Case 135: Claudication, Acute Leg Occlusion, Angina, Cerebrovascular Insufficiency and Renal Failure and the Boot; a Case History

This man was born October 16th, 1902. Vascular disease was familial and eventually when he died in his 90's, he had set a record for the men in his family; his father had died at age 65 with hypertensive arterosclerotic cardiovascular disease as did two uncles and a brother. His own history of vascular disease began in 1950 at age 48 when he had chest pain thought to be a manifestation of coronary heart disease; he stopped smoking. In 1954 he suffered from two block intermittent claudication and was evaluated at the University of Pennsylvania by Dr. Hugh Montgomery, a vascular medicine specialist, and Dr. I.S.Ravdin, Chief of Surgery. He was thought to have a partially blocked right iliac artery. A sympathectomy was considered but not accomplished. He was again evaluated by Dr. Montgomery in 1958 who then found both dorsalis pedis pulses and the right posterior tibial pulse to be missing. In 1965, he experienced some dizziness and had x-rays showing calcium deposits in his carotids. His overall care was supervised by Dr. Wallace Dyer who retired in 1968; his EKG's under Dr. Dyer were normal. He first consulted Dr. Dillon in 1968, again with intermittent claudication. His blood pressure was 185/95. An aggressive blood pressure program was instituted along with a walking program. In 1970, he was admitted to Bryn Mawr Hospital because of blurred vision and an unsteady gait. The neurologists and vascular surgeons noted modest narrowing in his carotid arteriograms but did not feel the lesions warranted surgical intervention. He was discharged on coumadin and phenformin; the latter was added both for mild type 2 diabetes and for its known effect in increasing fibrinolysins. His claudication disappeared. In 1975, his phenformin was discontinued as it was removed from the market because of the lactic acidosis scare. Within a few days of its discontinuance, he was admitted to Bryn Mawr Hosptial for chest pain. Clot lysis times on successive days revealed no lysis after 24 hours. He was again provided with phenformin and did well until our supplies were depleted. His symptoms of cerebrovascular disease recurred; in 1977, numbness at the corner of his mouth and in 1978, numbness of his tongue and left arm and leg.; he was treated with coumadin and persantine. In 1980, he was admitted for a briskly bleeding duodenal ulcer; the coumadin was discontinued. When his ulcer healed, he again noted signs of cerebrovascular insufficiency. Two clot lysis times revealed only 15% lysis after 30 hours. He was then given a treatment with the Long Circulator Boot; his clot lysis time increased to 100% at 24 hours. He was given a few weeks of Circulator Boot therapy as an outpatient; his cerebrovascular symptoms disappeared. To free him from boot therapy and increase his fibrinolysins at the same time, he was provided with metformin that was obtained from Canada. He did well until 1982.

He was wintering in Florida in 1982 when a cardiologist modified his medications substituting 250 mg of tolbutamide for the metformin (which was not available) and adding Procardia to the program; after the 4th pill of the latter, he collapsed presumably because of low blood pressure and the medication was discontinued. His claudication began to get worse. He flew back to Philadelphia and de-planed with a "Charley horse" in his left leg. He arrived in the office in a wheelchair able to take but a few steps. His brachial blood pressure was 170 supine and 130 sitting. His supine ankle blood pressures were 85 in the posterior tibial and absent in the anterior tibial and peroneal arteries. He was offered outpatient booting or hospitalization for arteriography and consideration for vascular surgery. Concerned about his head and his heart, he chose outpatient booting. He was booted daily for several days noting a small improvement after each treatment. He was then booted intermittently for several weeks and his blood pressure gradually increased to 122 in the posterior tibial, 68 in the anterior tibial and 105 in the peroneal arteries. In spite of restarting metformin, his clot lysis time was but 82% before boot therapy; it increased to 100% after boot therapy. With regular usage of the metformin, the additional fibrinolysis gained by boot therapy disappeared. He then took a trip to Canada and obtained a several months supply of metformin and regular booting was stopped. For the next few years, he did well. He returned for short courses of boot therapy when his legs seemed to ache. He remained very volume sensitive in his blood pressure. He was treated with nitrates, propranolol, minoxidil and hydrochlorthiazide. He was hypertensive without the latter and had marked orthostatic hypotension with a dose of 50 mg a day. By weighing himself daily and monitoring his blood pressure at home, he was able to take intermittent doses of the hydrochlorthiazide and control his pressure.

He was readmitted to the Bryn Mawr Hospital in May, 1985, with chest pain. His EKG showed poor progression of his R-waves across the precordium but no ischemic change was noted. He was found to have a recurrent duodenal ulcer and a hiatal hernia. His pain disappeared on his ulcer program but over the next few months he had leg edema possibly associated with an increase in his dosage of minoxidil. Lasix was substituted for the hydrochlorthiazide.

He did well in 1986 having only some claudication in his left leg for which he received some Long-Boot treatments. Some occasional chest pain appeared to be more gastrointestinal than cardiac in origin and did not respond to nitroglycerine. In May of 1987, however, his chest pain was more like angina and led to hospitalization. It was not clear if he had been taking his metformin; his clot lysis study revealed no lysis in 24-hours. Ultrasound studies showed non-critical carotid arteriosclerosis. He vacationed in Maine and returned with a paronychia that dried up with the local injection gentamicin and a single boot therapy. Persistent chest pain again led to hospitalization in late August. His carotid studies again showed signficant but non-critical disease. His ankle/brachial indices were 0.65 bilaterally. His coronary angiograms were read as showing an estimated 41% ejection fraction, a good but calcified left main coronary artery, moderate diffuse disease in the left anterior descending artery (one 80-90% stenosis was seen just beyond the 2nd diagonal branch), a long subtotal occlusion in the dominant circumflex and a subtotal occlusion in its first marginal branch and a total occlusion in the proximal non-dominant right coronary artery. The RAO left ventriculogram showed an akinetic basal segment while the other walls of the ventricle contracted vigorously. Subsequently on September 10th, 1987, his left common iliac artery was ballooned to allow the placement of an aortic balloon and triple aortocoronary saphenous vein bypass.grafts were placed to the 2nd diagonal and distal LAD and a separate graft was placed to the distal circumflex in the left anterior descending artery. Five days after discharge from the hospital, he came to the office for rest pain in his left foot; his Doppler studies showed a loss of amplitude in his posterior tibial and his anterior tibial and metatarsal arteries were essentially flat. His pain again improved with boot therapy. His weight was now down in the 135 pound range and his metformin had been replaced with tolbutamide in treating his diabetes. In June 1988, he developed another paronychia, this time on his right great toe; this responded quickly to local gentamicin and Mini-Boot therapy. His orthostasis and carotid disease contributed to his unsteadiness and occasional falls; in March 1989, he underwent a right carotid endarterectomy. His angina slowly returned leading to his hospitalization July 10th, 1990. His medications were altered and he remained ambulatory until he, having fainted at church, was again admitted for observation in September , 1990. Shortly thereafter, he contused his heart as a passenger in a car accident in Maryland in which a fellow passenger was killed. He attempted to return to his home for community living but was found unresponsive and hypotensive bringing him back to Bryn Mawr hospital. His red cell mass was found to be low and his condition improved with infusions of packed cells. In December, 1990, he again complained of discomfort in his left leg; the Doppler waveform was again low in the anterior tibial and his metatarsal arteries. His discomfort was relieved with Long-Boot treatments, three in December, one in January and three in April, 1991. The latter wre noted to help his leg edema which was not responding to his diuretic therapy (Lasix). Doppler testing in May showed the waveforms to be improved. Gout, gastritis secondary to non-steroidal pain medication, faintness, bradycardia and chest pain due to a sternal wire led to hospitalization on June 29th, 1992; the wire was removed. His blood pressure remained difficult to control without producing significant orthostasis; an ACE inhibitor (Vasotec), beta blocker (Lopressor), nitrate (Transderm nitroL and methyldopa were used in various combinations along with his diuretics (usually Lasix). He found leg swelling troublesome and gradually began to drink less to cure problem himself. In April 1993, he was admitted with a BUN of 100mg along with a falloff in the flow to his legs. A Foley catherter was placed in his bladder to bypass his prostate, he was encouraged to drink more and he was given Long-Boot therapy to assist his heart and legs. An ultrasound of his kidneys did not show any hydronephrosis. Still his BUN fell to 95 on the 3rd day, 71 on the 6th day and 46 on the 10th day of boot therapy. He was discharged on Norpace, minoxidil, Lasix, tolbutamide, allopurinol, Pepcid and Lopressor. Outpatient booting three times a week was recommended. On May 14th, it seemed to be effective: his BUN was 43 and his creatinine 2.4mg/dl. He now had moved into the medical care unit of his community living area and fell under the care of the physicians in the home. He subsequently died there.

Comments: The clot lysis time used here is an old test. The patient's blood is allowed to clot in a silicon-coated graduated tube with a string hanging in the tube and just touching its bottom end. A clot forms around the string, retracts and eventually should lyse. The tube is placed in a 20 degree C water bath. At various time intervals, the string is pulled up lifting the clot from any serum in the tube. If the volume of serum left in the tube when the clot is lifted is half the volume of clot and serum, the clot lysis is said to be 50%. If the volume of serum is 75% of the volume of serum plus clot, the clot lysis is said to be 75% etc. In this man clot lysis times were normalized by either therapy with biguanides or booting. See our "Clotting" library for references (Back N et al). Dr. Dillon actually began a study of clot lysis times as affected by boot therapy. But the clot lysis test is a crude test. If it is already well within normal limits, e.g 100% in 6 hours, no effect of booting will be seen. Hopefully, a more sensitive test such as a radioimmunoassay for TPA may be available someday. When we have presented this case to medical groups, someone commonly asks why we did not hospitalize this patient when he developed a leg occlusion on the airplane and get our vascular surgeons to do an embolectomy as it standard or at least common practice. In the past, we have had the surgeons introduce a Fogarty catheter down the thrombosed vessel and rake out large wads of clot. The lumen of the vessel is commonly restored by the procedure. However, the "rake" also traumatizes the endothelium of the artery and we commonly find the vessel re-thromboses in spite of heparin therapy. (See next case.) In this man's case we had a freshly thrombosed vessel which we had a good chance of opening with boot therapy alone. In other cases, we have combined booting and intravenous Streptokinase or urokinase therapy with some success. The latter, however, requires hospitalization and full laboratory support. In addition, it is more hazardous. The symptoms of cerebrovascular disease and of angina were lessened in association with boot therapy. See our library for pneumatic boots for the experience of others in this regard. Finally, his renal function improved significantly in association with his boot therapy. Elsewhere in these case histories we have described such improvement which we associate with an improvement in cardiac output. Our boot patients seem to survive a long time (see Case 34). This man set a record for the male members of his family.