Case 195: Two Numb Ice-Cold Mottled Feet with No Capillary Refill and No Doppler Sounds Below the Low Calf

Right knee and upper calf: The superficial femoral (not seen) and popliteal vessels were patent and smooth in outline. The anterior tibial and posterior tibial-peroneal trunk are occluded. Numerous collateral vessels are seen.

On January 12th, 2000, the vascular surgeon of this man requested a boot consultation. He described two quiet cold feet that he thought would likely come to amputation. The patient, a 60 year old engineer who had been born in India, had had two colon resections for Crohn's disease which presumably has become quiescent. With a short bowel, he has some diarrhea and had had calcium oxalate kidney stones which with an interstitial nephritis were thought to have led to uremia and need for hemodialysis. He visited India in the fall of 1999 and noted calf cramps after his dialysis while there. A few days later he noted difficulty walking and then a few days later, the onset of nocturnal pain in his feet. He returned to his Bryn Mawr dialysis center. He was advised he had neuritic pain and took Elavil with some relief. However, by the 3rd of January he found both leg were painful on awakening. The diagnostic label of neuritis persisted until his arteriogram on January 11th.

Left knee and upper calf: The popliteal is patent and smooth in outline. The tibial vessels are all occluded within 2 centimeters of their origin. Numerous collateral vessels are seen.

Right lower leg: Numerous collaterals are seen to the lower quarter of the tibia.

He had sought help in Emergency Room and was admitted on the vascular surgery service January 11th where he was advised there was no surgical remedy for his difficulty. The boot consultant advised the patient that the distribution of his occlusive disease was suggestive of diabetes, that he may have had neuritis but that the severity of his ischemia could account for his symptoms and that, left untreated, his feet would likely become gangrenous…. messages all distressful for the patient, his family and attending physicians. The use of topical oxygen was suggested and begun to support and maintain the integrity of his skin envelope and allow more time for booting. Therapy with the Mini-Boot was begun but the therapy was interrupted by his need for dialysis, his other medical problems, and the multiple consultations with other doctors his previous attending physicians felt necessary.

Left lower leg: Only a few collaterals were seen entering the level of the lower third of the tibia.

Right foot and ankle: Delayed films showed a small twig of a capillary between the right internal malleolus. Nothing was seen in the foot. Nothing was heard with the Doppler at the bedside in the ankle or foot.

His baseline laboratory data included a BUN 53 mg/dl, creatinine 8.0 mg/dl, a calcium 9.2 mg/dl (no PO4 available) and a prolonged prothrombin time of 17.3 seconds in the absence of anticoagulants. The boot consultant raised the possibility of calciphylaxis and the hazards of his dialysis (dehydration, hypovolemia, and elevation of his legs when his blood pressure was low) as factors potentially promoting his vascular crisis. As ischemic feet commonly develop osteoporosis and as measures like parathyroidectomy seemed excessive in this sick man, the boot consultant suggested therapy with intravenous pamidronate to minimize the development of osteoporosis and decrease the effect of his expected secondary hyperparathyroidism. The vascular surgeon agreed that foot elevation in the dialysis clinic had posed a hazard in his patients.

Left foot and ankle: No vascular structures were seen on delayed films at the ankle and foot. The lower leg had no Doppler sounds. He returned from the arteriogram with cyanotic feet.

Renal consultation: The patient has been on hemodialysis since May 1993 and has had longstanding hypertension. His AV shunt in his left upper arm is patent. Later the renal specialist noted that serum parathyroid hormone levels had not been elevated, that only on occasion was the serum PO4 elevated, but the serum calcium level was in the 9's (in spite of low albumins).

January 11th: Admitted and arteriogram done. The nutrition consultant pointed out his nutritional risk and recommended a renal diet supplemented by Magnacal three times daily and intravenous hyperalimentation. Laboratory: WBC 12.5, Hgb 11.1, prothrombin time 16.7 seconds, BUN 53 mg/dl, creatinine 8.0 mg/dl, albumin 2.8 g/dl (N3.4-5.0), SGOT 118 (N 15-40), alkaline phosphatase 174 (N50-136 U/L), D Dimer negative, .

January 12th: The plantar aspects of both feet were purple and mottled. Both feet were treated in the Mini-Boot between the above activities and consultations and appeared to be warmed to the ankles. The feet remained cold. Topical oxygen therapy was started and ran 24 hours a day through most of his hospitalization. Laboratory: iron saturation 16% (normal 20-50); rheumatoid factor negative; antithrombin III, Protein C and Protein S all normal, sedimentation rate 110 mm/hr, Staclot La negative, APC resistance V 2.0 (N >1.9), IGM 7.4 (N<10), IGA 11.9 (N <10), ferritin 1008 ng/ml (N 22-322), cryoglobulins negative and C3 and C4 normal, serum protein electrophoresis showed possible faint monoclonal band, ANA negative, neutrophil cyto antibodies (C ANCA, P ANCA and X ANCA) negative,

The right foot cold and had a non-blanching rubor. The nails are seen to be cyanotic. The dark areas of skin appeared to be non-viable.

January 13th The surgeons signed off the case. The patient was dialyzed. His feet were covered with a thin layer of gauze. A nasal oxygen catheter was placed around his arches. A plastic bag was then placed over his feet and gently contoured against his feet with loose gauze. Finally, pure oxygen was run through the nasal catheters at a rate of one liter a minute... all of this constituting the "topical oxygen" therapy he received through most of his hospitalization. The oxygen continued to run during the Mini-Boot treatments he received to both legs. His ankles were warmed but soles of both feet remained mottled. Laboratory: WBC 20.7, albumin 2.8 g/dl; homocysteine 6.0 uMol/L; IGG phospholipid 4.6 (N<10); negative tests for anti DNA (double strand), anti SS-A and anti SS-B, anti-SM, and anti-SM/RNP.

The left foot was cold and likewise had non-blanching rubor, cyanotic nails and questionable dark skin on the dorsum of the foot.

The toes were kept at a level below the pubic bone of the patient so that gravity might help keep the feet well hydrated. The Mini-Boot treatments are performed with the patient sitting in a chair with his feet on the floor again helping to pump fluids through the feet.

January 14th The boot specialist expressed concern about heparin therapy lest hemorrhage into ischemic tissue occur. The left foot was noted to show signs of breaking down. An intravenous morphine (PCA) drip was started successfully relieving his pain. Muscle enzyme elevations were thought to be compatible with muscle breakdown in his feet. His heart rhythm instability, the topical oxygen therapy and his IV morphine made it necessary to treat him in the hospital room rather than transport him to the boot clinic. Indeed, the cardiologist transferred him from his private room to the Intensive Care Unit because of his persisting tachycardia. His boot treatments were interrupted. Laboratory: blood gases: pH 7.43, PCO2 36.2 (N 35-45), PO2 69 (N 80-100) bicarbonate 24.5 (N 21.0-28.0); total serum calcium 9.4 mg/dl (N 8.5-10.5), magnesium 1.5 (N 1.5-2.4), ionized calcium 1.15 mM//L (N 1.09-1.33), glucose 137 mg/dl (N 70-110), phosphate 5.4 (8AM) and 3.8 (6PM)(N 2.5-4.6 mg/dl), cholesterol 73 mg/dl, potassium 6.0 mEq/L, LDH 373 (N 100-200), SGOT 115 (N 15-40) SGPT 66 (N 30-70), alkaline phosphatase 206 (N 50-136), GGT 78 (N 5-85), CPK 1440 (N 15-210 U/L), CKMB 24.5 (0.0-3.6 ng/ml), CKMB Rel Index 1.7 (N<1.5%; values <1.5 are probably of skeletal origin; values 1.5-4% are possibly and values > 4.0% are probably of myocardial origin) and serial blood cultures reported as "no growth". WBC 20.3. The pulmonary/critical care specialist listed sepsis or possible systemic inflammatory response syndrome as his first concern. Dialyzed from 7:40 to 11:40AM. Pulse 96-140.

The left foot remained well-hydrated also. A purple tissue infarction is seen in the proximal arch.

January 16th: The state of his feet (ice cold in temperature, mottled, presence of cyanotic areas that did not blanch with direct pressure) along with the muscle enzyme changes suggested that much of the feet were irreversibly damaged. The boot doctor suggested that in such feet and in the absence of any detectible pulsatile arterial flow, that treatment with vascular endothelial growth factor (VEGF) was likely fruitless. Something more rapid was necessary. His low serum albumin, normal total serum calcium levels, intermittently elevated serum PO4 levels and high alkaline phosphatase were all compatible with secondary hyperparathyroidism. The possibility of a process like calciphylaxis was mentioned. Again, it was pointed out that osteoporosis commonly develops in ischemic feet. It was suggested that the infusion of pamidronate 60 mg intravenously over four hours might be effective in treating both the osteoporosis and the secondary hyperparathyoidism. The gastroenterologist noted his persisting fever (100 degrees F) and atrial flutter. He added Medrol to the therapeutic program, agreed to the use of pamidronate (which was then administered) and made plans to transfer the patient to another institution for VEGF therapy. The cardiologist continued the Cardizem and heparin, decreased the beta blocker and added aspirin to the program.

January 17th: Now his 6th hospital day, his previous therapy included topical oxygen, some Mini-Booting, massage and intravenous administration of morphine, heparin, pamidronate and steroids. His blood glucose level rose with the use of the steroids suggesting the presence of latent diabetes. Both legs were booted in the morning and he was dialyzed in the afternoon. As his pulse rate rose to 130 during the latter, the cardiologist raised his dosage of Cardizem. The rheumatologist advised raising the dosage of Medrol to one gram daily (the patient refused) and obtaining a muscle biopsy. Dialysis 1:45PM-4:45PM. Pulse rate 95-135. Laboratory: albumin 2.3, calcium 9.4, PO4 5.2, BUN 140, creatinine 13.0. EPO 20,000.

January 18th: Doppler sounds were heard at bedside in the anterior tibials at the ankle and in the right foot, in the first dorsal metatarsal artery. The feet remained generally mottled and the toes blue. Insulin was prescribed to decrease the hyperglycemia stimulated by the Medrol. The boot doctor pointed out that steroids have not found use in the treatment of ischemic or thrombotic disease other than that associated with arteritis…. and that there was no evidence in this case of arteritis. Both legs were booted several hours. Atrial fibrillation persisted and the rate was controlled with an increased dosage of Cardizem. The rheumatologist still favored muscle biopsy. The gastroenterologist stopped the steroids.

January 19th: Dialysis 7:40-10:40AM. BP 103-190/58-110. Pulse 109-155. His heart monitor showed rapid atrial flutter. The cardiologist resumed intravenous Cardizem. EPO 40,000 units was given during the dialysis procedure. The mottling of the feet was less prominent. The left foot was warm over the tarsal bones and cold distally. The Doppler sounds in the left posterior tibial were modestly loud while sounds in the left dorsalis pedis and metatarsals were not found. The right foot was warm to the distal foot and strong Doppler signals were found in the right dorsalis pedis and 1st metatarsal arteries. The demarcation process was beginning in left foot. The vascular surgeon expressed worry about the need for bilateral BK amputations. Both legs booted.

January 20th: A small hematoma was found on his arm. His pulse rate was in the 80's on additional Cardizem. Fairly loud Doppler sounds were heard in the left posterior tibial at ankle and at the anterior tibial at the instep but no sounds were heard in the dorsalis pedis. The distal 60% of the foot was still cold. The rheumatologist noted negative tests for ANA, RF, ANCA, cryoglobulins, SSA and SSB along with normal C3 and C4. He still favored a muscle biopsy. He was given anesthesia for a successful cardioversion procedure ( a single 200 Joule synchronized shock). Amiodarone was started. Grossly heme-positive stools were noted and his heparin therapy stopped.

January 21st: Dialysis 1:15PM to 4:15PM and EPO 40,000 units administered. BP 159-216/84-101. Laboratory: albumin 2.0, CPK 208, WBC 21.2, CO2 18, glucose 118, BUN 144, creatinine 10.6. Doppler of left foot: strong posterior and anterior tibials at the ankle while the peroneal was weak and the dorsalis pedis absent. The distal left foot was cold and mottled. Both legs were booted. Patient refused transfusion. Patient's family talked to Dr. Isner at St Elizabeth's in Boston asking about angiogenic factors; Dr Isner suggested trying PGE1. Because of GI bleeding both heparin and coumadin were discontinued. Surgeons suggest transfer of patient to Boot service.

January 22nd: His blood glucose levels were monitored and an insulin scale prescribed successfully normalizing his glucose levels. The glucose remained normal after the Medrol was discontinued. The right foot was warm to toes with very little residual mottling while the left foot was cold to the proximal forefoot with cool mottled areas. Topical oxygen and Circulator Boot treatments were continued.

January 23rd: Several hours of boot treatment were administered. Patient had few complaints. Surgical options: transfer for angiogenesis factors to another hospital or discharge home with outpatient boot treatments. Surgical medical student noted that the patients was having "just a little vomiting".

January 24th: Dialysis 7:35-10:50PM. BP 173-192/80-95. Laboratory: BUN 126mf/dl, CO2 16 mEq/L, K+ 4.8mEq/L, creatinine 11.2mg/dl, FBS 144 mg/dl and white count 19.9. The high BUN was attributed to his gastrointestinal bleeding. The right foot was warm to the toes with some blistering of the toes. The proximal left foot was warmer. Both legs were booted. The cardiologist restarted Hydralazine.

January 25th: Distal half of left foot still cold and mottled. The Doppler of both the left anterior tibial and posterior tibial are now strong at the ankle level, but no left dorsalis pedis was detected. The right foot intact to the toes with good distal Doppler sounds. Gastroenterologist noted lack of further GI bleeding and lack of much pain in the feet. Cardiologist adjusts Amiodarone to 200 mg/day. Booted right foot one hour and left seven hours.

January 26th: Dialysis 9:35AM to 1:35PM. BP 157-185/70-105. 40,000 EPO. Purpuric spots on right toes still to resolve. Left proximal foot warm and distal foot less mottled. Advised not to walk on either foot yet as tissue plains and ligamentous structures were not solid. Advised that some of our patients, who were prematurely discharged and had been ambulatory of necessity, had dislocated their tarsal bones, resulting in one case in leg amputation with a significant mortality risk. His leukocytosis was thought to likely reflect damage to feet. Some low grade fever was recorded.

Right foot on January 27th: Patchy dark areas were seen on the dorsum of the foot.

January 27th: His right toes were warm but spotted with blue. His left foot was warm to the arch. He was still able to move his toes in spite of proximal mottling and coldness. The medial aspect of left heel was reddened and warm ("like a frost-bite injury", he was told). Desirable to change location of boot treatments to office as (1) can boot both legs simultaneously; and (2) easier for boot staff… but hospital treatments allowed non-weight-bearing, topical oxygen therapy, and long hours of booting to bad leg… along with no worry about snow and transportation problems to both dialysis and boot clinic. Patient having trouble with transfers to chair from his bed. Booted right leg all morning and the left leg all afternoon and evening.

January 27th: the patchy dark areas were more extensive on the left foot. The ruborous area over the proximal instep did not blanch on direct pressure. The distal half of the foot remained cold.

January 27th: Splotches of dark necrotic skin are seen on the toes and arch.

January 28th: Hemoglobin 6.9, the anemia due to his chronic renal failure, his gastrointestinal blood loss and the noxious effect of his necrotic foot. Booted both before and after his dialysis. Dialyzed 2PM to 6PM. EPO 40,000. BP 167-190/74-88. Right foot estimated to be 95% improved and left foot 50%. His WBC was down to 17.3 and his CpK down to 134. His pain was greatly diminished. Physician (Dr. German) reviewing the case for Blue Cross advised of continued need for hospitalization due to (1) his weakness and immobility; (2) his need for dialysis; (3) his need for transfusions; (4) the need to observe him for significant infection lest his leukocytosis represent infection in addition to tissue necrosis; (5) his need to avoid weight-bearing lest the associated shear forces tear his tissue plains or dislocate his joints; (6) his need for topical oxygen therapy to maintain the viability of borderline skin until the blood flow is re-established; (7) his need for many hours of booting; and his current observation by several physicians …. All of which would have been difficult or impossible had he been discharged especially in view of the bad weather.

January 27th: The distal two thirds of the left foot remained cold and mottled. A big blister appeared to be forming in the arch.

January 30th: Gastroenterologist noted the intestinal bleeding had ceased and aggressive booting still necessary.

January 31st: Dialysis 1PM to 4:30PM. BP 157-191/82-93. EPO 40,000. BUN 124, Na+ 136, K+ 6.1, CO2 13, CL98, CO2 13, Creatinine 10.6, WBC 9.2 - 13.2, alkaline phosphatase 339. Except for blood blisters on the right foot, the right foot normal. The bedside Doppler revealed strong signals in the left anterior and posterior tibials at the ankle and weaker signals in the dorsalis pedis but the distal left foot remained cold, quiet and mottled. Right fungus-laden toenails trimmed. Left heel warmer. Continued usual routine now booting left leg several hours. Gastroenterologist noted patient vomited non-bloody material. Cardiologist noted stable heart rhythm.

February 1st: WBC 8.9-10.0. TSH 10.61. Culture blister on right foot S4+ Staphylococcus aureus. Blood blisters peeling off right toes. Left foot warmer. Capillary refill developing on lateral distal left foot. Boot doctor noted that left beneath-the-knee amputation expected outcome if treatment lessened at present time. Vascular surgeon agreed more continuous therapy. Both legs pumped multiple hours.

February 2nd: The nailbeds are normal in color. Scattered areas of dark skin are peeling off the dorsum of the foot and toes.

February 2nd: Dialysis 7:15AM to 10:45AM. Laboratory: WBC 8.7-9.0, BUN 97, creatinine 8.5, blood sugar 116. BP 155-177/70-84. Pulse 79-91. Dopper signals from the left posterior tibial detected from the malleolus to the proximal arch and from the peroneal (lateral malleolar) artery from the malleolus to the proximal aspect of the 5th metatarsal. Left leg treatment included topical oxygen, tepid soaks with Sea Soaks containing gentamicin, and booting. TSH found to be elevated signifying the development of hypothyroidism possibly related to the usage of the Amiodarone. Thyroid replacement with Levothroid begun. The WBC now normal. Because of the persistence of low levels of serum bicarbonate, 1200 mg NaHCO3 started orally three times a day. 4+MR-resistant Staphylococcus aureus cultured from left foot blister fluid. Blood blisters still top peel off right foot. Left dorsalis pedis stronger. A second (but half dose) infusion of pamidronate administered. Gentamicin injected into the areas of the left foot suspected of infection and into the Sea Soaks foot soaks. Topical O2 and booting continued.

February 2nd: Four of the nailbeds are cyanotic. The reddened areas in the distal foot do not blanch. The foot remains well hydrated and blisters are seen.

February 2nd: A large blood blister is seen in the proximal arch. The distal foot was cold.

February 2nd: Note the black eschar that formed in the arch and the black areas on his toes.

February 3rd: WBC 7.5. Nutritionist noted low albumen (2.1) and advised dietary supplementation.

February 2nd: The left foot has not regained normal color and the distal two thirds of the foot is darkening.

February 4th: Dialysis 7:15AM to 12:10PM. Laboratory: WBC 7.4, Hgb 8.1, BUN 70. EPO 40,000. Right foot with black areas in the arch, beneath the 3rd metatarsal head and on the toes. The left foot warming in the arch but the blisters damper and possibility of infection considered. The potential adverse effects of gentamicin oi wound healing considered less of a risk than infection with Staphylococcus aureus. Patient advised to begin weight-bearing and exercises for right foot and to continue to rest the left foot. With his short-bowel syndrome and protein needs for healing, the gastroenterologist noted the patient should continue parenteral nutrition. Eight hours of booting. Modest temperature elevation noted possibly related to infection, the tissue necrosis in the foot or the pamidronate.

February 5th: Prothrombin time 17.8 seconds, INR 1.7 and PTT 31 seconds. Critical ischemia of left foot noted by boot service and importance of strict non-weight-bearing status emphasized.

February 6th: Sunday, eight or more hours booting accomplished. Now afebrile.

February 7th: The right foot was warm. The skin was peeling of the dorsum of the foot and toes. The toenail beds were well vascularized showing blanching on pressure and capillary refill.

February 7th: Dialysis 8:12AM to 11:42PM. EPO 40,000. BP 163-183/81-105. Loose skin debrided from right foot revealing normal skin beneath. Left foot warm and good Doppler sounds to mid-dorsum of foot where a pink tissue seen under the blisters. Potential outcomes considered: Right foot mostly healed at present and weight-bearing started. Percentages of healing estimated for left foot procedures done today: BKA 100%, transmetatarsal 20-30% and healing of whole foot still possible but unlikely.

February 7th: The left foot was still cold. The skin was blistering of the middle of the foot. The second and third toenails appear pink but do not blanch. A demarcation process across the midfoot appears to be beginning.

February 7th: Parts of the black eschar in the arch and under the 3rd-4th metatarsals were removed from time to time revealing normal skin. Likewise dried blood blisters were debrided off the toes.

February 8th: Laboratory: Prothrombin time 14.7, INR 1.4 and PTT 32 seconds. On no anticoagulants. More blood blisters debrided from right foot. Left foot had lots of drainage distally (not a bad sign… desiccation and mummification bad signs). Patient able to move all of this toes. Left foot given cleansing soak with Sea Soaks containing gentamicin and the latter also used to infiltrate the plantar blisters. Topical oxygen applied and booted ten hours. Unable to advise patient what if any procedure required on his left foot.

February 7th: The pink area under the left first metatarsal is misleading: it represents an area of "rubor mortis"; the skin is pink on removal from the oxygen bag but slowly becomes cyanotic where the cells can consume the oxygen while in dead areas the skin may remain pink.

February 10th: More black eschar debrided from right foot. Ceftazidime and gentamicin used in Sea Soaks cleansing soaks. Skin peeled off mid-foot leaving pink tissue which appeared to be covering with skin. Capillaries appeared to be invading a devitalized three cm round necrotic spot over middle third of the 3rd metatarsal bone. The left toes appeared to be blistering not desiccating. TSH 19.80, a rise in spite of the prescription of 0.075mg levothyroxine a day. The rise thought to be due to the effect of his Amiodarone on thyroxine-deiodinase. Cytomel started. Foot culture left foot: 1+ Enterobacter and 2+ Staphylococcus aureus.

February 10th: The skin was peeling off the distal necrotic parts of the left foot. Some capillaries seem to be invading the white necrotic area in the midfoot.

February 10th: The right foot was warm and except for the black eschar on the sole and the blood blisters on the toes was warm.

February 11th: Dialysis 8:40AM to 12:10PM. BP 180-191/83-95. EPO 40,000. Usual treatments in the afternoon and evening: foot soaks, topical O2, and continual booting. The nutritionist recommended in addition to his usual oral diet and supplements, parenteral feedings to include 250 ml 20% dextrose, 500 ml 15% aminoacids and 250 ml 20% lipids. The cardiologist stopped the Amiodarone. The hematologist remained concerned about the possibility of amyloid and asked pathology to stain any tissue they might have for amyloid over the last five years. More "blood blisters" were debrided from right foot.

February 10th: The volume of the left toes was beginning to shrink.

February 13th: More black skin has peeled off the right toes. The toenails are pink and healthy.

February 13th: Skin peeling off the dorsum of the right foot. The oxygen flow over the left foot served the function of drying the drainage, oxygenating the tissue and preserving the skin envelope. The loose skin from the heel and proximal left mid-foot were debrided leaving healthy skin.

February 13th: The skin over the middle three metatarsals is necrotic. The proximal half of the foot is healthy with new shiny unpigmented skin.

February 13th: Right toes fully extended.

February 13th: Right toes fully flexed.

February 13th: Left toes extended.

February 13th: Left toes equally flexed.

February 15th: Black skin debrided from right toes and distal foot.. Both legs booted. Skin on dorsum of the left foot floating off during soaks and the dorsum of the foot noted to weep. The hematologist noted that liver tissue from 1995 was negative for amyloid with congo red.

February 16th: Dialysis 7:43AM to 11:20AM. BP 181-217/87-102. Pulse rate 71-100. More black skin removed from toes of right foot. The pedal pulses were palpable in the right foot. The left foot booted 8 hours after his cleansing soaks. Still able to wiggle his left toes.

February 17th: On the right toes a little black skin is still seen rimming the toenails. Less brown material is seen at the base of the center toe. The right foot was still being booted an hour a day.

February 17th: His oral temperature was 99 degrees F. More skin was removed from the right toes. In the left foot, weak Doppler sounds were heard along the margin of medial demarcating area. Strong sounds were heard on the dorsum of the foot and at the distal end of 5th metatarsal bone laterally.

February 17th: Granulations were forming in the mid-foot. It was uncertain how far distally they might develop.

February 17th: In the right arch, only a small amount of black eschar remained to be debrided.

February 18th: He received hemodialysis from 7:45AM to noon. His blood pressure remained labile (BP 154-235/62-107). He received 10,000 units of Epogen. Due to pressure from his insurance company to bring hospitalization to a conclusion, some of the eschar was debrided from the left arch exposing red raw tissue that likely would have been better left covered. The dorsum of the foot had a modest odoriferous drainage. He was able to move all of his toes. He continued to receive daily cleansing soaks with Sea Soaks containing ceftazidime and gentamicin. He received several hours of booting.

February 17th: Much of the distal thick plantar skin had dried out to a stiff dark leather consistency. He could still flex his toes.

. February 20th: Sunday: The patient admitted to having little pain. Discharge was noted on the dorsum of the left foot and the dressings were odoriferous. Usual treatments with topical oxygen and booting administered.

February 21st: His dialysis treatment aborted 30 minutes early because of nausea. Small amounts of dead black skin removed from right foot. One eighth to one inch of eschar removed from various areas of the circumference of his left foot. In the arch the debridements required deeper cuts to get down to viable tissue. Usual boot treatments administered.

February 22nd: The remaining eschar was removed from the right foot which was now 99.99% healed. The left foot was demarcating in the mid-foot. Strong Doppler sounds were found up to the margin between the dark and good tissue. He was still able to move his toes, but his 2nd to 5th toes were beginning to dry out and lose bulk. The loose eschar along the demarcation line was debrided. Both legs (one at a time) were booted over eight hours. The vascular surgeon noted that the right leg now was normal and the left leg progressing with the only alternative to his booting being left leg amputation. X-rays were taken of the feet and showed preservation of the structures and shape.

February 22nd: Right foot: The roentgenologist reported modest osteopenia and soft tissue swelling in both feet.

February 22nd: Left foot: Less soft tissue is seen under the big toe sesamoid bone... otherwise the feet are very similar.

February 22nd: Right toes fully extended.

February 22nd: Right toes fully flexed.

February 22nd: Left toes extended.

February 22nd: Left toes equally flexed.

February 24th: The plantar eschar was again debrided revealing viable tissue both medially and laterally while the mid-arch was necrotic. He received foot soaks with Sea Soaks containing gentamicin and ceftazidime, topical oxygen and his booting. As the distal left foot was still unstable and the final demarcation line uncertain, non-weight-bearing, topical oxygen and booting still thought to be desirable.

February 25th: The improving status of the left foot was increasing the likelihood that the proximal half (or more) of the left foot could be salvaged. Topical oxygen was continued along with his other therapies to conserve as much skin as possible. The more skin preserved, in general the shorter is the long term healing time. The cardiologist noted continued "mild" hypertension and recommended more hydralazine (100 mg twice daily).

February 26th: Saturday: Loose black skin was debrided from the area over his left lateral 5th metatarsal and normal skin was found underneath. He received his usual soaks, oxygen therapy and booting. His TSH was noted to be normal at 1.8; the Cytomel was discontinued and the Levothroid continued. Normally, the patient was told that we amputate toes with the appearance of his left toes... but that we usually do not amputate toes that continue to wiggle.

February 27th: Sunday: Noninvasive vascular testing was performed to assess the healing potential of the left foot. He spent two hours booting before the tests and six hours after the tests. The boot doctor suggested the blood pressure medicines be changed to include an ACE inhibitor, Procardia in place of Carfdizem, and possibly some Minoxidil.

February 27th: The ankle brachial index was obtained with a bidirectional Doppler. The brachial pressures were undesirably high and taken only in the right arm because of his hemodialysis shunt in his left arm. Both ankle presssures were also high. It was uncertain how much the blood pressure readings were elevated by vessel calcifications.

February 27th: The pulse volume curves were close to equal in both feet even though the mid-foot cuff enclosed some of the black eschar in the left arch. Overall, there was good flow down to the mid-foot areas in both feet. It was noted that the "J" channel, which is the lowest amplification available on the recording device, was used at all levels of the leg and foot.

February 27th: The Doppler detected all of the tibial vessels at the ankle. High pitched sounds ("streaming") was heard at points in all of the vessels suggesting stenotic areas. The right dorsalis pedis could be traced out to the various digital arteries.

February 27th: Right toes fully extended.

February 27th: Right toes fully flexed.

February 27th: Left toes extended.

February 27th: Left toes equally flexed.

February 27th: The dark left distal foot remained cold. The proximal areas were warm.

March 2nd, 2000: The patient is walking into the Boot Clinic for treatment.

Comments: The right foot was salvaged intact. He has some numbness in the right foot but admits to have experienced some numbness previously. The left foot was only partially restored. The arteriogram showed the blood flow in the left lower leg was worse than that in the right leg. There is, of course, only a certain duration of time that a leg can survive severe ischemia. We were not quick enough to restore the left leg and may possibly have been too late when we began aggressive boot therapy. The cause for his ischemic episode was not clear. Calciphylaxis has been described in patients with Crohn's disease and chronic renal failure (Barri YM, Graves GS, Knochel JP: Calciphylaxis in a patient with Crohn's disease in the absence of end-stage renal disease. Am J Kidney Dis 29:773-6, 1997. Oh DH, Eulau D, Tokugawa DA, McGuire JS, Kohler S: Five cases of calciphylaxis and a review of the literature. J Am Acad Dermatol 40(6 Pt 1):979-87, 1999). The Doppler studies at the end of his hospital stay did suggest distal arteriosclerotic and calcific arterial disease. His total serum calcium level was well maintained in spite of hypoproteinemia. His serum phosphorus levels were intermittently elevated. He may be expected to have had secondary hyperparathyroidism. Patients requiring dialysis commonly have widespread arteriosclerotic vascular disease especially if they have diabetes and/or hypertension. Such patients are less likely to benefit from bypass surgery and more likely to come to leg amputation. Increases in blood homocysteine levels (Manns BJ, Burgess ED, Hyndman ME, Parsons HG, Schaefer JP, Scott-Douglas NW: Hyperhomocyst(e)inemia and the prevalence of atherosclerotic vascular disease in patients with end-stage renal disease. Am J Kidney Dis 34:669-77, 1999) and usage of erythropoietin (Wakeen M, Zimmerman SW: Association between human recombinant EPO and peripheral vascular disease in diabetic patients receiving peritoneal dialysis. Am J Kidney Dis 32:488-93,1998.) have also been associated with vascular events in dialysis patients. Our patient has at least latent diabetes, clearcut hypertension and usage of erythropoietin. His homocysteine level was normal. He may have had calciphylaxis (whatever this syndrome is). The most common problem we have seen in our vascular patients going to dialysis is hypovolemia and hypotension requiring elevation of the legs for a few hours; during such elevation, blood flow to arteriosclerotic legs may be totally obliterated. In short, our patient was at risk for developing occlusive disease in the legs and did develop it. The problem was not immediately recognized and he belatedly came to boot therapy. His gastrointestinal bleeding prevented therapeutic anticoagulation. Besides his natural healing processes, the only therapeutic measures for his legs were his pamidronate infusions, the topical oxygen therapy, the foot soaks and his boot therapy. Pamidronate has found use in treating osteopenia, hyperparathyroidism and, more recently, Charcot feet (Guis S, Pellissier JF, Arniaud D, Turck F, Witjas T, Roux H, Mattei JP Healing of Charcot's joint by pamidronate infusion. J Rheumatol 26:1843-5, 1999.) Topical oxygen alone has no proven role in the treatment of ischemic leg disease. Some authors find topical hyperbaric oxygen a helpful adjunctive therapy (Landau Z: Topical hyperbaric oxygen and low energy laser for the treatment of diabetic foot ulcers. Arch Orthop Trauma Surg 117:156-8, 1998; and Heng MC: Topical hyperbaric therapy for problem skin wounds. J Dermatol Surg Oncol 19:784-93, 1993.). On the other hand, some have found topical hyperbaric oxygen to even possibly slow healing (Leslie CA, Sapico FL, Ginunas VJ, Adkins RH: Randomized controlled trial of topical hyperbaric oxygen for treatment of diabetic foot ulcers. Diabetes Care 11:111-5, 1998.) In the case of our patient, we sought to maintain the skin envelope until booting restored blood flow sufficient to support the foot. As far as the effect of our boot therapy on his revasularization, the demonstration of normal pulse volume tests in both mid-feet and the healing he did accomplish is proof enough. To accomplish these things, however, he required long hours of therapy, bedrest and close observation. When his feet were solid enough, he was allowed to ambulate and was discharged. He will now require debridements, possible maggot therapy and additional booting to heal his left foot. We are grateful to the Bryn Mawr Hospital which allowed this man to continue his therapies while the physicians from Blue Cross, who were reviewing his status, urged that he be discharged from the hospital. Discharge at the time they requested would likely have resulted in amputations of both legs and possible loss of life. Their Senior Medical Director as 3/09/2000 has denied the days between 2/05-2/27/2000. What do you think about that?