Case 178: Eighteen Years of Boot Therapy for Multiple Foot Lesions, Claudication, Arteriosclerotic Heart Disease, Congestive Heart Failure and Chronic Renal Failure. Still Going at 81.

Referred by his diabetologist with a cyanotic tender right first toe 11/12/80 in Bryn Mawr Hospital. Born November 14th, 1916 and a paratrooper in WWII, he had a chronic problem with an old left ankle fracture but was still playing regular golf. He had a ten year history of type 2 diabetes and a 40 year history of smoking two packs of cigarettes a day. He had a family history of diabetes and recalled that three of his four paternal uncles had had amputations associated with peripheral vascular disease. His Doppler testing showed normal flow in his posterior tibial and peroneal arteries at the ankle but an obstructive pattern in the distribution of his distal anterior tibial. The vascular surgeon was unable to palpate the dorsalis pedis and recommended a course of antibiotics.

He was treated with Circulator Miniboot in hopes of opening up the flow in his distal foot. Carotid flow studies, done because of a carotid bruit, were found to be normal. He was given Dymelor for his diabetes and Aldomet and Dyazide for his hypertension. He was discharged for outpatient booting and did well until he resumed his smoking and business activities. His diabetologist again hospitalized him on January 17, 1981 for "threatened breakdown" of his big toe.

In his admission note, the diabetologist diagrammed the area of "threatened breakdown" and noted that the patient also has a history of cold exposure to his feet years ago.

The toe area in question, after various consultations, proved to be but further resolution of his initial problem. His sock had stuck to some secretions and when the sock was removed a small spot of skin had come off causing bleeding. His wife and, subsequently, his doctor had become anxious and sought immediate hospitalization. Doppler testing showed that the flow in his big toe had become close to normal.

While it was apparent his booting was associated with an improvement in his peripheral blood flow, the control of his diabetes by oral agents was not good; his glycohemoglobin was 10.3%. His doctor asked for the opinion of another vascular surgeon. The latter noted his improvement by history and suggested consideration of a sympathectomy if healing did not continue. He did heal and was referred back to the care of his diabetologist ... still smoking and still on Dymelor. He returned to the boot clinic on December 11, 1981 again with a cold painful distal foot. His Doppler sounds were again grossly abnormal in the foot.

He began to receive outpatient boot therapy seeming to improve. However, about December 28th he discovered some loose skin over a callus and cut it back himself. He was hospitalized on January 1, 1982 with a plantar abscess and cellulitis of the dorsum of his foot. Staphylococci and E-Coli were cultured from his foot. He was given intravenous Ancef and local gentamicin along with four Mini-Boot treatments daily.

His physician diagrammed the admission status of his foot on the hospital record.

January 12, 1982: His Doppler sounds were again restored to his distal foot.

He again healed his lesions and did well. He returned to work and smoking. He presented again on August 27th, 1982 with ischemia of his right foot and again his foot was pumped out successfully. On October 26th, 1982, he presented with a blue first toe and a 1 cm ulcer under his 4th metatarsal head. Both were successfully treated as an outpatient. He was still smoking and enjoys a few cocktails a week. He was now on Diabenese (chlorpropamide) and experienced a flush with the alcohol. He next reported with an ischemic foot on November 11th, 1983 when again the Doppler sounds were reduced in his first dorsal metatarsal artery. And again his foot improved with his boot treatment. On January 29th, 1985 he returned with a small paronychia; it was cured with local antibiotics and the Mini-Boot. His diabetologist retired in 1985 and he sought care for his diabetes at the boot clinic. Insulin was substituted for his oral agents. His chemistries included creatinine 1.5mg/dl, BUN 29 mg/dl and cholesterol 210 mg/dl. His brachial blood pressure was 148-166 / 86-93. In September of 1986, he complained of claudication in his right calf. He had no palpable dorsalis pedis pulse in either foot while his posterior tibials were 2+ (easily found and distinct with firm palpation). A routine EKG was normal. On December 3, 1986 he presented with red-yellow spots on the sole of the right foot suggesting infarction of skin. His BUN (31) and creatinine (1.7) were noted to have risen a small amount. On December 31st, the systolic blood pressure in his tibial vessels at the ankle level had fallen significantly below his brachial pressures while his Doppler tracings were monophasic and showed a little widening (arm 152 mm Hg vs 100 in the anterior tibial, 115 in the posterior tibial and 114 in the peroneal at the ankle).

By June 21st, 1988 his claudication had progressed limiting his walking to one block. Besides his insulin, his drugs now included Vasotec, Dyazide and Clinoril and ASA... and, unfortunately, nicotine; he was still smoking. His diabetes was better controlled (Hemoglobin A1C 7.5%). While his total cholesterol was 217mg/dl, his cocktail habit perhaps helped his TC/HDL ratio by raising his HDL to 53 mg/dl. He was given Trental for several months but discontinued it feeling it had no benefit for him. He found more relief with his boot treatment. However, he presented in November 1988 with a new problem: seeing him through the winter without access to booting. He wanted to spend the winter in Florida. His non-invasive vascular testing suggested he had developed either total occlusions or marked stenoses in his superficial femoral arteries bilaterally: the blood pressure fell 45 mm Hg from his high thigh to his low thigh and a further 30-40 mm Hg to his ankles. He, hence, was admitted to the Bryn Mawr Hospital for arteriograms and consideration of either bypass or angioplasty procedures. The films showed advanced ulcerated atherosclerotic disease involving the abdominal aorta and iliofemoral system. Bilateral renal artery stenoses, greater on the right, and an occluded left hypogastric artery were noted.

Bilateral superficial femoral artery occlusions measuring 4 cm on the left and 6cm on the right are seen.

Popliteal reconstitution above the knee with 2 vessel runoff on the right and three on the left

In the left leg all three tibial vessels could be traced to the foot as could the posterior tibial and peroneal arteries in the right foot. The right anterior tibial was discontinuous. In the right foot the pedal arch was not well seen while in later films the dorsalis pedis did visualize perhaps through collaterals from the peroneal artery.

His blood pressure was 190/90 raising the possibility of dilating his renal arteries. The diabetes service noted small blue lesions in the toes that did not blanch on pressure and worried about ischemic infarcts. The latter together with his neuropathy and poor distal vascular tests led to the recommendation of bypasses... which he turned down in view of improvements he experienced during his concurrent hospital boot treatments. He wintered successfully in Florida. By July 1989, he again had one block claudication and again had a series of treatments with the Long-Boot. On August 13, 1990 he returned after a fall with an ecchymoses and abrasions of his left ankle and again had several treatments with the Long-Boot. His smoking, diabetes and hypertension were continuing to exact a toll in the early nineties: his BUN and creatinine rose from 33 and 1.9 to 46 and 2.5 from June 1991 to July 1993. His EKG showed left ventricular hypertrophy and left atrial enlargement in September 1993, while his ankle/arm indices (0.48 right and 0.58 left) and claudication (two blocks) remained fairly constant. He fell on his stairs in August 1994 sustaining a traumatic synovitis of his right knee. The knee continued to bother him leading him to his orthopedic surgeon in September 1995 when a degenerative meniscal tear of the right knee and a right shoulder impingement syndrome were noted. His carotid bruits persisted and increased in the meantime leading to a left carotid endarterectomy on June 20th, 1996.

On August 5, 1996, he was admitted to the Bryn Mawr Hospital with congestive failure and a myocardial infarction. His R-wave was lost in leads V1-V3, his admission blood gases included: pH 7.22, PO2 61 and PCO2 37.9; while his serum chemistries included: CO2 17mEq/L, creatinine 4.5mg/dl, BUN 62 mg/dl and glucose 117mg/dl. A PSA of 13.6 and palpable abnormalities pointed to prostatic cancer. The cardiology consultant thought that his multiple disease (chronic lung disease, azotemia, peripheral arteriosclerosis obliterans and his low estimated ejection fraction of 36% all made him a poor candidate for invasive procedures. Hence, he was treated with intravenous heparin and boot therapy. His BUN fell to 55 mg/dl and his creatinine fell to 3.6 mg/dl. He was discharged to take Cozaar 50mg qd, Isordil 5mg BID, Ecotrin, Apresoline 25 mg QID, Lupron and his usual insulin scales.

The heart attack had weakened him. We suggested he might benefit from participating in our Long-Boot heart (Angiology 1998) from which he was eventually dropped for failing to attend many of his visits and eventually for leaving for Florida.

His EKG tracing is shown on the 1st and 3rd lines. His dZdT curves obtained from a Renaissance IQ electrical impedance monitor are shown on the 2nd and 4th. The 1st and 2nd lines were taken from his baseline study when the monitor gave 6.32 L/min for his cardiac output and 91.6 ml for his stroke volume. During Long-Boot therapy, 3rd and 4th lines, his cardiac output increased to 10.9 L/min and his stroke volume increased to 155.7 ml.

Here we see his Q-med Holter heart monitor RST histogram prior to his series of Long-Boot treatments.

And here we see his Q-Med Holter heart monitor RST histogram after a series of treatments and before he was dropped from our study. The number and severity of RST depressions were diminished.

His cardiologist put him through a stress test on October 4, 1996. He developed fatigue during the test and dropped his ST segments in the inferior lateral leads reaching a peak pulse rate of 112. The patient again wanted to go to Florida. We advised him of his borderline renal function and pointed out that while his BUN and creatinine had improved with his booting, we expected the values to deteriorate somewhat without booting. Golf in Florida beckoned him and off he went until Christmas. He returned to the Bryn Mawr Hospital on December 26, 1996 in congestive heart failure with a BUN of 86 and a creatinine of 4.7 mg/dl. His CPK rose to 98 and his SGOT to 167. Again, his cardiologist recommended conservative therapy and again he was booted and given intravenous heparin. He improved markedly and was discharged on coumadin, Apresoline, Ismo, Cozaar, Rocaltrol, TUMS, Epogen, Lasix and a 3-times/week Long Boot program. Florida and golf again beckoned. He was warned that both heart failure and an increase in his renal failure were likely in the absence of his boot therapy.... and his Florida doctors would likely begin dialysis. To the Florida golf links he went.... and on March 8, 1997 he was admitted to the North Collier Hospital in Naples Florida, still smoking, with unstable angina and an acute myocardial infarction. His BUN was 98 and creatinine 6.7 mg/dl. His glycohemoglobin was 4.1 (N 4.4-6.4%). Dialysis was begun.

He returned to Bryn Mawr where his dialysis was continued and proved quite troublesome. His shunt has clotted off several times requiring multiple shot hospitalizations. On one occasion the shunt became infected and he became septic and developed pneumonia. Removal of excessive fluid has left him faint and unsteady on his feet of many occasion. When his pressure is especially low, his dialysis chair is tilted backward and his feet elevated to maintain cerebral blood flow; during these episodes he has no arterial flow to his toes and on two occasions his feet have broken down and required boot therapy.

On September 28th, 1997 he presented with focal necrosis of the end of his right 1st toe, an avulsed and cracked left 1st toenail, infection of the left 1st toenail bed, a small abscess under his left 4th toenail and a small area of focal necrosis under the tip of his 5th left toenail.

On November 7th, 1997 his left 5th toe was still devitalized. He was continually advised he had to stop smoking. Would a toe amputation heal if the boot failed him? Would he lose a leg? Could he golf? He stopped smoking!

January 15th, 1998: His toes are healed. He is ambulatory.

He continues with his dialysis three days a week and intermittent boot therapy. An 18-year veteran of the boot.... he is one of our most experienced boot patients.

Comments: In Dillon's Angiology 1997 paper (see our library), he reported on 2177 episodes of foot care. The computer used in the study allowed only for three relapses a patient. This man had possibly 20 episodes over the years between 1980 and 1998. Sometimes, it was not clear when one episode was over and another beginning. In spite of 28 years of diabetes, 57 years of smoking (over 100 pack-years?) and 18 years of symptomatic peripheral vascular disease, this man is still alive at 81 year old and has all of his parts. The Circulator Boots have helped him with Buerger's disease, with toe infections, with claudication, with his heart failure.... and to some extent with his renal function. His last 24 hour urine volume was about 1000 ml in March, 1998. His kidneys are not ideal for boot support; they are somewhat small likely due to his renal artery disease. We think we are more likely to benefit the large diabetic kidney.. Still, over the years booting has seemed to help his kidney volumes and function. Can we claim a role in his longevity? Can we claim a role in his quality of life? I suspect golfers might think so..