Case 195a1: Renal Failure, Hemodialysis and Leg Ischemia - Follow-up of Case 195.

Discharged from the hospital on February 28th, 2000, he continued with his hemodialysis three days a week and his boot therapy. He was treated in the outpatient boot facility 5-6 days a week. His routine included Long-Boot treatments to both legs followed by cleansing foot soaks in Sea Soaks and dilute hydrogen peroxide, followed then by local gentamicin injections into the soft potentially infected areas of the left foot and, finally, followed by Mini-Boot treatments (the right foot dry and the left frequently immersed in Sea Soaks and antibiotics). On March 3rd, he was found to have an increased amount of drainage on his dressing and a slight odor. Parts of the distal left foot were soft and "mushy". To ensure adequate drainage from his foot, the soft necrotic areas were debrided back to firmer tissue.
The soft necrotic tissue around the 3rd and 4th toes was removed.

Dorsal aspect left foot on March 9th.

Over the next few days, the remaining toes of his left foot were removed. He could still flex his big toe when it was removed on March 7th. As yeast was recovered from his foot culture on March 13th, he was given oral Fluconazole and Fungizone was added to his Mini-Boot bath. He continued to do well until March 22nd when he came from dialysis where he had had his feet elevated again for a period of hypotension. His feet were cold and painful and his vascular tests had deteriorated.
Plantar aspect left foot on March 9th.

March 22nd: His ABI had fallen from 1.10 on the February 27th to 0.45 in the right leg and from 0.89 to 0.54 in the left. His pulse volume at the ankle had fallen from 1.1mmHg to 0.28mmHg in the right leg and from 1.48mmHg to 0.40mmHg in the left leg.

He was started again on an aggressive boot program, essentially pumping both legs a few hours both morning and afternoon 3 days a week and after dialysis 3 days a week. His requirements for pain relief with Percocet receded over several days and his feet gradually regained their warmth. The eschar was gently debrided back from the margins on the left foot to expose granulation tissue. Reganex was added to his program to hasten epithelization over the exposed tissue. He remained ambulatory but was advised to limit his walking to necessary activities.


The area of necrosis in his arch showed the least healing.
Granulations were developing under the eschar in the medial aspect of the lesion and some new skin was forming at the edges of the granulations.
The lateral foot had good granulations both on the dorsal and plantar surfaces.

Cardiology consultation on May 18th: The patient was noted to have a rapid pulse rate in the boot room on May 17th and later in the evening was aware of palpitations. He telephoned his cardiologist for an appointment on the 18th. He was asymptomatic on awakening the 18th and denied having had any dypsnea or chest pain. His daily medications were noted: Levothroid 0.088mg, Captopril 50 mg every 8 hours, Catapres 0.4mg patch (weekly), hydralazine 100mg every 12 hours, Cartia 180 mg in the morning and 120 mg in the evening, Plavix, Diflucan, Elavil, and Epogen. His beta-blocker had been discontinued by his renal specialist. The cardiologist speculated that the palpitations had been a recurrence of his paroxysmal atrial fibrillation and increased the dosage of Cartia to 400 mg daily. He also recommended considering restarting the beta-blocker.

.

June 9th, 2000: The pulse volume tracings had recovered at the ankle and mid-foot. The waveforms in the left mid-foot, where there was no distal runoff, were actually larger than in the right foot.

June 23rd, 2000: More debridements and more healing....
June 23rd, 2000: The tissue bleeds well when nicked....
October 10th, 2000: More debridements and more healing... Still work to do. Ambulatory.

March 14, 2001: Pain in the area of the 4th metatarsal stump and a sed rate of 54 mm/hr suggested the possibility of osteomyelitis. Three views of the foot were obtained.
March 14, 2001: The roentgenologist noted little soft tissue about the ends of the remaining metatarsal bones. No gas was seen in the tissues. The medial cortex of the remaining portion of the 1st metatarsal was eroded, and there were some erosive changes at the base of the 1st metatarsal.
March 14, 2001: The findings were suggestive of osteomyelitis. The suspicious areas were subsequently targeted with local antibiotic injections (vancomycin for MR resistant Staphylococcus aureus and Amikacin for Pseudomonas).

On April 10th his foot cultures grew out Alcaligenes xylosoxidans, Stenotrophomonas maltophilia and methicullin-resistant Staphylococcus aureus. He was treated with foot soaks of dilute peroxide in Sea Soaks, 3-minute ultraviolet light exposure and Sufladine cream in addition to his local injections and boot therapy.


April 18th, 2001: Slow healing and some foot pain associated with infection with resistant organisms and ambulation. His foot pain abated with curtailing his ambulation.
April 18th, 2001: His skin was allowed to grow up to the islands of bone which were then flecked back to expose marrow that the skin could then cross. Still some healing to do.

On May 21st, his culture grew out a scant amount of Staphylococcus aureus (treated with local vancomycin) and a heavy growth of Pseudomonas aeruginosa (sensitive only to Tobramycin [which was subsequently used locally] and Imipenem). His ulcer appeared to be doing well. In June, the possibility of allergy to his Silvadene cream was raised and the medication was discontinued. In early July, his ulcer again appeared to be doing well, but it now grew out but a light growth of Coagulase-negative Staphylococcus (the Vancomycin was stopped) and a heavy growth of Pseudomonas now resistant to all antibiotoics tested except Amikacin (the Tobramycin was discontinued and local Bactroban was prescribed). On July 6th, he developed shaking chills while in dialysis and was admitted to the hospital for 8 days. His past medical history was noted:


For these conditions, he was taking Labetalol 400mg 3x/day, Plavix 75mg daily, hydralazine 100 mg 2x/day, amitriptyline 40mg at bedtime, Cartia XT 180mg in the morning and 120mg in the evening, Levothroid 0.088mg/day, Captopril 50mg 3x/day,Creon 10, sodium bicarbonate, L-arginine, vitamins E and C, fish oil, multivitamins, Rengel and protein supplements.

His temperature on admission was 101.4F and pulse 119. He had bi-basilar crackles in his chest and diminished breath sounds. His foot ulcer was little changed but did have a gray-greenish discharge. His chest x-ray showed cardiomegaly, mild pulmonary congestion and a retrocardiac infiltrate with bilateral pleural effusions. He had a right bundle branch block and lateral wall T-wave inversions on his EKG. His white count was 7.0 with 90% polys and 1% bands. The platelet count was 70000. The serum albumen was 2.8G/dl and bilirubin 1.1mg/dl. His blood cultures grew out Pseudomonas aeruginosa resistant to all antibiotics except Imipenem (sensitive) and amikacin (intermediate). The infectious disease consultant recommended leg amputation noting that the infection could cost him his life. The infectious disease consultants, his renal specialists and his boot doctors all discussed the advantages and disadvantages of amputation versus outpatient antibiotic therapies. His last blood culture was negative and he felt well. He chose outpatient therapy and was discharged on intravenous imipenem and amikacin along with his usual medications. His discharge diagnoses included besides the above:


He continued with his boot therapy and his dialysis. The latter left him weakened and commonly febrile in spite of an infusion of antibiotics at the end of the procedure. The antibiotic susceptibilities of his Pseudomonas caused confusion raising the question as to whether his foot ulcer was indeed the source of his bacteremia: his foot culture on July 20th grew Pseudomonas aeruginosa resistant to all antibiotics while his blood culture grew Pseudomonas aeruginosa susceptible to piperacillin and intermediate to aztreonam and ceftazidime in spite of his then receiving pipercillin and aztreonam intravenously. Could the foot bacteria mutate into the blood bacteria against the pressure of appropriate antibiotics? While the foot and blood Pseudomonas organisms might have been derived from a common source, was their different antibiotic sensitivities due now to their coming from different sources, one the foot and the other an intravascular site somewhere else in his body? Why, he and his wife asked, did he get chills and positive blood cultures after his dialysis. Was the dialysis filter contaminated? Were protective antibiotics dialyzed away? Were osmotic forces generated that sucked bacteria from his foot into his blood stream? He did not have chills and fever after his boot therapies in spite of the compressions delivered to his foot. His habit of picking his nose was also a problem: methicillin-resistant Staphylococcus aureus and Coagulse-negative staphylococcus were cultured and probably transferred to his foot ulcer as he would examine his foot. (Bacitracin was prescribed for his nose.) He fell and suffered a right perioribital contusion (no fracture) on July 26th. Other x-rays showed persistent cardiomegaly with left basilar effusion/consolidation and possible changes of osteomyelitis of the 1st metatarsal head (little change from the above films). The fall along with his fever and weakness led again to hospitalization.

Hospitalization July 26th to September 29th: Salient points on his admission physical examination included his thin frame, a lack of acute distress, the right periorbital hematoma, a protuberant abdomen, a perianal fistula with visible tracts into his left buttock, an intact right foot, his left foot ulcer with a slight serous discharge, and his A-V graft dialysis fistula in his left upper arm.

During the hospitalization, he had multiple blood cultures positive for Pseudomonas with sensitivities different from that of his foot. Some of the blood isolates were reported as being sensitive to no antibiotic. He had tagged white cell bone scans that showed some activity on the ends of his metatarsals where the bone had been cut back along with activity in his enlarged spleen and liver. His abdomen was protuberant both because of ascites and hepatosplenomegaly. In reviewing his past abdominal x-rays and ultrasound examinations, it was recognized that his spleen had been slowly enlarging over the past few years. A literature review showed that his hemodialysis might be a cause of the splenomegaly, thrombocytopenia and anemia. Further, splenic abscesses were now possibly a source his bacteremia. (Platts MM, Anastassiades E, Sheriff S, Smith S, Bartolo DC. Spleen size in chronic renal failure. Br Med J (Clin Res Ed) 289(6456):1415-1418, 1984.) (Vanherweghem JL, Drukker W, Schwarz A: Clinical significance of blood-device interaction in hemodialysis. A review.Int J Artif Organs 10(4):219-232, 1987.) (Liang JT, Lee PH, Wang SM, Chang KJ: Splenic abscess: a diagnostic pitfall in the ED. Am J Emerg Med 13(3):337-343, 1995) (Najean Y, Messian O: Anemia of kidney failure treated by periodical hemodialysis. III. The effect of splenectomy. A retrospective study of 25 cases. Presse Med 12(37):2307-2310, 1983.) The infectious disease specialists favored leg amputation throughout his hospitalizations, but noted that it was quite likely that amputation would not cure his bacteremia; it was likely, they thought, that there was seeding to an intravascular site that would eventually lead to his death. When the patient developed a sore nodule in his arm a few inches distal to his arm AV shunt, the nodule was needled and biopsied expecting such a vascular focus, but a sterile granuloma was removed. His A-V shunt was considered as a possible locus of infection, but the white cell scans did confirm the suspicion (one of the infectious disease specialist did not consider the scan definitive proof of a lack of infection while the renologist were very jealous of their shunt (it worked and other sites had already been exhausted). Seeding to his ascitic and pericardial fluid was also considered. The latter fluid was loculated behind his heart and was not not to be easily removed. Why not remove his leg? The following considerations were discussed with the patient and his wife:


While the above and multiple other studies were performed, he continued with his dialysis and, on many days, his boot treatments. Local foot debridements, bone scraping, ultraviolet light therapy, and vinegar soaks were utilized in attempts to rid his foot of Pseudomonas. DNA studies of the blood and foot Pseudomonas species returned showing that in spite of their differing antibiotic susceptibilities, they shared the same DNA.



August 21st, 2001: The hemorrhagic spot was the site of a bone debridement. The sheen over his ulcer was left in place a few days in hopes it represented growing epithelial cells; it proved to be a membrane rich in Pseudomonas.
September 10th, 2001: Further sharp debridements did not produce a sterile wound.

Athough he was weak and intermittently febrile, he was discharged to continue his treatments at home. Maggot therapy had been intermittedly suggested. Now, it was offered in hopes they would sterilize his ulcer and remove infected necrotic material his physicians could not appreciate.(The maggots were obtained from Ronald Sherman, M.D., University of California, phone 949-824-5829)



The maggots swarmed over his ulcer centering their activity over his arch and the bony area previously debrided.
October 17th, 2001: With each application, the maggots were allowed to stay on for 48 hours. They left a clean red meaty wound.
October 22nd, 2001: After 3 applications, the wound appeared to be closing and the necrotic bony area cleaner.

With the possibility that the maggots might clean up his foot infection when our local and systemic antibiotics could not, he was advised that we would do well to apply the maggots regularly three days a week. We would remove each maggot application after 48 hours, rinse the foot, treat his foot in the Miniboot and reapply another batch of maggots. Such a regular program was not to be. Searching for other avenues of treatment, they consulted an nearby wound-healing center and an academic center where hyperbaric oxygen was to be considered. As some raised again the question of surgical vascular reconstruction, repeat noninvasive tests were done:



October 29th, 2001: Good pulsatile flow was seen at both the ankle and midfoot bilaterally even when the feet were raised two feet off the examining table. The transcutaneous gas tests were not as favorable, however. The patient kept twitching his feet breaking the seal between the skin and the electrode making it necessary to tape the electrode firmly against the skin and unfortunately blanching the skin; TcPO2 readings of 4-6 and TcPCO2 readings of 56 were recorded. Such low readings are not usually found with pulse volume tracings as good as his and may have been due to the application of tight electrodes, ischemia, cellulitis or change in the skin permeability due to chronic inflammation.

The consultations, a social trip and fatigue interrupted his boot and maggot sessions. His lack of cardiac assist was associated with (not necessarily the cause of) increasing ascites and dypsnea. He was readmitted to the hospital on November 7th because of increased shortness of breath. A parencentesis removed 1.75 liters of sterile dark yellow fluid relieving his dypsnea somewhat. A MRI of his cervical spine was done because of complaints of neck pain. Discitis and osteomyelitis of C4 and C5 were demonstrated; here was another focus of infection besides the foot.. and a focus that was neither operable or curable, given the reported resistance of the organism. He was discharged on November 18th with a neck brace (he rarely wore) and intravenous antibiotics (Vancomycin and pipercillin). He subsequently received few boot treatments and no maggot treatments. His wife applied honey to his foot ulcer at home and during his next and last hospitalization with some benefit (reduction in drainage and little enlargement of his ulcer). He was readmitted on November 19th because of low blood pressue. His sclera were now deeply icteric. He died on December 3rd.


Comments: It is obvious that his man had multisystem involvement of his arteriosclerotic disease and needs care of appropriate physicians. The determination of appropriateness and need for consultations is best left to the medical vascular specialist and not the family doctor. This man had numerous unnecessary and potentially dangerous consultations. As in this case, a rheumatology consultation may lead to a trial of steroid therapy, which in our experience is rarely helpful and commonly harmful (infection is a common cause of death with chronic steroid therapy). The recurrence of his ischemia and its successful treatment with booting is worth emphasizing. First, the relapse associated with dialysis is evidence that hypovolemia and hypotension associated with excessive dialysis was likely the cause of his initial episode. Second, little additional tissue damage was associated with the second episode because there was little delay in initiating boot therapy to restore the circulation. Third, it may be noted that his feet were still there at the time of his death (albeit one foot still ulcerated and infected). The risk of managed care is again to be recognized. When a patient from such an organization in our area is referred as an urgent case, we must apply immediately to the HMO to obtain permission to treat the patient. Further, we are asked to send the patient to a capitated vascular testing site to document the vascular status of the patient. If we do send the patient to the capitated site, routine segmental pulse volumes and an ankle/arm index will be scheduled in the near future (rarely if ever performed the same day). If we do the vascular testing in our office to appropriately document the vascular pathology for a specific patient, we will not be paid. If we appropriately treat the patient immediately and successfully reverse a vascular occlusion, their response has been that the care was likely not necessary and, hence, not covered. It is quite likely that in this man had he been referred early in the course of his first episode, he would not have had any loss of tissue. It should be noted that his relapse was treated as an outpatient. Maggot therapy deserves some comment: it might have been done much earlier. It does not pose the risk of allergy and resistance to antibiotics. It is likely cheaper than home antibiotic infusions. It is not, however, covered by most insurance programs. Again, the question of insurance coverage. What happened when our hospital appealed to Blue Cross to reverse their denials? On June 2nd, their Vice President of Quality Management wrote us denying days 1/23-1/27 and 1/30-2/27 on the basis that wound care could have been done in an alternate setting. We have no alternate setting where we could have given this man the treatments described. Do you? The families of patients like this one do not need the additional stress of insurance controversies. This man was blessed with a loving, informed and attentive wife whose work and life was greatly disturbed by his long illness.


Return to start of this case
Return to CBC Homepage
Return to Menu of Case Histories
Next Case