At age 69, this lady had had diabetes 29 years and an ulcer on her left big toe for 1.5 months when she was hospitalized in Philadelphia on February 22nd, 1991. The ulcer had not responded to rest and ciprofloxacin and osteomyelitis was suspected. Her pre-admission medications included Synthroid 0.1mg daily, Cipro 500 mg twice daily, Inderal LA 20 mg daily, Allopurinol 100 mg daily, Lasix 20 mg daily and Micronase 5 mg daily. She was given intravenous antibiotics (Ancef 1 gram every 8 hours) and consultants in vascular surgery and podiatry were called. Her noninvasive vascular tests showed a decrease in systolic blood pressure in the left popliteal, posterior tibial and dorsalis pedis arteries suggesting stenoses in the distal left superficial femoral artery and other occlusions in the calf. Her serum tests for hepatitis A and B were noted to be positive. She refused to have an arteriogram or local surgery on her toe and was discharged March 5th with prescriptions for Bactroban ointment and more Cipro. As the ulcer did not heal and drainage persisted, she was referred to the Circulator Boot Clinic on May 14th, 1991.

May 14th, 1991: Her big toe on presentation to Bryn Mawr.

May 14th, 1991: On the first row, the Doppler velocity curve of the 1st dorsal metatarsal artery was found to be rounded, widened and low. There was significant flow between pulse waves and the zero flow line (the short line at the lower left) as may be seen in collateral vessels and neuropathic feet. On the second line, similar findings were present in the anterior tibial at the instep. In the 3rd line, only trace flow was documented in the posterior tibial. In the 4th line, monophasic flow was noted in the peroneal behind the lateral malleolus. In the 5th line, the pulse volume, magnified 5-fold, was found at the ankle to be widened and low. In the last line, the PPG tracings of the big toe are seen to be timed with respiration as alteration in venous back-pressure with respiration had a bigger effect on the flow through the big toe than the arterial blood pressure did.

The treatment program we prescribed included: (1) oral tri meth sulfa (Bactrim -DS ); (2) local injections with gentamicin into the bed of her ulcer before boot treatments; (3) Mini-Boot treatments; (4) foot soaks at home using Sea Soaks containing gentamicin; and (5) local debridements of callus around the ulcer as it developed. Her treatments were all accomplished as an outpatient. Her ulcer drainage was cultured periodically through her treatment leading to substitution of Fortaz for her gentamicin for a period.

November 1991: Her big toe had healed. Her sensation improved over the course of her treatments; initially she did not sense her local antibiotic injections while at the end of her treatments, she did.

An abscess of her 3rd toe was found. The culture probe appeared to penetrate into the toe to the bone of the distal phalanx. A heavy growth of Coagulase-negative staphylococci was recovered and reported to be sensitive only to vancomycin and tetracycline. Her BUN was 21 mg/dl. A sedimentation rate of 51 mm/hr was compatible with the diagnosis of osteomyelitis.

January 12th, 1999: Crusty dry secretions were present on the plantar aspect of the 3rd toe. The left popliteal pulse was faint but clearly palpable. The right was more easily found. No distal pulses were present on either foot. Vascular tests were obtained.

January 12th, 1999. The Doppler velocity waveforms are shown for her RAT and LAT (right and left anterior tibial arteries) in the instep, over her R-DP and L-DP (right and left dorsalis pedis on the dorsum of the foot, over her R-PT and L-PT (right and left posterior tibial arteries behind the medial malleolus and over her R-Per and L-Per (right and left peroneal arteries above and behind the lateral malleolus). The examiner noted that all of the sounds were monophasic, that both posterior tibials were undetectable at the ankle, that the flow in the left anterior tibial was weak at the ankle and in the dorsalis pedis, that the lateral malleolar arteries (peroneal) were detected but weak, and that the studies pointed to advanced ASO (arteriosclerosis obliterans) of the tibial vessels.

January 12th, 1999. The PPG (photoplethysmographic) curves showed reduced flow in the right toes. The sensor was not able to pick up any flow in the left toes and when the gain was turned high to magnify any signal the write-out ran off the chart.

She was started on daily weekday treatments in the Boot Clinic. Initially, she was given Trovan for systemic antibiotic coverage. Her daily routine began with a cleansing foot soak in Sea Soaks (one cup) and hydrogen peroxide (one tablespoonful). Then the toe was infiltrated with gentamicin (0.5 ml from a 40 mg/ml vial), vancomycin 0.5 ml from a 500 mg vial diluted with 5 ml of Sea Soaks) and urecholine 0.2ml from a vial containing 5 mg/ml). The foot was then placed in a bag containing 100 ml Sea Soaks and about 0.3 ml of the gentamicin and vancomycin solutions. The foot, bag and all were then placed within a Mini-Boot and pumped for 40 minutes after every third heartbeat. When the culture results became available, the Trovan was replaced by Doxycycline. By January 29th, her pain and swelling were greatly reduced and she was able to walk comfortably. Her booting was reduced to four times a week. By February 22nd, she had no pain but a little drainage persisted. A culture was taken and her pumping was reduced to three times a week. The culture proved sterile except for a light growth of yeast. Amphotericin B was added to the Sea Soaks during her Mini-Boot treatments.

February 25th: The small fissure into the toe persisted. Overall the toe appeared to be doing very well.

While the plantar aspect of the toe appeared to be doing well, it was not clear how the dorsal aspect of the toe was faring. She came to the clinic on April 1st with more swelling, rubor of the dorsum of the toe and a small purple area suggesting pus. The foot was given a cleansing soak and the skin over the purple area punctured. The small amount of material gained by squeezing the toe was cultured. Daily booting and local antibiotics were begun again while the culture "cooked". The bacteriology laboratory reported "no growth". The toe resumed its normal color.

April 1st, 1999: New discoloration of the toe! Uncontrolled infection? New trauma? A response to bleeding and irritation induced by our local injections? It is hard to know at times. We treat such setbacks as evidence of uncontrolled infection.

May 13th, 1999: A little callus remains at the site of her previous ulcer. She was discharged from the clinic and advised to return immediately if the toe developed any discoloration, swelling or drainage.