Case 185: Boot Treatments Successful and Cheap over 7 Years Compared to the Cost and Complications of Standard Therapies the Last Six Months of Life

May, 1991: Patient RA was born 1/4/34. Now at age 57, he was referred to Bryn Mawr for care of his diabetes and its complications by his ophthalmologist. The latter noted RA had had diabetes 25 years with a history of neuropathy, nephropathy, bilateral carotid endarterectomies (1985) and a mild stroke in 1990. After pan-retinal photocoagulation in 1990, his visual acuity was 20/50 OD and 20/25 OS.

RA arrived for evaluation on August 6th, 1991. He gave a history of having weighed 260lb (117 Kg) in 1959. He was still 216lb (98 Kg), 20% above the ideal weight of 179lb (81Kg) calculated for his height (70.7 inches or 179.6cm) and weight history. He had a 25 pack-year smoking history which he discontinued in 1970. He was taking an ACE inhibitor (Prinivil) and two fixed doses of insulin twice a day. His supine blood pressure was 145/76 (pulse 96) and erect blood pressure 115/65 (pulse 100). His nasal mucosa was reddened. His pupils were 4 mm in size and changed little on exposure to bright light. He had moderate lenticular clouding bilaterally. He had occasional red spots, laser burns and some vessel dropout in his retina. His thyroid gland was firm and slightly irregular. The interosseous muscles of his hands were atrophied. He could only partially abduct his right shoulder. He had no heart murmurs. His left border of cardiac dullness was outside of the midclavicular line suggesting modest cardiomegaly. His abdomen was expansive and protuberant in the supine position. He had faint bruits in his left groin and over each carotid. His testes were soft and slightly small. His prostate gland was smooth but modestly prominent. The distal phalanx of his right big toe was surgically absent. Stasis pigmentation was found beneath both internal malleoli. There was a focal 2 mm black spot under the end of his 4th left toenail. Hair was absent beneath the mid-calf bilaterally. Both feet were ruborous on dependency. His femoral pulses were 1+ bilaterally (found after searching and then not strong). His popliteal pulses were trace-to-absent. His distal pulses were absent. His radial, patellar and Achilles reflexes were absent. Vibration sense was absent. He presented, hence, with insulin-dependent diabetes complicated by retinopathy, cataracts, nephropathy by history, arteriosclerotic cardiovascular disease (an old stroke, S/P carotid surgery and peripheral arteriosclerosis obliterans) and both autonomic and peripheral neuropathy (insensate feet, muscle atrophy, orthostasis and impotence).

His baseline laboratory data included a normal EKG, normal thyroid studies and a BUN of 35mg/dl. The R-R interval of his EKG, however, changed little with a Valsalva maneuver. A nose culture grew out abundant Morganella morganii and moderate Staphylococci coagulase-negative; the infection was treated with oral trimeth sulfa and nasal lavage with Sea Soaks containing gentamicin (A repeat culture in November revealed a few Diphtheroids and coagulase-negative Staphylococci.). Vascular studies were performed as he was unable to walk a block at a normal pace. Photoelectricplethysmographic tracings of his toes were flat in the right foot and showed only trace broad waveforms in the left foot signifying dangerously deficient blood flow in both feet. Formal Doppler mapping was next done. For the reader, a normal study is first shown.

With care the ultrasound technician may demonstrate all of the arteries in the above diagram. The height of the Doppler signal is related to the proximity of the probe to the vessel examined, the amount of blood detected and the speed with which it is moving. The shape of the Doppler tracing is related to the speed with which the flow of blood changes and, hence, indirectly with the patency of the vessels.

The tracings for his left foot are shown. Those from the right foot were equally abnormal. Such low rounded waveforms are grossly abnormal and signify advanced occlusive disease. His blood pressures were 70, 0 and 60 in the anterior tibial, posterior tibial and peroneal at the ankle respectively; at the calf they were 70, 84 and 38 compared to 154 in the arm supine. The pressure above the knee was 96 and that in the upper thigh over 200 mm Hg. Not shown above were the Doppler curves of the femoral and popliteal which showed progressive widening and loss of amplitude down the thigh. In short, both legs showed pseudohypertension in the upper thigh pointing to significant atherosclerosis, loss of pressure and Doppler velocity down the thigh pointing to occlusive disease in the superficial femoral and popliteal, further progressive loss of flow down all three tibial vessels and minimal flow at level of the ankle.

!991: He was given 10 treatments with the Long-Boot to both legs during August and September and his walking impairment was followed with the Walking Impairment Questionnaire of Regensteiner et al (see our "Claudication" library); his distance score improved from 0.246 to 0.49 and his walking speed score improved from 0.183 to 0.33. At that time, he felt his neuropathic gait was more of a problem than his claudication. In regard to his diabetes, he was instructed in diet, a four/day home glucose testing program and a four times daily insulin-injection program.

April 22nd, 1997: His foot was obviously ruborous compared to a normal foot. His ankle edema is not well appreciated in the photograph.

June 30th, 1997: The osteomyelitis of the proximal phalanx was well established and not to be cured. The dead tissue over the bone was continually trimmed back.

September 15th, 1997: The skin on the distal foot was less ruborous. Virtually the entire proximal phalanx of the big toe was now either exposed or trimmed back.

1997 - continued:In August his BUN was 28 and creatinine 1.2 mg/dl. His LDL-cholesterol was 112 and HDL-cholesterol 25 mg/dl. His hemoglobin A1c was 7.8% in October. His ophthalmologist found his visual acuity to be stable at 20/25 in both eyes. Vascular tests were repeated to assess his chances of healing his toes. His boot record showed he had 21 treatments in August, 17 in September, 16 in October, 10 in November and 14 in December.

October 30th, 1997: His Photoelectricplethysmography tracings (PPG's) showed pulsatile flow in the stub of his right big toe and in all of the other toes. The pulsations were weaker in the right foot ("B" scale 0-0.5 vs "C" scale 0-1.0 for the left foot).

October 30th, 1997: The cuff pressure necessary to occlude his systolic blood pressure is shown for various levels of both legs (center diagram). His pulse volume curves for the same levels are shown on the sides of the page. The lack of a sharp dicrotic notch on the pulse volume curves in the upper thigh, the decrease in the thigh blood pressures below the brachial level and the presence of femoral bruits pointed to some inlet disease (occlusive disease in his iliacs or femorals). While the Doppler was biphasic at the groin, it was monophasic at the popliteal level and fell off distally. He had a progressive falloff in arterial flow down the leg with preservation of some flow to the toes. He was advised that such vascular tests are treated with the Circulator Boot systems using a Long Boot from groin to ankle or midfoot (to continue to support his heart and kidneys and to improve flow in the upper leg... followed by Miniboots from the knee to the toes with appropriate antibiotics for his toe in the Sea Soaks solution.

!997 continued: Discussions of alternate forms of therapy were a weekly occurrence. He was advised that he would need either an arteriogram or an MRA of his legs to evaluate his possibilities for distal arterial bypasses. While his renal function had actually improved since 1992, he had been made aware of his renal disease at that time and had appropriate concern. Again, he recalled his experience with arteriography and his carotid disease which was associated with stroke. The MRA, hence, was suggested. He was also advised that the fact that he had had a stroke and had advanced peripheral arterial disease made it highly likely that, in spite of a "normal" resting EKG, he had significant coronary artery disease and that many centers would prefer to see coronary angiograms and repeat Duplex scans of his carotids before they would risk peripheral arterial surgery.

On April 3rd, an MRA was performed at the University of Pennsylvania. The right common femoral artery had a distal stenosis. The superficial femoral occluded at Hunter's canal. The right popliteal artery was not visualized. "No name" collaterals were present in the distal right thigh and around the knee . The peroneal and anterior tibial reconstituted in the mid-calf. The anterior tibial carried into the foot while the peroneal was not seen beyond the ankle. The left superficial femoral was occluded at its origin. The left deep femoral was normal. Numerous collaterals were seen throughout the left thigh. The left popliteal reconstituted at the knee joint. The left anterior tibial continued down to the ankle but was not continuous with the dorsalis pedis. The left posterior tibial was not seen and the left peroneal terminated at the ankle.

On April 14th, his toe culture report listed a light growth of Pseudomonas fluorescens-putida group (sensitive to the prescribed Fortaz, gentamicin and Cipro all of which were continued) and a heavy growth of Cornynebacterium species. On May 1st, RA sought another opinion form an infectious disease specialist of the University of Pennsylvania. The ID specialist concluded that the current therapy had no hope of success and recommended amputation of the 1st metatarsal and surgical closure of the open wound. He also advised consultations with vascular surgeons, cardiologists and orthopedists at the University of Pennsylvania. On June 4th, he had a Sestamibi study with persantine. A reversible anteroseptal perfusion abnormality, a partially reversible apical perfusion abnormality, a fixed inferolateral perfusion abnormality and mild left ventricular dilatation with stress were noted. His left ventricular ejection fraction was estimated to be low at 33%. Clinically these findings were associated with decreased exercise capacity due to fatigue but no signs or complaints of congestive heart failure or angina.

On June 16th, he underwent coronary bypass x 5: sequentual left internal mammary artery to diagonal left anterior descending, sequential saphenous vein to 1st and 2nd circumflex, and saphenous vein to posterior descending. His arteries were sclerotic and the anastomoses difficult. Postoperatively, following heparin reversal there was persistent bleeding from the circumflex anastomosis requiring reinstitution of his cardiopulmonary bypass and a few extra hours in the operating room. He left the operating room in guarded condition.From June 26th to July 16th, RB was a resident of the extended care nursing facility. He received 17 boot treatments during this 21-day period. He had fever of undetermined origin during much of his stay perhaps related to atelectasis, his bilateral pleural effusions and/or his right great toe. His foot x-ray now showed an absent right great toe (it had auto-amputated). Various foot cultures grew Stenotrophomonas multiphilia and Acinetobacter.

January 21st, 1998: The total removal of his big toe now left a large open wound.

June 3rd, 1998: With his continued treatments, his wound had begin to close. His surgical consultants believed revascularization was necessary to complete healing.

August 25th, 1998: During the postoperative period after his heart surgery, the dorsum of the right 2nd toe and the end of the left 1st toe broke down perhaps due to the weight of his blankets. Boot treatments began again on the 26th of June. By the end of August, the lesion over the right metatarsal head was close to healed although no revascularization procedure had been done.

1998 continued : In August, his insurance coverage became an issue and his treatments were cut back to 4 for the month. Laboratory tests on August 22nd included: hemoglobin 11.7 gm/dL, WBC 7000/mcL, BUN 29 mg/dL and creatinine 1.1 mg/dL. In September, he began a twice a week boot schedule and received 10 treatments. At the end of the month, his insurance company determined that his Circulator Boot treatments were medically necessary and extended coverage for the treatments until January 1st 1999. His having followed a less aggressive boot schedule, however, proved to be unfortunate.

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August 26th: Like the right 2nd toe, the left big toe had not done well postoperatively and was now under therapy.

September 29th: While his right foot continued to close, he developed an infection in his left foot which he watched for four days before calling for a boot appointment on the 29th. Cultures were taken. He preferred outpatient treatment to hospitalization. He was given Trovan orally and both gentamicin and Vancomycin were injected at multiple sites in his toe and foot. His white count was 17.0 with 87% neutrophils.

October 1st: While the black had extended to include the entire dorsum of the toe, he was feeling better, his fever was gone and a white count obtained September 30th was improved (14.7).

October 5th: A methicillin-resistant Staphylococcus, sensitive only to vancomycin, had been reported on October 4th. He was telephoned and advised to come in for treatment. He thought he could wait until his next appointment on the 5th. Now he presented with an obvious extension of his infection and symptoms of sepsis.

October 5th: The Staphylococci were now digesting the plantar tissue under the whole first metatarsal bone. He was admitted to the hospital and begun on intravenous Vancomycin therapy. Except for arterial calcifications and a previous amputation of part of the first toe, his foot x-ray was unremarkable.

October 15th: Septic emboli found there way to the heel of the right foot which also had begun to breakdown. Here the process was stopped with local injections of vancomycin.

He was a sick man when he was admitted on October 5th. His temperature was 104 degrees F (40 degrees C) and his white count 22.4. The infection on the left foot was associated with rubor of the entire foot and lower leg. The plantar aspect of his right heel was blue. He had a white streak beneath his sternum from which pus was aspirated; he had paradoxical sternal movements (it collapsed inward with inspiration). The infectious disease consultant began intravenous Vancomycin, Azactam and Flagyl. The throracic surgeons incised and irrigated the sternum and the next day, October 6th, the plastic surgeons debrided the sternum. Persistent fever, hypotension and mental confusion led to the urgent amputation of his left leg on October 9th. His Staphylococcus proved very difficult to eradicate. It was grown from his left foot, from his proximal left leg amputation site, from his sternum, his right heel, from multiple blood cultures from the 5th of October to the 19th of November, from the tip of his intravenous catheter on October 30th, from his sputa on November 16th and finally from his nose on December 1st, two days before he died. The pathology report of the left leg read: "Beneath knee amputation: gangrenous necrosis of portion of the left foot. Posterior tibial vessels with mild atherosclerosis. Monckeberg's medial calcification involving anterior tibial vessels. Skin from the proximal margin appears histologically viable. Muscle from the proximal margin shows moderate to marked degenerative change." Postoperatively, his chest x-rays showed minimal density at the left base with obscuration of the left hemidiaphragm and minimal atelectasis at the right base, a central line in the superior vena cava and an endotracheal tube in satisfactory position. The chest x-ray October 12th showed atelectsis vs pneumonia of the left lower lobe. On October 19th, a right femoral arteriogram showed complete obstruction of the distal common femoral artery with reconstitution at the origin of the superficial femoral and profunda arteries. The superficial femoral was diffusely diseased with occlusion at the adductor canal. There was no popliteal reconstitution. The peroneal reconstituted at the midcalf and was continuous to the distal calf with reconstitution of the distal anterior tibial artery just above the ankle. There was no complete plantar arch. On October 21st, an in situ femoral/peroneal bypass was performed taking blood approximately 22 cm below the knee. On October 26th, a CAT scan of body showed large pleural effusions with some compressive atelectasis, tiny collections under the staples in his right leg, gallstones and cardiomegaly. An esophageal ECHO on October 28th showed worse heart motion but no evidence of endocarditis. On the 31st, his chest x-ray showed pleural effusions and interstitial edema. On November 2nd a Duplex scan of leg showed no DVT or other cause for fever and a 2 and 24-hour whole body white blood cell scan was normal. Episodes of dypsnea attributed to congestive failure were noted to occur after meals raising the possibility of intermittent aspiration. On November 5th, oral feedings were stopped and a Dobhoff tube was placed in his stomach. On November 9th, his chest films still showed bilateral pleural effusions in spite of his diuretic program. Thorancentesis showed sterile fluid. Chest x-rays showed large pleural effusions on November 10th and worsening of findings at left lung base due to pleural effusion or infiltrate on the 16th. A bone scan on November 18th showed degenerative changes in his major joints along with increased activity within the sternum, ribs and sternoclavicular joint suggestive of findings common after recent CAGB surgery; the study provided no help in his current management. On November 19th, a video fluoro swallowing function study showed vallecular and pyriform sinus pooling along with penetration and aspiration. It was thought he might be aspirating his saliva and possibly regurgitated tube feedings. On November 29th, a portable chest x-ray showed increased opacity of the lungs, cardiomegaly, bilateral effusions. On December 1st, he had a surgical consultation for placement of jejunal feeding tube. On December 3rd, he had another episode of congestive failure and died. His autopsy revealed an acute myocardial infarction.

Comments:This man is included for many reasons. First, he was a long term success in the support of his legs, heart and kidneys over the seven years prior to his final illness. Both of his legs deteriorated when his self-determined need for booting was twarted by his insurance company. The right big toe developed an osteomyelitis that ended in an autoamputation over many months. The chronicity of his lesion, however, eventually led to less frequent booting, more aggressive therapies (his CABG) and surgical complications during which his right foot improved without his ever having a bypass. His CABG did not prevent later episodes of congestive failure and a fatal myocardial infarction. A relatively benign lesion of his left foot was neglected again associated with insurance issues and became infected with an extremely aggressive staphylococcal infection that cost him his leg and eventually essentially his life. His right leg was eventually bypassed after the embolic lesion of his right heal was sterilized and stabilized; then, as he had become an amputee, it was thought that he was not likely to be able to come to the office for outpatient booting and that his lesion was not likely to heal without either booting or bypass. While we have only rarely seen such aggressive embolic spread of infection, its occurrence here emphasizes the need for appropriate systemic antibiotic coverage during boot therapy. The patient had had long courses of antibiotics over the last years of his life. None of his foot cultures had included a resistant staphylococcus until his final illness. Of interest was his final positive culture: one of his nose while his blood and lesions were negative. The nose is a known reservoir for staphylococcus. It is possible that he infected his left foot during his period of self-care at home when his boot therapy had been cut back?. See Lowy FD, "Staphylococcus Aureus Infections" in our library on Cellulitis, Osteomyelitis and Sepsis. Finally, there are the issues of costs of care and indications for surgery. Patients with severe diffuse vascular disease are rarely if ever normalized by surgical revascularization procedures. The mortality, morbidity and complication rate in such patients is high. Should invasive procedures be done if the patients are "getting along" with less aggressive but chronic therapies? This man continued to fail after his heart surgery. The financial costs of hospital and rehabilitation care the last six months of his life was $448,437.41 (not including his doctor bills). The pain and suffering of the patient and his family cannot be measured.