Case32: Case in Progress: Patient with End-Stage Kidney Disease Would Like to Avoid Dialysis by Booting. Both Legs Preserved in Spite of Serious Lesions.

This Caucasian male was born 2/24/58. He has had diabetes since age nine. His diabetes was followed many years by a general practitioner who took an interest in diabetes. In recent years, he had no doctor and monitored his sugar only on occasion. He suffered a stroke in November 1995 and has been unable to do his work as a carpenter since. After his stroke he began to monitor his sugar three times daily and believed that his diabetes was reasonably controlled. He had been found to have arterial hypertension prior to this stroke and had noted some swelling of his legs. His vision had been diminished for many years; he had been legally blind in his left eye for ten years. A vitrectomy was attempted in 1995 with no success. Finally, he had had sores on his feet intermittently in recent years and had responded to conservative measures.

He was referred to our office by a friend in December, 1995 with the above history. His review of systems then revealed he was having some lightheadedness, blurring of vision in his remaining eye, a decrease in hearing, bilateral tinnitus, night sweats, swelling of his ankles, two pillow orthopnea (shortness of breath if lying lower than two pillows), nocturia, back pain and numbness, cramps and weakness in his feet.

On physical examination, he was found to stand 69.5 inches tall and weigh 146 pounds. His blood pressure in the left arm sitting was 168/105, in the right arm sitting 175/100, in the right arm standing 168/98 and in the right arm supine 175/100. His teeth were in good repair but he did have moderate retraction of his gums. His left eye was slightly sunken and had a dense opacity. In the right eye, his pupil was 2.5 mm in size and barely responded to light. He had old laser scars in his retina and it was obvious that his vision was diminished. He had some red telangiectasia spots across his shoulders and neck. He had no goiter. His hands were warm but he had atrophy of his interosseous and hypothenar muscles. He had lots of chest hair. His lung fields were clear. His chest was slightly funnel-shaped. His left border of cardiac dullness was about the midclavicular line. He had no significant heart murmurs. His abdominal exam was unremarkable. Slight fatty hypertrophy was found on his anterior thighs at his insulin injection sites. There were no bruits in his flanks, over his groin or over his carotids. His genitalia were normal. His stool was loose and watery on the examining glove. He had pigment spots over both shins and both ankles were slightly swollen. Vibratory sense was present on his toes. Light touch sensation was missing on the dorsum of his feet. He was not able to detect a stick pressed against his skin distal to his mid-shins. His hand grip was reasonably strong. The skinfold thickness was 3.1 mm on the dorsum of his hands, over his biceps 2.7mm, over his triceps 10mm, over the subscapular area 16.7mm, over the iliac crest 11mm and over the abdomen 17.5mm. His Achilles reflexes were absent while his patellar reflexes were 1+. His femoral, radial, ulnar, and dorsalis pedis pulses were 2+ (easily found and palpable with firm touch) while his posterior tibial pulses were trace to absent. He walked with a broad-based gait. Laboratory values included a glycohemoglobin of 10.9%, creatinine 2.7mg/dl, potassium 5.6mEq/dl and urine protein 2+.

His diagnoses , hence, included: (1) Type 1 diabetes mellitus; (2) cerebral arteriosclerosis with past stroke; (3) diabetic nephropathy; (4) diabetic retinopathy, cataracts and blindness; (5) peripheral neuropathy, and (6) likely arteriosclerotic heart disease with mild congestive heart failure. As he was unable to work at his trade (or any trade for that matter) he was applying for disability... which still had not been approved at the time this history was first written here.

He was advised of his diagnoses and their proper treatments: sugar control, blood pressure control and diet modification. The latter included restrictions in protein, sodium, potassium and phosphorus. He came taking Procardia 60mg XL, Vasotec 10mg, Zocor 20mg and aspirin daily. The Vasotec was replaced with Accupril 40mg a day. Leg swelling led to the addition of 40mg furosemide. Further rises in his blood pressure led to the addition of Tenormin 25mg/day and hydralazine 25mg three times a day. Marked hyperkalemia (7.5mEq) and weakness necessitated the discontinuance of his Accupril. Minoxidil and more furosemide was added to attempt to reduce his pressure and edema. Digoxin was added because of increased dypsnea on exertion and orthopnea. Rocaltrol was added because of hypocalcemia and an elevated alkaline phosphatase. TUMS was given after meals to help bind his intestinal phosphorus. Epogen was added to correct his anemia (8.1gms/dl). His heart failure persisted and he was unable to sleep at night. Chlorthalidone was added to his program to be taken a few hours before his furosemide. His failure persisted. He was instructed in his likely need for dialysis: his BUN was 95mg/dl and his creatinine 4.0mg/dl. He was advised his anorexia might improve and his excessive fluid could be removed with the dialysis.... such was the standard approach in a patient with his problems.

He was also advised of our current research in following the response of the heart to boot therapy.... three weeks of free boot therapy during which his heart is monitored on an Omni Holter monitor and a Renaissance IQ monitor. The former is used to follow both rhythm and RST depressions over 24 hours weekly. The latter is an electrical impedance apparatus (IQ Renaissance Technologies, Inc) which allows us to follow his cardiac output, stroke volume, ejection fraction, systemic vascular resistance etc. Noninvasively before, during and after the boot treatments. He was advised that our boot patients commonly experience a significant improvement in renal function but that the mechanism of the improvement was not certain. He was interested to enter the program in hopes of delaying or escaping dialysis.

The baseline IQ study is shown here; his EKG is on the top line and the dZdT curve below it. His hemodynamic parameters were 6.32 L/min for cardiac output, 83 ml for stroke volume and 3.59 ohms/sec2 for acceleration index.

Here are his tracings after 22 minutes of booting both legs. His cardiac output has risen to 8.76/L/min, stroke volume to 115.3 ml and his acceleration index to 5.07 ohms/sec2.

He has done well with the program. His initial Omni study revealed significant depressions occurring when his heart rate rose to 97 with modest exertion. After one week of therapy no depressions were seen. At three weeks he was again free of RST depressions except when, feeling pretty well, he involved himself in moving furniture. During his boot therapy, his cardiac output rose significantly on one day, for example, from 6.32L/min. to a maximum of 12.39 L/min. As hoped, his symptoms of congestive failure have diminished, but, unfortunately not totally disappeared. Weekly BUN determinations have also improved: 95, 91, 89 and 74. Creatinine levels also improved: 4.0,3.9,4.0 and 3.2mg/dl. The research protocol is over. He still would like to avoid dialysis and would like to continue with boot therapy. His family and friends are looking for sources of support. Their search has led to the addition of this case history to our Website. Hopefully, interested persons may find the details of his case here and respond.

Comments: A few years ago, I (Dr. Dillon) attended the Council for the Diabetic Kidney at the American Diabetes Association Meetings. Perhaps a thousand people were in attendance. The half dozen professors summed the bleak outlook for the diabetic patient with end-stage renal disease noting that new avenues of approach were needed. I stood up at a microphone in the audience and noted that we had then pumped on perhaps a thousand diabetic patients and had generally found with prolonged therapy approximately a 50% fall in BUN and creatinine levels. I allowed that I was not sure of the mechanism whereby the kidney appeared to benefit but suspected that various factors were involved: an improvement in cardiac function, an elaboration of fibrinolysins, an elaboration of various vasodilators known to be stimulated from the endothelium of the vessels in the legs (nitric oxide, prostacyclin etc.). I offered to meet with any interested physicians after the meeting. The professors looked at one another and expressed no knowledge of the boot or its physiology. No one in the audience came to express an interest. Now, I would be surprised if boot therapy can permanently avoid dialysis in all diabetics or even in a significant portion of diabetics. On the other hand, we have patients who have avoided dialysis for months to a few years and during that time have enjoyed a quality of life far superior to that of the dialysis patient and at a greatly reduced cost. Our patient here has not yet leveled off in his improvement in cardiorenal function. If we are lucky, he will level off back at a BUN of 30-40 and will slowly rise back to his current levels over 2-4 years. During that time, he might require leg pumping for one hour three days a week. A few of our patients have been able to stop pumping altogether. There is no question that booting can benefit the renal function of some patients. Hopefully, we may interest the NIH or again some folks in the American Diabetes Association to study these effects and find what if any role booting should have. If a mechanism of benefit can be determined, why even the molecular biologists might find a role and produce a new humoral substance to allow a cure??? (Molecular biology has been getting a large proportion of the research dollar in recent years.)

Update 11/8/96: BUN 68mg/dl, creatinine 3.3mg/dl. Would expect a further drop in both the creatinine and BUN as he seems to be responding and the maximum effect we have seen on other patients took a few months. He has been given free treatments three days a week the last few weeks. He is off our study protocol and will likely be dropped from therapy in the absence of any funding.

A heavy growth of Staphylococcus aureus was recovered from his blister drainage. The heel was meaty red and had no capillary refill, an ominous picture. His oral temperature was 100o F. He was given oral Cipro and started on the local measures as above.

While fever and drainage were quickly remedied, the avascular tissue was soon to mummify through to the os calcis. He was told we can heal such lesions, but over many months.

Update 4/22/97: BUN 41 and creatinine 3.8. He is eating well and feels stronger. He has been receiving boot therapy as an outpatient and his heel has improved. He had been approved for Medicaid and his HMO had allowed that they would cover three boot treatments a week.

His heel lesion demarcated well and began to heal at the edges. On 5/23/97 his BUN was 46 and creatinine 3.8mg/dl.

On 8/26/97, he was found to have a new blister, this time on his left foot. The picture does not display the lateral ankle well where he had a diffuse erythrema. He was started on local gentamicin and oral Cipro until his culture returned showing a coagulase-negative Staphylococcus sensitive only Clindamycin and Vancomycin. The latter given orally and locally did not control his cellulitis. He developed nausea and vomiting and was admitted to the hospital where he remained as of October 12th, 1997.

Update 10/14/97: With his infection, fever and antibiotic load, his renal function again deteriorated somewhat; his BUN rose to 80 and creatinine to 5.8mg/dl in early October. As his hospital room has allowed only booting on one leg at a time, he was taken to another room to allow treatment to both legs resulting in a diuresis and a drop of his creatinine to 4.5 mg/dl. He is now scheduled for discharge home on 10/15 where hopefully his HMO will allow daily booting and IV antibiotics for a week and then indefinitely three times a week booting in lieu of dialysis and surgical procedures on his feet.

10/16/97: The right foot was holding and his heel lesions slowly resolving. The inflammatory process in the left foot extended almost across the full dorsum of the foot.

10/16/97: The cellulitis process was a challenge to the entire plantar surface of his left foot. Capillary refill was lost along the lateral margin of the foot where the skin is seen to be separating.

Update 1/8/98: His HMO had mandated his discharge from the hospital. They allowed one week of daily therapy and did agree to three treatments a week thereafter.... the therapy to be reviewed periodically. Such a schedule might be compared with our usual programs: "level 1" or maximal therapy: 4-6 treatments per day in the hospital for patients with severe disease and threatened or progressing loss of tissue; "level 2": 1-2 treatments per day in the hospital; "level 3": 2-3 treatments per day as an outpatient; "level 4": 1 treatment per day as an outpatient; "level 5": 2-3 treatments per week as an outpatient; "level 6": 1 treatment a week as an outpatient; and "Level 7" 1-2 treatments a month as an outpatient. Our man was removed from the hospital and reduced by the HMO from a "Level 1-2" to a "Level 5". At office expense, extra treatments were added to the "Level 4". The HMO approved IV Primaxin at home from 10/16 to 10/30. With the tissue destruction in his left foot, his white count was quite elevated: 23.5 on 10/27, 21.8 on 11/18, 13.6 on 12/16 and 9.2 on 1/5/98. In addition to his IV antibiotics, he received oral doxycycline and local injections of Fortaz and vancomycin into his foot at the time of his boot sessions. The Fortaz was continued as a heavy growth of Pseudomonas was reported on 12/17. With his continued booting, a long black area demarcated on his lateral foot, his sense of well-being returned, his BUN has dropped from 82 on 10/27 to 65 mg/dl on 1/5/98, his creatinine has dropped from 5.4 to 4.7 mg/dl and his serum albumen has risen from 2.3 to 3.3 G/dl. (See case 53 and 96 for similar feet that have healed).

January 7th, 1998: The color has considerably improved on the dorsum of the left foot. The distal dorsal half of his left 4th toe has mummified.

10/16/97: The plantar surface of the left foot has also improved. The medial aspect has regained most of its normal color and texture. The inflammatory streak from his 4th toe to his heel has demarcated and mummified. The ulcer and osteomyelitis of the right heel is slowly closing.

He is again subject to the review of his HMO which seems to have a different reviewing physician every few weeks. He remains in need of regular booting until he is healed... and thereafter perhaps 3 times a week to maintain his heart and kidney function. Without such therapy, he is likely to come to prolonged hospitalizations for bilateral leg amputations, placement of dialysis catheters, dialysis and congestive heart failure. The HMO will be faced with significant costs with this man until he dies. As of 1/8/98, the HMO has cut him off his therapy and he continues at office expense. An appeal has been made... but HMO's may not recognize appeals.

February 5th, 1998: The dorsum of his foot has returned to normal. His fourth distal toe is mummified and will be allowed to autoamputate. His laboratory studies included BUN 75mg/dl, hemoglobin 11.1 g/dl and white count 9.1. He ambulates on crutches and is eating and sleeping well..

February 5th, 1988: He is developing granulation tissue under the eschar on his right lateral foot. We weekly trim back the edges of the eschar to allow the skin to move in.

February 5th, 1998: The osteomyelitis under the calcaneus has been controlled and the heel ulcer continues to close. He has been getting both Long Boot and Mini-Boot therapy three days a week.

May 7th, 1998: New skin has crossed the lower third of the eschar which has generally become narrower. The skin of the rest of the foot is normal.

June 4th, 1998: An angled view of the left foot shows the eschar yet to be healed.

June 4th, 1998: The osteomyelitis and necrosis of the right heel also had been doing well. Only a small lesion is seen to remain.

His HMO presumably agreed to pay for his January 1998 treatments; as of August 1998 no payments have been made. His therapies generally three times a week were continued at office expense. He was depressed about his financial and social circumstances and his physical disabilities. His BUN rose with increases in his diuretics and decreased frequency of boot therapy. In May 1998, his BUN rose to 103 and his creatinine rose to 8.0mg/dl. Dialysis was again discussed. The possibility of increasing his water intake and daily booting was also proposed. He continued his booting until June 11th when he decided to trust in his medications alone. He died June 18th, 1998.

Comments: TG presented with all of the complications of diabetes: blindness, hypertensive arteriosclerotic cardiomyopathy, renal failure, peripheral neuropathy, peripheral arteriosclerosis obliterans (missing posterior tibial pulses). Boot therapy helped both the function of his heart and kidneys. Reduction in therapy was associated with peripheral edema and skin blebs that led to limb-threatening infections. The latter were stabilized with boot therapy and local and systemic antibiotics. Major foot lesions, which commonly might have led to leg amputations in many hospitals, were reversed and close to healed. The restrictions of his HMO were always in the background. The HMO was spared the costs of amputations, hospitalizations for congestive heart failure and dialysis. Dialysis in his last few weeks would likely have improved his sense of well-being, but, as the nephrologists pointed out, does not improve cardiac output and heart function. He was advised initially that booting might help him for two years; he died 2.5 years after presentation. The course of his therapy has been described here every few months as his case progressed.... a "case in progress".