Case 12:Leg Cramps, Mononeuritis, Congestive Failure, Necrobiosis Diabeticorum

At age 69 with a history of having had insulin-dependent diabetes for 33 years, this man was referred for his first formal diabetes education in September 1988. He had no claudication but was troubled by leg cramps and a painful mononeuropathy down his left leg. Both improved with boot therapy. In January 1992, he presented with congestive heart failure. His estimated ejection fraction by ultrasound was 34%. Furosemide and chlorthalidone did not reduce his leg edema. In March 1992, he complained of purple feet. In an effort to support his heart and reduce his edema, he was given 42 Long-Boot treatments with QRS to boot ratio of 1:1 (i.e. the boot compressed the legs in end-diastole of every heartbeat). His heart failure and his walking distance improved.

Shin Ulcer and Necrobiosis Diabeticorum

Two years later, July 1994, he presented with an ulcer in his shin and well-circumscribed plague in his lower anterior leg. Except for a few veins visible in the area of the anterior ankle, his venous findings were unremarkable. He also had a small ulcerated callus or corn on his left 5th toe. His ankle/arm indices were 0.78 and 0.76 in his right and left legs respectively. He was again begun on Long-Boot therapy. Over the next two months, his ulcers healed and the skin plague faded..

Two Weeks Later

And after an Additional Eight Weeks

The next several months were uneventful for him. His diabetes required periodic adjustments as did his dosage of digoxin. Quinine sulfate proved helpful for nocturnal leg cramps. By November of 1996, his congestive heart failure was becoming symptomatic again. His EKG showed multiple premature ventricular beats occurring occasionally in triplets. The RST segments were depressed 2-3 mm in leads V4-V5. He had no exertional chest pain but did get short of breath. He was interested in more boot therapy but had no foot lesions to qualify for Medicare coverage. He volunteered for current boot studies on heart function. First, he had 24 hour Holter monitor (Monitor One TC 100, Omni Series by Q-Med)> The baseline tracing had a 2-3mm depression over V5. During the study he had a one mm depression for 22 hours, 23 minutes and 52 seconds; a 2 mm depression for 43 minutes 31` seconds; and a 3 mm depression for 1 minute and 28 seconds. He was aware of no chest pain. After one week of boot therapy, a repeat study showed 2 mm depressions for 1 minutes and 1 second and no 3 mm depressions. At the end of three weeks, he no longer had nocturnal leg cramps and was walking further. Again, he had no 3 mm depressions but, perhaps because of his increased activity had 2 mm depressions for 16 minutes and 34 seconds.

Baseline RST Depression in V5

RST Depression after 3 Weeks Long-Boot Therapy

Tracings were also made of his cardiac output using the electrical impedance apparatus of IQ Renaissance Technologies. In the tracings below, the upper tracing is the EKG and the lower curve the cardiac output.

Baseline EKG and Cardiac Output (7.45L/Min)

Boot Releasing Both Legs Just Before Each Heartbeat - Cardiac Output 11.3 L/Min

Our patient and his wife have been a devoted couple for many years. At December, 1997, he appears dependent on boot therapy to control his congestive heart failure (having problems with pulmonary congestion and leg edema), his renal and pre-renal azotemia, and his tendency to form leg blisters and leg ulcers. Three treatments a week may keep him out of the hospital and reasonably comfortable.

Comments: This man was plagued by sequential problems that were difficult to treat. Leg cramps are common in patients with vascular disease and disappear generally for weeks after boot therapy. Diabetic mononeuritis is attributed to a vascular lesion of the nerve. We have booted patients with success in relieving their pain over a three to six week period. We have booted the worst leg in patients with pain in both legs, using one leg as a control. When the one leg gets better, we then treat the other leg and assume the sequence of events attests to the efficacy of our treatment. We have no controls for the treatment of neuritis in one leg only. The pain of this man was relieved. Next he arrived with congestive heart failure that was little benefited by a vigorous diuretic program. The boot is a counter-pulsation device and has obvious beneficial effects in assisting the heart. Patients with dyspnea due to failure, commonly talk comfortably while in the boot. Further, they may lie back flat in their beds. The murmurs of those patients with mitral insufficiency decrease during therapy. Elevated lactic acid levels commonly fall. The contour of pulse volume or PPG tracings in the arms or fingers may be shown to change as the boot monitor settings are changed; the sudden release of the legs by the boot may produce a sharp falloff in the various tracings. More recently as in this man, we have found large changes in cardiac output during boot therapy documented with the use of the Renaissance electrical impedance apparatus. Again, recently we have begun to tabulate the effects of therapy on angina, the baseline EKG and the Holter monitor. (See Dillon RS: Angiology 49: 523-535, 1998 in the Pneumatic section of our website library) This man benefited from the cardiac-assist action of the boot. He passed large volumes of urine after each treatment. His clinical status improved and the improvement has lasted for weeks to months. Finally, he develops a ulcerated leg plaque similar to necrobiosis diabeticorum. It might be argued that the lesion was due to venous stasis but he had no long term history of stasis disease, no obvious abnormalities of his venous testing and his lesions healed and pretty much faded with treatment. This man had multiple circulatory problems. It is because of the multiple circulatory benefits of treatment with our end-diastolic boot that we have named it The Circulator Boot.