Case 189: Postoperative Bilateral Foot Ischemia and Toe Necrosis Relieved with Boot Therapy

Born October 13th, 1928, this man was to become well acquainted with surgeons. He had a herniorrhaphy in 1950, colorectal cystectomy in 1974, a cholecystectomy and appendectomy in 1989 and coronary artery bypass surgery on August 5th, 1998. There was a question of his having had cholesterol emboli to his feet at the time of surgery. He was discharged with foot sores but no severe pain. The feet became progressively worse over the next several weeks. He returned to his surgeon who had nothing to offer except the comment: "Let nature go..." Referred by friends, he came for consideration of therapy with the Circulator Boot on October 13th, 1998.

October 13th, 1998: The soles of his feet were cyanotic and painful. The right middle toes and the left 1st and 4th toe had distal necrosis.

October 13th, 1998: His left heel was likewise very tender and cyanotic with a coin-sized black eschar on its posterior lateral aspect.

October 13th, 1998: The dorsums of the feet were not cyanotic, but ruborous compared to a normal foot.

He recalled weighing 145 pounds at age 18 and 180 pounds at age 25. He had reached a maximum weight of 228 pounds about 1995. He denied having diabetes but recalled being told he had a high sugar count about 1994 and was advised to diet. He had hypertension for six years and had a small stroke in 1995. He had smoked a pack of cigarettes a day for 40 years and quit in 1996. He was now impotent and had a bruit in his right carotid. His feet hurt at rest and he was capable of minimal walking. His femoral pulses were easily palpable with firm palpation (2+), popliteal pulses palpable with light touch (3+), the posterior tibial pulses 2+ and the dorsalis pedis likely present after searching (1+). Vascular tests were done.

October 13th, 1998: There was good flow down the posterior tibials at the ankle level. Manual pressure on the posterior tibial arteries quieted the sounds in the dorsalis pedis in both feet, in the faint anterior tibial in the left anterior ankle and in the right perforating peroneal artery; in all of these vessels the waveforms were inverted signifying backward flow. The right anterior tibial could not be found.

October 13th, 1998: The pulse volume waveforms fell off progressively down the legs. While low at the ankle, they were especially low in the left midfoot.

Hence, he was thought to have occlusive disease in his anterior tibial and peroneal vessels, diminished overall flow in the mid-feet and negligible flow distally. His serum homocysteine level on October 14th was 31.2 (normal 4.9 to 14.6 micromol/L. Subsequent values for folic acid and vitamin B12 were 9 ng/ml (normal > 1.9) and 195 pg/ml (normal >200 and indeterminant 160-200). He was started on vitamin B12 injections. Pus from the 4th right toe grew out 4+ Pseudomonas aeruginosa. He was given a prescription for Cipro and gentamicin was injected into the necrotic portions of the toe before his Mini-Boot treatments until the infection was gone. Pus became apparent in the right great toe in December when heavy growths of Alcaligenes xylosoxidans and coagulase-negative Staphylococci were recovered. He was then treated with oral Doxycycline and local vancomycin. Patients with feet like these have pain day and night, and they do not tolerate debridements without anesthesia. We provide whatever oral analgesics they require. His daily treatments included: (1) a cleansing foot soak with Sea Soaks and dilute hydrogen peroxide (they are asked to keep their feet out of unsterile home baths and tubs); (2) local antibiotic injections into areas of obvious infection; and (3) Mini-Booting with the foot immersed in Sea Soaks and appropriate antibiotics if infection is present... or Mini-Booting the dry bandaged foot if no infection is present. The patient is often more comfortable in the Sea Soaks solution. His serial photographs document his course.

November 17th, 1998

Color improving

Demarcation progressing

Heel eschar discrete.

Eschar beginning to separate.

Partial autoamputations of right 2nd and 3rd and left 4th toes.

Tips of the big toes still to heal.

Ten toes with good color mostly intact

Tip of left big toe epithelizing

Heel ulcer close to healed

Cap of left 4th toe debrided.

Bone tip of left 1st toe shelled out giving good bleeding.

Heel site reddened but intact.

Comments: Whether this man had cholesterol emboli to both feet or whether he had advanced distal arteriosclerosis obliterans in his anterior tibial and peroneal vessels which occluded in the remote postoperative state is not clear. The symptoms of cholesterol emboli depend on the area where the emboli are created. Loosened plaque in the proximal aorta, for example, may embolize anywhere in the body from head to toe. The descending thoracic aorta may be the source of emboli to the kidneys, intestines, and muscles and skin from the abdomen to the toes. In this man, there were no symptoms of ischemia except in the feet. One might conjecture that plaque from the abdominal aorta embolized down both iliacs, spared the thigh, took a 90 degree turn into the anterior tibials blocking them and showered smaller emboli into the feet blocking flow into the heel and toes. The possibility of pre-existing occlusive tibial disease with new occlusions occurring due to a decrease in cardiac output, stasis and bedrest associated with his surgery is easier to imagine. A tissue biopsy might have helped to make a definite diagnosis but would also have created a new and likely painful lesion to heal. Practically, the exact diagnosis is not important in cases like his unless his surgeons entertain the possibility of operating on some source of recurrent emboli, an abdominal aneurysm for example. In regard to the legs, he was not a candidate for any other form of treatment (thrombolysis, angioplasty or bypass). With his disease beginning below his knees, he was a candidate for our Mini-Boot therapy. His prolonged treatment course would likely have been shortened with hospitalization to allow multiple treatments a day. He was at risk of losing both feet and is presented to illustrate the time course of outpatient treatment in such cases. He had several advantages in a sense: others had told him he might lose his feet, that there was no surgical procedure to help him and that he must "let nature take its course." He stuck to our program and did well. We have started on other patients who have panicked and gone elsewhere when advised that their disease was advanced enough to require amputation in many centers. Others have flown in for a day to have three or four treatments and left disillusioned they were not cured. Necrotic tissue just does not heal in a few days. One might have noticed that this is another current case. Now that we know we have a website where we can demonstrate our method, we are becoming better at taking pictures.

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