Hyperbaric Oxygen as Primary Treatment for Ischemic Foot Ulcers: Case Report

A 67-year-old man with diabetes presented with painful hammer-toe deformities of the left foot. His podiatrist recommended surgical correction of the hammer-toe deformities but was concerned about wound healing, since no pedal pulses were palpable. The podiatrist referred the patient to a vascular surgeon who felt that the patient had adequate vascular supply to the foot to support wound healing. The vascular surgeon did not recommend a pre-operative arteriogram or transcutaneous oxygen monitoring. On June 4, 2004, the podiatrist performed surgical correction of the hammer-toe deformities. Three of the incisions on the dorsum of the left foot subsequently dehisced and over the next 8 weeks formed enlarging ulcers with exposed tendon (Figure 1, Day 1). The 2 largest ulcers measured 1.4 cm x 1.4 cm x 0.4 cm and 1.2 cm x 1.0 cm x 0.3 cm. Despite regular debridement and treatment with becaplermin (Regranex Gel 0.01%, Ortho-McNeil Pharmaceutical, Inc., Raritan, NJ), the ulcers failed to improve. A second vascular surgeon was then consulted. The patient’s exam revealed palpable left femoral and popliteal pulses but no palpable dorsalis pedis or posterior tibial pulses. The ankle-brachial index could not be calculated because of non-compressibility of the vessels due to intimal calcification. On August 12, 2004, the patient underwent left lower-extremity arteriography, which showed occlusion of the proximal portions of the anterior tibial, posterior tibial, and the peroneal arteries at the popliteal trifurcation (Figure 2). After the proximal occlusion of the peroneal artery, the peroneal artery then reconstituted through collateral vessels at the level of the mid-calf and was considered a good-sized vessel suitable as a target for arterial bypass. Collateral vessels from the distal peroneal artery supplied the foot by reconstituting the anterior and posterior tibial arteries at the level of the ankle joint. The vascular surgical consultant recommended bypass to the peroneal artery for limb salvage, since 2 months had now elapsed since the initial surgery, and the wounds were continuing to enlarge. The patient was concerned about the morbidity of distal bypass procedures and was aware of other patients who had sustained wound-healing problems with leg incisions after bypass. He was familiar with hyperbaric oxygen (HBO) and requested evaluation at the authors’ wound care center. Transcutaneous oxygen measurements (TcpO₂) obtained August 25, 2004, showed a TcpO₂ of 30 mmHg at the dorsum of the left foot with the patient supine. After the left leg was elevated to 30° for 5 minutes, the TcpO₂ fell to 16 mmHg. After breathing 100% oxygen by facemask, the TcpO₂ increased to 51 mmHg. The low TcpO₂ on room air followed by the more than 3-fold increase after oxygen breathing suggested that the patient might benefit from HBO. On September 4, 2004, the patient began a series of 20 HBO treatments, breathing 100% oxygen for 90 minutes at 2.0 atmospheres. By September 29, 2004, the wounds were nearly completely healed (Figure 1, Day 25), and the HBO treatments were discontinued on October 1, 2004. By October 27, 2004, the wounds were completely healed (Figure 1, Day 57). The patient returned for follow-up 7 months after completion of HBO. His left foot wounds remained completely healed. Follow-up transcutaneous oxygen measurements at the dorsum of the foot were obtained on March 31, 2005. Discussion In this case, the first vascular surgeon who evaluated the patient was clearly in error in his assessment that the patient had adequate arterial inflow to heal the proposed surgical incisions. The ankle-brachial index or other noninvasive studies may have been difficult to interpret due to intimal calcification of the tibial arteries. Tibial artery calcification is very common in patients with diabetes.¹ This case demonstrates the value of transcutaneous oxygen monitoring or arteriography before elective foot surgery in the patient with diabetes, unless pedal pulses are clearly palpable or other noninvasive studies are unequivocal. Once the wounds had dehisced and continued to enlarge over an 8-week period, it was apparent that some form of intervention would be necessary. The room-air TcpO₂ of 30 mmHg could be considered borderline, but after elevation of the legs to 30° for 5 minutes, the TcpO₂ fell to the clearly ischemic level of 16 mmHg. There is debate in the wound care literature regarding the exact level of TcpO₂ that defines critical hypoxia. Bacharach et al.² found that lower-extremity TcpO₂ > 40 mmHg reliably predicted healing of amputation sites, and TcpO₂2 of 20–40 mmHg, Bacharach et al.² noted that prediction of amputation failure was more accurate if the TcpO₂ level fell by 15 mmHg after leg elevation to 30° for 3 minutes. By this definition, the wounds in the authors’ present case could be reasonably classified as hypoxic. It should be noted that this patient’s ulcers were post-surgical with concomitant ischemia and, thus, may differ physiologically from primary ischemic ulceration. The sustained increase in the TcpO₂ on the dorsum of the foot documented at 7 months post-HBO treatment confirms long-term alteration of the microcirculation. Marx³ documented long-term increases in capillary density after HBO treatment of hypoxic tissue. He demonstrated that elevation of TcpO₂ and increased capillary density, which he terms the angiogenic effect of HBO, persists at the same level as long as 4 years following HBO therapy. In the authors’ case, this angiogenic effect was seen even though the proximal large-vessel occlusive disease at the popliteal trifurcation was not corrected by angioplasty or bypass. Conclusion This case suggests that HBO can function as a primary method of wound revascularization even in the setting of advanced, large-vessel occlusive disease. In carefully selected wounds with limited necrosis, it may be reasonable to offer HBO as a primary treatment or as an alternative, not just as an adjunct, to arterial reconstruction by angioplasty or bypass. Hyperbaric oxygen can lead to sustained increases in TcpO₂ distal to severe large-vessel occlusive disease. Prospective studies are necessary to confirm these concepts.