three times per week with 1-hour sessions. Following each treatment session, the wound was dressed with the hydrocolloid dressing,

After 2 weeks of treatment with VCT added, the wound had decreased in size by 25% and was healing at a rate of 0.59 [cm.sup.2] per day. By the end of the fourth week of treatment, several 0.5x2-cm wounds remained. All wounds were completely epithelialized by the end of the eighth week (Fig. 3). Overall, the wound healed at a mean rate of 0.58 [cm.sup.2] per day. During the next 2 months, the wound continued to remodel to its present appearance (Fig. 4).

Discussion

Several factors that had the potential of affecting the outcome of this case need to be addressed. Smoking has long been known to cause arterial vasoconstriction and can delay or prevent wound healing in individuals with arterial insufficiency.[8,9] Although it is highly likely that cigarette smoking served to complicate the healing in this case study, this was not a variable that changed during the course of the treatment. The patient continued to smoke despite admonishments to quit.

The healing rate of wounds is affected by the type of dressing used in treatment. The literature abounds with information about the properties of various synthetic dressings on the market and why each is better than traditional gauze dressings.[10-12] Hydrocolloid dressings have been reported to facilitate wound healing by promoting autolytic debridement. Autolytic debridement is felt to occur because endogenous enzymes and macrophages are contained within the wound by the dressing. These dressings also create a moist environment that encourages the proliferation of capillaries.[13] The use of a hydrocolloid dressing in this case likely provided a proper moist environment for the wound, but it is unlikely that the dressing alone can be credited with the major changes seen in the patient's wound. The dressing was begun 2 weeks prior to initiation of VCT, and the wound did not change in size during that period.

Vacuum-compression therapy appears to have been the factor most responsible for facilitating healing in this case. The volume of an elastic vessel can be increased by the application of a vacuum force on its outer wall.[14] In the negative pressure phase of VCT, just such a force is exerted on the extremity and its vessels. The change in the transmural pressure gradient results in a passive hyperemia that we commonly visualized within 60 seconds during treatment and that theoretically resulted in better capillary filling.[15]

This case seems to demonstrate the potential benefits of VCT in promoting capillary filling and assisting the healing of wounds of individuals with compromised arterial circulation. Controlled studies that examine larger numbers of patients with similar wounds and other traditional therapies need to be conducted. Likewise, the potential usefulness of such a device in the management of symptoms associated with small-vessel disease, such as diabetes, and in the treatment of slow-healing arterial wounds warrants investigation. Until such time as more data are available, however, the use of VCT for wound healing should still be considered experimental.

Acknowledgments

We thank Ms Beverly Lane and Mr Bruce Neal, who assisted in the management of this patient. Equipment discussed in this report was made available by a loan from Henley International Inc. [dagger] ER Squibb & Sons Inc, General Offices, PO Box 4000, Princeton, NJ 08543-4000. [double dagger] DuoDERM [R], ConvaTec (a Bristol-Myers Squibb company), CN 5254, Princeton, NJ 08453-5254.

References

[1] McCulloch JM, Hovde J. Treatment of wounds due to vascular problems. in: Kloth LC, McCulloch JM, Feedar JA, eds. Wound Healing Alternatives in management Philadelphia, Pa: FA Davis Co; 1990:177-195. [2] Griffin JE, Jones HH. A clinical study of testing and treatment of peripheral vascular diseases. Phys Ther Rev. 1950;30:375-377. [3] McCulloch JM. Peripheral vascular disease. In: O'Sullivan SB, Schmitz TJ, eds. Physical Rehabilitation: Assessment and Treatment. Philadelphia, Pa: FA Davis Co; 1988:371-383. [4] Bier A. Hyperemia by suction apparatus. In: Hyperemia as a Therapeutic Agent. Chicago, Ill: Roberts Publishing; 1905:74-87. [5] Blair DA, Glover WE, Greenfield ADM, Plassaras GC. The increase in tone in forearm resistance blood vessels exposed to increased transmural pressure. J Physiol (Lond). 1959; 149:614-625. [6] Coles DR, Kidd BSL, Moffat W. Distensibility of blood vessels of the human calf determined by local application of subatmospheric pressures. J Appl Physiol. 1957;10:461-468. [7] Tielrooy WF. Vacuum-Compression Therapy (VC7) in Peripheral Arterial Circulatory Disorders. Delft, the Netherlands: Enraf-Nonius Delft; 1986:10-14. [8] Mosely LH, Finseth F. Cigarette smoking: impairment of digital blood flow and wound healing in the hand. Hand. 1977;9:97-101. [9] Winniford MD. Smoking and cardiovascular function. J Hypertens Suppl. 1990;8:517-523. [10] Falanga V. Occlusive wound dressing: why, when, which. Arch Dermatol. 1988; 124:872-877. [11] Varghese MC, Balin AK, Carter M, Caldwell D. Local environment of chronic wounds under synthetic dressings. Arch Dermatol. 1986; 122:52-57. [12] Katz S, McGinley K Leyden JJ. Semipermeable occlusive dressings: effects on growth of pathogenic bacteria and reepithelialization of superficial wounds. Arch Dermatol. 1986;122: 58-62. [13] Madden MR, Nolan E, Finkelstein JL, et al. Comparison of an occlusive and a semi-occlusive dressing and the effect of the wound exudate upon keratinocyte proliferation. J Trauma. 1989;29:924-930. [14] Nave CR, Nave BC, eds. Physics for the Health Sciences. Philadelphia, Pa: WB Saunders Co; 1975:73-75. [15] Murray RH, Thompson LJ, Bowers JA, Albright CD. Hemodynamic effects of graded hypovolemia and vasopressor syncope induced by lower body negative pressure. Am Heart J. 1968-76:799-811.