Case 196: Diffuse Cardiovascular Disease, Possible Distal Emboli Following Heart Catheterization and Bilateral Leg Amputation Avoided with Boot Therapy.

Born 4/29/21, this gentleman was referred on November 21, 1998 by his family physician for cellulitis of the left foot and gangrene of the toes of both feet possibly secondary to emboli subsequent to a coronary angiogram. The latter had been accomplished on 9/28/98 and was noted to show an ejection fraction of approximately 40-45% area and akinesia of the high lateral wall and the inferior walls of the left ventricle. The aortogram showed multiple lesions along with a 50% obstruction of the lower abdominal aorta. Subsequent to the aortogram, his wife thought he was confused and his physicians found that he had a retroperitoneal bleed and pain and discoloration of his feet. The latter were treated with analgesics as an outpatient. However, the discoloration and pain increased in the left foot suggesting lymphangitis and cellulitis to his family doctor who hospitalized him on November 3rd for intravenous antibiotic therapy. His antibiotics were continued after his transfer to the Transient Care Unit and physical therapy and walking exercises were instituted. The infectious disease consultant suggested his rubor was more likely due to arterial insufficiency than cellulitis leading to consultations with the vascular surgery service. The latter noted ankle/ arm indices of 0.87 in the right leg and 1.2 in the left. The pulse volume waveforms in the midfoot were noted to be low. The surgeons thought the right foot was improving and the left deteriorating with progressive necrosis of the toes. They saw no opportunity for reconstructive surgery.

On November 21st, we found his feet to show multiple signs of ischemia. The left foot was especially discolored. There was a lack of blanching of the rubor after application of direct pressure to the skin of the toes, the distal plantar surface and the lateral dorsum of the foot suggesting extravasation of blood and a discontinuity of the small vasculature, a pregangrenous condition.

Doppler tracings on November 21st showed a left posterior tibial artery that was strong but not normally biphasic. The left anterior tibial at the instep and the left dorsalis pedis could not be detected. The left peroneal was weak. In the right leg, the anterior tibial, posterior tibial and peroneal were all detected at the ankle level but were weak and monophasic. The right dorsalis pedis was faint to absent.

Pulse volume tracings on November 21st showed better flow at the left ankle than at the right ankle. No flow was found in the left midfoot and that in the right foot, amplified 100% in these tracings over the ankle flow, was widened and diminished.

Perhaps because all three tibial vessels were detected at the right ankle and possibly fed into the foot, the right foot appeared to be in better condition than the left. Both feet, however, had areas of necrosis in the first and fifth toes. Once the above vascular testing was completed, the referring physicians and his wife were advised that he would do well to have Mini-Boot treatments to both legs over the next several weeks twice daily until he was pain free and his feet obviously stable. Until arterial flow was re-established in his left foot, they were advised that we might not be able to prevent an increase in the mummification process that was involving the left foot. He received 6 treatments from the 21st to the 30th of November and 15 treatments during December.

By December 23rd, the color was improved in both feet but the necrotizing process in the left foot had extended to the distal aspects of all of the toes.

The necrotizing process was arrested in the right big toe and reversed in the right fifth toe.

Doppler studies on January 18th, 1999, showed strong flow in both posterior tibials, detectable but diminished flow in both the anterior tibials at the instep and in the dorsalis pedis. Overall, the flow was improved since his November studies.

Pulse volume curves in the midfoot were still abnormal but again significantly improved.

January 19th, 1999: The distal left foot remained painful. The distal half of toes 2-5 were trimmed back. In an attempt to minimize any infection contributing to his pain, the black eschar was infiltrated with gentamicin and gentamicin was added to the Sea Soaks used in the Mini-Boot.

Prior to each treatment, his foot was cleaned in a Sea Soaks dilute hydrogen peroxide soak. The local gentamicin proved safe in spite of the elevation of his BUN (51 mg/dl) and creatinine (3.2 mg/dl) that had been noted since his arteriogram.

February 19th, 1999: The inflammation and pain had subsided.

The demarcation process was almost complete; the tissue was close to normal up to the mummified tissue.

April 6th, 1999: The toe stubs were yet to be debrided back to the marrow which skin can grow across.

Again, it is seen that the plantar surface was now normal up to the toe stubs.

September 20th, 1999: The radiologist noted the multiple amputations through the toes of the left foot at the level of the proximal interphalangfeal joint or within the proximal phalanx itself. No bony destruction was seen in the remaining bones but there was some osteopenia.

January 13th, 2000: He had had a stroke on October 13th, 1999 causing a non-fluent phasia and an increased awareness of pain in his left foot. His neurologist considered the possibility of reflex sympathetic dystrophy and prescribed Neurontin without much benefit. His stroke made it difficult to assess the severity of his pain.

The eschar on the end of the right first toe had been debrided the previous summer and is now seen to have closed over. He had been treated three times a week until his stroke. Subsequently, he missed several treatments and then as his feet were largely healed was cut back to one to two treatments a week.

May 11th, 2000: His walking was limited by fatigue likely due to his heart disease. He continued to complain of foot pain, but, again due his aphasia, his discomfort was hard to evaluate.

Comments:This man had diffuse arteriosclerotic cardiovascular disease and likely had significant tibial disease before his arteriography procedure. The degree of his ischemia was not appreciated by his cardiologist and family physician and his symptoms were mistaken for cellulitis. He had progressive necrosis of his toes during his two months of conservative observation. The necrosis prolonged the duration of his pain and the time needed for boot therapy to heal his feet. Delayed recognition of ischemia post-angiography is common likely due to the natural inclination of the physician to deny a complication of his procedure, the acceptance of some physicians that distal emboli is an accepted risk of their procedure and their hope that the complication will spontaneously improve. In view of the progressive necrosis of his toes in both feet and in the absence of detectable Doppler sounds in his feet at the time of referral for boot therapy, it is likely that this man was headed for bilateral leg amputation prior to his boot therapy.