Case 184: Treatment of Osteomyelitis (1991), Leg Ulcers (1995) and Heart Failure and Chronic Renal Failure (1998)


Treatment of Chronic Osteomyelitis: This lady presented at age 74 for boot therapy on July 29, 1991 because of a persistent infected ulcer in her right foot. She had had bypass surgery in her right leg in 1986. Worsening angina led to sextuple coronary bypass surgery with the use of her mammary artery on January 5th, 1990; a postoperative sternal infection had required muscle-flap closure. Ultrasound showed normal left ventricular function on July 9th, 1990 accompanied, however, by aortic sclerosis, mild aortic insufficiency, moderate mitral insufficiency and concentric LVH. The development of the ulcer in her right foot led to study of her legs on the 30th of July 1990; an ABI of 0.61 in left leg and 0.95 in right leg along with diminished pulse volumes in left leg with especially low readings in the left midfoot were reported. Foot x-rays on August 28th, 1990 showed advanced degenerative joint disease of right 1st MP and 5th MP joints. Her rubor and drainage were thought to be associated with osteomyelitis which was treated under the guidance of her endocrinologist, vascular surgeon (various debridements), orthopedic surgeon and infectious disease specialist over the next year. Her hyperkalemia (K+ 5.1-6.0 mEq/L), anemia (Hgb 10.1), mild azotemia (BUN 26-32 mg/dl) and creatinine retention (2.1 on May 13th, 1991) were attributed to chronic renal insufficiency by her physicians. A repeat bone scan on May 6th, 1991 showed increased uptake over the right first MP joint. On June 4th, the orthopedic specialist was able to probe the ulcer showing extension into the joint space. An elevation of her sedimentation rate to 103 mm/hr on the 17th of July 1991 was attributed to the osteomyelitis in her right foot, then present for a year. In the meantime, her ophthalmologist had found 20/400 vision in both eyes associated with with macular degeneration, cataracts and minimal background retinopathy. Her vascular surgeon recommended amputating her first toe and removing the joint. The orthopod recommended a resection of her first ray. She refused and was referred by another patient to our boot clinic on July 29th, 1991. She was then taking insulin 15 units, atenolol, furosemide, Volataren, Ascriptin, Augmentin, vitamins and iron. Her HgbA1c of 8.4% (N< 6.1%) pointed to a lack of ideal control of her diabetes. Her walking capacity was limited to 1-2 blocks. She was treated on 13 occasions as an outpatient with local injections of gentamicin into the joint space followed by Mini-Boot treatments. Her ulcer healed and she was dismissed on September 3rd. X-rays at Bryn Mawr were thought to be as suggestive of gouty arthritis as osteomyelitis. Her uric acid level was found to be only mildly elevated at 7.23 mg/dl, a value in keeping with her renal dysfunction.



Her first metatarsal head had destructive changes compatible with the diagnosis of osteomyelitis... but gout was also suggested.

!992-1994: As the endocrinologist at her hospital died, she began coming to our office for diabetes management in January, 1992. Her hemoglobin A1c 8.8 (N<6.2) was still elevated . Her thyroid function was normal (TSH 1.53). In May 1992, her cardiologist noted bilateral leg edema (right leg more than left) and started Pravachol 20 mg per day for her modest hypercholesterolema. In August 1992, her creatinine was noted to be holding at 2.0 mg/dl. Her ophthalmologist reiterated that her visual loss was more due to macular degeneration than to her diabetes. In January 1993, her cardiologist attributed her dypsnea to left ventricular hypertrophy and possible diastolic noncompliance of her left ventricle. On February 2nd, 1993 her serum creatinine was again 2.0 mg/dl and a thallium persantine test was negative for ischemia. During the rest of the year, she was noted to have two-block claudication, her cardiologist added Procardia for her hypertension, her ophthalmologist began Pilocar and Betoptic for glaucoma and she ate excessively enough to maintain her weight at the 180 pound level.


Nocturnal Leg Cramps, Claudication and Ulcers in 1995: On January 10th, 1995 she complained of nocturnal leg cramps and groin pain walking two blocks. No pulses were found below her groin. The ABI in the right leg was 0.71 and in the left, 0.50. She was given nine Long-Boot treatments to both legs from January 16th to 27th. Her nocturnal leg pain was relieved and her walking improved. On February 28th, her renal function was found to be stable (creatinine 1.9mg/dl and BUN 21mg/dl) and, in spite of her obesity, her total cholesterol to be 214 mg/dl and HDL-cholesterol 42 mg/dl. She was taking in addition to her insulin: Zocor 20mg, atenolol 50mg, Procardia 60mg, Lasix 20 mg, and twice daily Apresoline 20 mg. Repeat renal function tests included those on March 15th (BUN 32 and creatinine 1.7 mg/dl.) and July 11th (BUN 36 mg/dl, creatinine 2.2 mg/dl and potassium 5.5 mEq/L). On July 31st, her cardiologist added Zaroxolyn to her furosemide in view of bilateral dependent edema and a left pre-tibial laceration. On September 25th she had cataract surgery. On November 14th, she returned to the Boot Clinic with an ulcer on the right lateral calf and an one-block limit in walking. The right leg was firm and swollen. Venous outflow studies were normal. Photoelectricplestysmographic (PPG's) tracings of the left 2nd to 5th toes and right 4th toe showed no pulsations. Her right ABI was 0.69 and left 0.58. She was given nine Long-Boot treatments to both legs from November 20th to December 9th. Again, her ulcer healed and her discomfort was alleviated.



November 14th: An edematous ulcerated leg not responding to the diuretics of her cardiologist.

November 27th: Less swelling and the ulcer drying up and healing.

December 12th: Dismissed from the Boot Room.

1996: Her cardiologist noted on January 19th that her ECHOcardiogram showed mild pulmonary insufficiency, mitral annular calcification, severe mitral regurgitation, aortic stenosis (mild with valve area 1.4 cm2), mild aortic insufficiency and tricuspid insufficiency with normal function and size of her left ventricle. On January 22nd, her hemoglobin was noted to have fallen (7.2 gm/dl). Her renal function (creatinine 2.4mg/dl) was not abnormal enough to explain her anemia. Her cholesterol had dropped to 152mg/dl. A barium enema showed a sessile polyp in her proximal ascending colon. Her chest showed cardiomegaly with mild congestive heart failure. On January 29th, her surgeon removed a 1.3x1x1 cm villanous adenoma with moderate atypia. She was discharged with prescriptions for Lanoxin 0.25 mg qd, Isordil 10 mgTID, Aldactone 25 mg qd, Lasix 40 mg qd, Apresoline 25 mg BID, Losartin 50 mg qd, Zocor 20 mg qd, Tenormin 25 mg qd, Aminophylline 100 mg TID, and Ferrous sulfate 300 mg BID. On February 7th, her hemoglobin was 11.5 gm/dl and her digoxin level was in a toxic range (2.8 mg/dl). On March 19th, her hemoglobin was 10.8 gm/dl and her renal function unchanged (BUN 36 and creatinine 2.4 mg/dl). In July, her cardiologist found her ankles swelling to have increased and increased her diuretics to include Zaroxolyn 2.5 mg 3 days a week. On July 22nd, her BUN was noted to have increased to 81 mg/dl and her creatinine to 3.4 mg/dl. She was advised to avoid phosphorus in her diet. Oral calcium carbonate was prescribed to bind phosphorus in her intestines and Rocaltrol (Dihydroxy-vitamin D) was given 0.25 mg daily.


1997 and Metastatic Cancer: In February, complaints of back pain led to x-rays showing severe degenerative joint disease at L3-4 and L4-5 along with degenerative spondylolisthesis of L3 on L4. On February 25th, her BUN was 78 and her creatinine 3.1 mg/dl. On February 26th, a chest x-ray and a subsequent CAT scan showed multiple lung nodules suggesting metastatic disease along with a destructive lesion of her left glenoid. A search for a primary tumor began (mammograms etc.). On the 11th of March, her BUN was 94mg/dl and her creatinine 3.4 mg/dl perhaps explaining her hemoglobin of 9.4 G/dl. On March 13th, a bone scan showed a pathologic fracture of her proximal right humerus and a lesion in her left glenoid fossa. On March 18th, her orthopedic surgeon stabilized the right humerus and obtained a specimen from the fracture revealing her tumor to be metastatic follicular carcinoma of thyroid, quiet a surprise as no one could feel a thyroid nodule or goiter. Her preoperative ECHOcardiogram on March 24th showed mild aortic insufficiency, 3+ mitral insufficiency, 2+ tricuspid insufficiency, moderate pulmonary hypertension, an estimated ejection fraction of 42% and a reduction of her left ventricular function to perhaps 40%. On March 27th, a total thyroidectomy revealed a focal lesion in the lower left lobe and another in the right lobe. Postoperatively, her BUN rose to 99 mg/dl while her creatinine remained at 3.3 mg/dl. With hydration and modest protein restriction, her values were improved on April 7th (BUN 55 mg/dl and creatinine 2.8 mg/dl). She was given no thyroid replacement but her serum thyroxine level remained in the upper normal range and her TSH remained suppressed. A lemon-sized mass had now developed in her left glenoid. A radioactive iodine scan on April 18th showed evidence of functional metastatic disease involving left scapula, right acetabulum, mediastinum and right lung. Minimal activity was seen in the right humerus. Her chest x-ray on April 21st showed an increase in the size of the lung nodules. She was discharged to a long term facility on May 1st taking Tapazole to block the thyroid hormone production of her tumor and to allow her TSH to rise. Her other medications included Isordil 10 mg TID, Aminophylline 50 mg TID, 1 gtt Pilocarpine OD TID, 1 gtt Betaxolol BID, Cozaar 50 mg qd, Metamucil, Senocot, Calcium gluconate 500 mg TID, Lanoxin 0.125 mg on odd days, Apresoline 25 mg BID, Tenormin 25 mg qd, Zocor 20 mg qd, furosemide 120 mg on odd days, insulin and Epogen 10,000 units 2 times a week. When her TSH was over 60, her tapazole was stopped and a few days later on May 12th, 66.4 mCI I131 was given. A follow-up scan on May 20th showed intense uptake in left shoulder and prominent uptake in the proximal right humerus, the thyroid bed, mediastinum, right hilar region, and pulmonary parenchyma bilaterally. Increased uptake was also noted in the right pelvis, acetabulum and possibly the proximal right femur and the left inguinal areas. Her serum thyroglobulin level was over 7000 ng/ml. On May 27th her BUN was 41 mg/dl and creatinine 2.5 mg/dl. Over the next few months she was given increasing doses of thyroxine to suppress her TSH. However, 125 mcg a day brought her TSH only to 2.7 while her symptoms of heart failure increased. On July 15th, her BUN was 57 mg/dl, creatinine 2.5 mg/dl and thyroglobulin 1000 ng/dl. The mass in her left glenoid was now no longer visible or palpable. By October 7th, her thyroglobulin had fallen to 33 ng/dl. On October 19th, an ambulance took her to a hospital near her home with an acute stroke and a left hemiparesis. She returned to Bryn Mawr continuing on her same medications. On November 17th, her TSH was 1.13, glycohemoglobin A1c 7.3% and thyroglobulin 3500 ng/dl. On December 1st, the nodular densities were not seen on her chest x-ray, but cardiomegaly, a left sided pleural effusion and interstitial edema were noted. A body scan on December 9th suggested progression of metastatic disease. Shortness of breath led to re-admission to Bryn Mawr on December 19th; her BUN was 43 mg/dl, creatinine 4.0 mg/dl and thyroglobulin 7350 ng/dl. Her thyroxine replacement was discontinued and tapazole again prescribed to allow her TSH to rise in preparation for another radioiodine treatment. She was transferred to a nursing home to await the proper time for her treatment.
1998 - More I31 treatments of her cancer and Boot treatments to support her legs, heart and kidneys: In a few weeks, her TSH was again over 40. The nursing home was asked to discontinue her Tapazole and a few days later on the 26th of January, an I131 scan was performed revealing uptake again in her left glenoid area, the right proximal humerus, the right supraclavicular region and the left pelvis. On January 30th another 32.7 mCi of I131 was given. Five days later her L-thyroxine was started again 125 mcg a day, a dose her heart seemed to tolerate. Laboratory values on February 23rd included BUN 77mg/dl, creatinine 4.6 mg/dl, albumen 3.1 G/dl, Na+ 140mEq/L, K+ 5.4mEq/L and HCO2- 20mM/L (the tendency towards hyperkalemia and acidosis attributed to her chronic kidney disease). Sugar control and hydration were emphasized and on April 13th the laboratory values had improved: glycohemoglobin A1c 6.7%, BUN 56 mg/dl, creatinine 3.9 mg/dl and thyroglobulin 940 ng/ml. Thereafter, she seemed to fail. On May 4th, her BUN was 74 and her creatinine 5.2 mg/dl. On May 26th, her BUN had risen to 83 and her creatinine to 5.7 mg/dl. Her TSH could not be adequately suppressed without raising her dosage of thyroxine and was 3.5. Her thyroglobulin had bottomed out at 470 ng/ml. Her legs were swelling and she was developing foot ulcers. Boot therapy was begun in early July when a 1.5 sq cm scab on the right 5th toe and small areas of focal necrosis were noted on the right first and second toes. The entire top of the left fourth toe was blistered and a few scabs and callus were found on the left big toe. With the therapy her BUN fell to 66 mg/dl and her creatinine to 5.2 mg/dl. Her thyroglobulin, however, had risen to 2100 ng/ml. It was time for the family vacation at the shore and she joined them for two weeks. She returned on July 21st again with swollen legs with infected blisters of her left 2nd, 3rd and 4th toes and right 4th toe. Her family brought her into the clinic for Long-Boot treatments July 21, 24, 27 and 31st. Meanwhile, her thyroxine had been discontinued and triiodothyronine substituted to decrease her body pool of thyroxine in preparation for another treatment with radioactive iodine. Her intermittent booting was sufficient to decrease her leg swelling and allow healing of her ulcers to begin. Her booting was continued every 2 to 3 days through mid-August ( 3,5,7,10,12, 14 and 17). She then attempted to go 5 days without treatment, began to retain water and was admitted to the hospital on the 5th day (August 21st) with a new stroke manifested by garbled speech and confusion. The admission CAT scan of her head showed old small infarcts. The neurologiy consultant advised us to avoid thrombolytic agents. Because her BUN had risen to 103 mg/dl, her creatinine to 6.4 mg/dl and her CO2 had dropped to 16, a nephrologist was consulted to advise her about hemodialysis, which she and her family declined. He reviewed her renal ultrasound which showed a left kidney 12.2 cm and right kidney 9.6 cm in length. The renal parenchyma was somewhat diminished compatible with global parenchymal loss bilaterally. The kidneys were somewhat echogenic, a finding which can be seen in medical renal disease. No hydonephrosis was apparent. He observed her fluid overload (congestive heart failure and swollen legs) and recommended fluid restriction and hospice care advising the family she would likely be dead in the near future from her renal failure.



August 21st: Basal congestion and cardiomegaly pointed to congestive heart failure.

The boot service, on the other hand, noted the warm weather, the confusion of the patient, the unlikely possibility that she had been drinking an adequate amount of fluid, her known cardiac dysfunction and the possibility that she had a combination of dehydration and congestive heart failure. If the latter were true, further fluid restriction would worsen her renal failure and indeed possibly kill her in the absence of dialysis. A fluid challenge accompanied by heart support with the Circulator Long-Boots was accomplished.



Our IQ electrical impedance apparatus was used to document we could indeed improve her cardiac output. Here are shown her dZ/dt waveforms representing changes in her cardiac output on a beat-by-beat basis during booting on alternate heartbeats. The top line is her EKG. On the bottom line, the red arrows show her assisted beats and the black arrows the unassisted beats.

She was first given 5% glucose in half normal saline at 40 ml per hour for two days. Her urine output increased and the infusion was increased to 80 ml per hour. On the 27th of August, her BUN had dropped to 69 mg/dl and her creatinine had dropped to 4.9 mg/dl. She continued on the Cytomel. Her TSH was less than 0.05 and her thyroxine serum level was less than 1.0 ug/ml suggesting that her thyroid cancer no longer made thyroxine and might not now take up radioactive iodine. On August 28th, she was transferred to our Transient Care Unit to continue her stroke rehabilitation, to await a new thyroglobulin level and to continue her booting. There she achieved her lowest values for BUN (49 mg/dl) and creatinine (4.2 mg/dl).



September 4th: Her dypsnea had improved and her lungs cleared with her boot therapy.

Over the Labor Day weekend, she again received no booting for four days; on the 4th day she again appeared to have a new stroke and her creatinine were found to have risen to 4.6 mg/dl. With reinstitution of booting, her cerebral function improved and she was discharged home to receive her boot treatment as an outpatient. A rising thyroglobulin level (3775 ng/ml) appeared to necessitate more I131 therapy. Her Cytomel was discontinued and TSH allowed to rise. Subsequently, an I131 scan revealed multiple foci of tumor and another 31 mCi of I131 was administered as an outpatient. She is to continue booting as an outpatient to support her heart and kidneys... until the effort is no longer in her interest because of the spread of her tumor.


Comments: This lady is included for many reasons. Her initial osteomyelitis had resisted the best care her hospital had to offer for over a year. A short course of local antibiotics and boot therapy had a long-lasting benefit and the foot remains intact today. Her leg ulcers developed in spite of the vain attempts of her cardiologists to prevent peripheral edema. The cardiac-assist action of our Long-Boots helped her control her edema and heal her legs. Suffering from potentially terminal congestive heart failure and uremia, she was benefited again by the cardiac-assist action of booting. Her multiple medical problems and lack of any remaining peripheral veins made her no candidate for any form of surgery. Could her problems have been treated by any other method? Her mitral valve disease contributed likely to her heart failure but does not prevent immediate benefit from booting. Her aortic valve, fortunately, did not have significant insufficiency; if it did, Long-Booting would have had no cardiac benefit. These patients do not need to be booted everyday. Booting Monday, Wednesday and Fridays seems to keep them free of problems. As with this patient, however, a four or five day lapse in therapy is commonly associated with a return of heart failure and a worsening of renal function. In this patient, cerebral function seems also to fail.



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