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Pages S54-S58 of Methods of Treatment
Support of legs, heart and kidneys. Patient JM was born 9/5/29 and was found to have diabetes mellitus at age 16. He first sought the care of a diabetes specialist in July 1954. In November, 1954, a gastrojejunostomy for dilated duodenum was performed resulting in a circus movement and marked weight loss; a re-anastomosis was necessary in April 1955. In 1964, early cataracts, advanced diabetic retinopathy and proteinuria were noted. Hypophysectomy was considered. By 1971, no vision was present in the left eye and vision was limited to 10/70 in the right eye.
In July 1973, he had his first major foot problem: an amputation of the right 4th toe for osteomyelitis. In December 1974, a paronychia left first toe was treated successfully with bedrest and antibiotics. In June 1975, he developed lesions on both feet; a 3.7 cm black spot on left heel and 1.2 cm black spot under the left 1st metatarsal head remained non-responsive to bedrest and antibiotics. Revascularization was considered and an arteriogram was performed with subsequent complete renal shutdown. The study showed several areas of stenosis in the left superficial femoral and both popliteal arteries and decreased runoff in both legs below the knees. A peripheral vasodilatation test showed extremely poor flow in both feet: toe temperatures in the right foot varying from 19.8 to 21.6 degrees C and in the left foot from 19.6 to 21.4 degrees C (constant temperature room at 20 degrees C, patient under warm blankets with only his toes and face exposed). Normal patients have toe temperatures in such circumstances over 30 degrees C while those with severe impairment are listed in the 21-25 degree C range (5). Here evaporation in a dry room allowed his toes to cool below room temperature. After two weeks in the hospital, his lesions were improved but not healed. He was admitted to the Clinical Research Unit of the Philadelphia General Hospital where he received treatment with a Circulator Boot prototype. A large rise in subcutaneous PO2 was noted after boot treatment by the polarographic method. His foot ulcer healed and renal function improved.
On July 4, 1976, he was hospitalized for two weeks for chest pain, a myocardial infarction and hypertension (195/105). A creatinine of 4 mg/dl was noted. In September, 1976, he was hospitalized for partial intestinal obstruction, cause undetermined. Laboratory values included serum BUN 87 and creatinine 4.4 mg/dl. In November, 1977, he was hospitalized for a subendocardial myocardial infarction and uremia. Denervation of his bladder, nephrosclerosis, Kimmelstiel-Wilson’s disease and prostatic hypertrophy appeared to be contributing factors; hydration and scheduled urination at two-hour intervals helped. EKG 12/77 showed inverted T-waves in V4-V6.
In April 1978, he was hospitalized for extreme malaise, tired legs and uremia. Kidney transplantation, hemodialysis and peritoneal dialysis were offered. The patient requested a trial of boot therapy in that it had helped his malaise in the past. His BUN fell from 116 to 85 mg/dl and his creatinine fell from 6.3 to 5.6 mg/dl. He was discharged to receive outpatient long boot treatments to one leg, from groin to toes, three days a week with a boot:QRS ratio of 1:1. The fatigue in his legs lessened. In June 1978, boot therapy was discontinued lest it had a placebo effect. His malaise quickly returned as his BUN rose. Boot therapy was re-instituted 3 days a week. On February 13, 1979, boot therapy was again discontinued because of snow and frozen air lines.
He was admitted to the hospital February 20, 1979, with anorexia, extreme malaise and nausea. He had palpable femoral pulses and Doppler pulses distally; his blood pressure was 130 in the left PT and 118 in the right. His ankle reflexes were absent. He was treated with hydration and boot therapy; his BUN fell from 119 to 85 and his creatinine fell from 6.7 to 6.0 by the tenth hospital day. The precordial EKG leads returned to normal. On the ninth and tenth hospital days both echocardiograms and isotopic myocardial scans were normal with an estimated ejection fraction of 75%; an 11% increase in the ejection fraction was estimated on the ultrasound while no significant change was seen during or immediately after boot therapy on the scans; the patient expressed no surprise at the results because, he explained, he felt well at the time of both tests. On the 13th hospital day, he received Lasix at 8AM and a Foley was inserted into his bladder to reveal a residual volume of 180 ml. He passed an average of 152 ml of urine per hour from 8AM to noon; he was then given a 35 minute boot treatment; his urine flow increased to 211ml/ hour. Urine and serum measurements showed an increase of 20.4% in creatinine clearance and 24.8% increase in the clearance of BUN with the boot therapy. On the 14th hospital day, the Lasix was omitted; his average urine flow was 71ml/hr of urine from 8AM to noon before boot therapy , 175 ml during a one-hour boot therapy and 165ml the hour following boot therapy. Still wary of the risks of peritoneal and hemodialysis, he chose to add the gastrointestinal dialysis technique of Young and Lee to his boot program(6). His serum BUN dropped to 72 mg/dl.
On October 5th, 1979, he arrived outside our office door with chest pain of eight hours duration, dypsnea, cough, diffuse rales in his chest and an apical gallop; he refused to go to the hospital emergency room and allowed that he had come for boot therapy. With the start of the boot therapy, he rapidly improved and found total relief of his symptoms in ten minutes. He then agreed to go to the hospital where nonspecific EKG changes were noted along with an initial BUN of 113, creatinine 8.0mg/dl and persistent arterial hypertension in the 195/90 range. The mechanism whereby boot therapy appeared to be helping him was not clear. He agreed to the insertion of an arterial line, which proved difficult and could be advanced but a few inches above the wrist. The catheter showed changes in the shape of the arterial waveform during boot therapy but no pressure or flow measurements were possible. Ultrasound tracings were made of his carotid waveforms both when the time of boot compression was placed in systole (giving giant carotid pulse waves that were terminated by a sharp drop-off when the boot deflated) and when boot compression was placed in end-diastole (resulting in narrow wave forms as the sharp drop-off due to boot compression is buried in the waveform). The changes were made more apparent by pumping on alternate beats. The tracings were interpreted as showing a rapid significant reduction in cardiac afterload induced by decompression of the boot (Figure 12).
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Figure 12. Patient JM: Doppler tracings of carotid artery are shown. The top tracings were taken before boot therapy. Boot compressions (black rectangles) were timed to coincide with cardiac systole on every third beat (second line), every other beat (third line) and on every beat (fourth line). Small arrows mark the moment of expected boot decompression and are associated with a sudden dropoff in blood velocity when actually occurring after a boot pulsation (after end of black rectangle). Boot compressions were timed in late diastole (hatched rectangle) in the bottom line; here the dropoff in velocity is buried in the next waveform which is narrowed. |
His medications now included metoprolol 50mg TID, hydralazine 50mg TID, isosorbide dinitrate 5 mg TID and digoxin 0.25mg 5 days a week. Serial cardiograms showed marked T-wave inversions V2-V4 and less marked inversions in V5 and V6 in November 1979. By December 1980 only minimal T-wave inversions were seen in V4-V6.
In April 1980 he was admitted for abdominal pain thought to be associated with yeast enteritis and stomach and bladder paresis. He was now on peritoneal dialysis. He developed congestive heart failure having retained excessive dialysis fluid. He was treated successfully with boot therapy, furosemide and intermittent positive pressure respiration. His discharge medications now included minoxidil, calcitriol, metoclopramide, allopurinol, isosorbide dinitrate, furosemide, Alternagel, nystatin and his insulins.
A few weeks later, he arrived in the emergency room in congestive heart failure. His home program now had included boot therapy which had been omitted a few days because of a sense of well-being and preoccupation with his dialysis. His systolic admission blood pressure was 210. Morphine, oxygen, furosemide, insulin, a nitroprusside drip and intermittent positive pressure respiration were tried without relieving his failure. Boot treatment was then started in the emergency room; his failure improved perhaps due to the boot therapy or possibly the gradual effects of his previous treatments. Hypertonic dialysis fluids were subsequently used to remove excessive fluid. Serial EKG’s suggested that he had sustained an anterior wall infarction. An echocardiogram the 3rd hospital day showed good function of the left ventricle but a somewhat enlarged left atrium.
In June, 1980, he was hospitalized for uremia and congestive heart failure perhaps precipitated by a prescription of tetracycline that had been prescribed for a suspected overgrowth of his intestinal flora. His BUN was 135 and creatinine 11.3 on admission falling after two weeks of peritoneal dialysis in the hospital to a BUN of 49 and a creatinine of 8.6mg/dl. During the hospitalization he had periods of fluid overload associated with congestive heart failure and various heart arrhythmias. The latter were treated successfully with nitroprusside IV drips and boot therapy.
On December 26, 1980, he was admitted with bronchitis, fever, congestive heart failure and uremia. He responded to oxygen, antibiotics, peritoneal dialysis, morphine and boot therapy. He was instructed in our chronic ambulatory peritoneal dialysis program. He installed his own boot system at home.
He was admitted again in November 1981 with nausea and repeated hematemesis. Conservative measures failed and he was taken to the operating room where a large blind loop, that originated in the duodenum and extended to the pelvic rim and bladder, was removed. Postoperative congestive failure responded to vasodilators and boot therapy. Hemodialysis was performed postoperatively on three occasions and then his peritoneal dialysis was resumed. On the 17th of December, he developed septic shock associated with a staphylococcal peritonitis. His blood pressure was successfully restored and maintained over nine hours with the Circulator Boot until his intravenous and peritoneal antibiotics became effective. On the 30th of December, a bedsore on the back of his right heel was noted and daily boot therapy for the right leg was begun. He was discharged intact but weak on January 12, 1982 on calcitriol, metoclopramide, propranolol, minoxidil, Nitropaste, and his insulin regimen.
At 11 PM in May, 1982, his wife phoned that he was again in failure and that his heart was too fast to operate the boot. She was instructed set the boot monitor to unload every other heartbeat. The boot functioned and a regular boot cadence of about 75 beats per minute was audible over the phone. Over the course of five minutes the cadence slowed to approximately 50 beats per minute; she was then instructed to set the monitor to unload every heartbeat. His pulse continued to slow and he was out of trouble.
He was hospitalized August 12th, 1982 and died on the 13th; no boot treatments were performed.. Autopsy revealed end-stage kidneys with evidence of Kimmelstiel-Wilson disease and advanced arteriosclerosis, an enlarged heart with three-vessel non-occlusive disease and an old subendocardial infarction of the posterior and lateral left ventricles. Bilateral pleural effusions and congested liver and spleen suggested that congestive heart failure was the cause of death. Foot lesions had also developed but were not mentioned on the autopsy report.
Comment: With boot therapy, JM maintained his legs seven years. He successfully postponed dialysis two years. He worked at least part time until his last year. The boot was able to successfully assist his heart both in the hospital and at home; it aborted an infarction, reversed heart failure and supported his circulation during an episode of septic shock. Clinical bedside studies suggested that pumping either leg alone was able to reduce afterload enough to benefit him; when treating himself for heart failure, he might comfortably lie flat after a few minutes in the boot. He was a prince of a fellow and we were honored to take care of him. He is included here because of his long and interesting history, because his results encouraged us to pursue the development of boot therapy to help similar unfortunate people and because we continue to observe such multiple benefits in other patients.
The Circulator Long-Boot is a cardiac-assist device similar to other devices designed specifically for treating heart disease (7,8). Like these other devices, it does not involve the significant risks of the intra-aortic balloon(9). In view of the available literature on these other devices and our emphasis on the peripheral circulation, we have not collected data for publication on the cardiac effects of the Circulator Boot system. With the availability of increasingly accurate non-invasive methods, we are now doing so. Anecdotal bedside obeservations and laboratory findings suggesting a significant clinical benefit have included: heart ausculatory findings ( a decrease in the murmur of mitral insufficiency and an increase in the murmur of aortic stenosis); an increase in the talking capacity of the patient in congestive failure (more long-winded); improvement in congestive failure (clearing of pulmonary edema); reflex slowing of the pulse rate; fall in elevated levels of lactic acid in patients with congestive failure or septic shock; appropriate alterations in waveform tracings obtained by Doppler, pulse volume or photoelectricplethysmographic monitors; and an improvement in cardiac output in patients followed with a catheter in their pulmonary artery or with an electrical impedance monitor (Renaissance IQ monitor). Patients with low cardiac outputs, of course, constrict the peripheral arteries and decrease peripheral flow in attempt to maintain flow to the important proximal organs. An improvement in cardiac output may markedly increase peripheral flow in these patients. Cardiac output is, of course, at slow heart rates directly proportional to the pulse rate. In some patients with a marked bradycardia, peripheral flow may increase dramatically after the insertion of a pacemaker. The effect of gravity has been previously addressed (Table 5); blood inflow to the foot is increaesd by dependency and decreased by elevation. Both cardiac output and gravity are added to our formula for peripheral effective blood flow:
VI. Effective blood flow = f(variables)(Cardiac Output)(Gravity) or EBF=f(V)(CO)(Grav)
or EBF = f(V)(CO)(Grav) / (VP)(IFP)(Neur)(ASO)(Inf)
Success in the treatment of patients with foot problems is dependent on how well each of these factors is addressed by the physician. Boot therapy appears to have a beneficial effect on each factor. “F(V)” in the formula allows for the effect of other functions and factors. Vasodilatation with boot therapy due to the elaboration of local tissue hormones like nitric oxide and prostacyclin has been shown by others. These factors are ignored here because they are not readily appreciated, addressed or measured.
1. Ellenberg M: Diabetic neuropathic ulcer. J Mt Sinai Hosp NY3:585-94, 1968.
2. Regensteiner JG, Steiner JF, Panzer RJ and Hiatt WR: Evaluation of walking impairment by questionnaire in patients with peripheral arterial disease. J Vas Med and Bio12:142-152, 1990.
3. Lofgren EP: Present-day indications for surgical treatment of varicose veins. May Clin Proc 41:515-523, 1966.
4. Fitzgerald DE and Carr J: Peripheral arterial disease: assessment by arteriography and alternative noninvasive measurements. Am J Roentgenol 128: 385, 1977.
5. Horwitz O and Abramson DG: A modification of the vasodilatation test. Am J Cardiol 6:663-666, 1960.
6. Tze-Kong Young and Shih-Ching Lee, Gastrointestinal dialysis in the therapy for uremia. Kidney International, Vol. 13, Suppl.8 (1978), pp S-185-S-187.
7. Soroff HS, Hui J and Giron, F. Current status of external counterpulsation. Critical Care Clinics 2:277-295, 1986
8. Yu S, Da H and Zhen Z: External Counterpulsation, Review Article. Chinese Med J 103 (9): 768-771, 1990.
9. Goldman BS, Hill TJ, Rosenthal GA, Scully HE, Weisel RD and Baird RJ: Complications associated with use of the intra-aortic balloon pump. Can J Surg 25:153-156, 1982.
10. Montgomery H and Horwitz O: Oxygen tension of tissues by the polarographic method. J Clin Invest 21:1120, 1950.
11. Guyton DP, Khayat A, Husni EA and Schreiber H: Elevated levels of 6-keto-prostaglandin-F1a from lower extremity during external pneumatic compression. Surg Gynecol Obstet 166: 338-342, 1988.
12. Morgan RH, Carolan G, Dsaila JV et al.: Arterial flow enhancement by impulse compression. Vasc Surg 25: 8-15, 1991.
13. U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research. Clinical Practice Guideline. Number 15. Treatment of Pressure Ulcers. Pages 12-13. December 1994.
14. Wagner FW: The diabetic foot and amputations of the foot. In Surgery of the Foot. 5th ed. Mann, R editor. St Louis, Mo. The C.V. Mosby Company.