Case 183: Circulator Boot Used with Thrombolytic Therapy to Salvage Leg with Acute Thrombosis of Femoral-Popliteal Graft and Distal Vessels, Used to Support Blood Flow to Heart, Head and Kidneys and Used to Avoid Fasciotomies Associated with Compartment Syndrome

Previous History: This 68 year old lady was previously treated with the Circulator Boot for postoperative ischemia possibly due to cholesterol emboli and peripheral arteriosclerosis obliterans. This episode and her previous medical and surgical history were described in Case #122 (She is the only patient listed twice in these reports). She returned to the care of her primary physician and did well until the end of March 1998 when she had gastroscopy, colonoscopy and an abdominal CAT scan at a nearby hospital for intestinal bleeding from an undetermined source. She received 8 units of blood and plasma. Her coumadin was discontinued. In April she fell back on her buttocks and incurred a compression fracture at T12. She spent two weeks in a convalescent facility when her toes began to hurt. She came to the outpatient boot facility on June 23rd when a bony remnant was removed from the end of her left fifth toe releasing perhaps a ml of pus; a heavy growth of coagulase-negative Staphylococcus was cultured. Twenty milligrams of gentamicin was injected into the abscess cavity and the toe was massaged a few minutes. Augmentin was prescribed. On the 24th of June the toe was noted to be improved and the swelling reduced. She also allowed that her right leg had been cold and had had decreased sensation since March. She was advised that vascular testing was indicated ... but, of course was uncovered at our site by her HMO. She visited her vascular surgeon who found Doppler studies at the right ankle to be adequate and offered her no particular therapy.

Comments: It was clear she had a occluded leg. The cause of the occlusion was not clear. Her ischemic symptoms since March supported the diagnosis of chronic ischemia with a sudden propagation of thrombus. The possibility of embolus from her aorta or heart were also to be considered. Cases 135 and 137 are examples of effective booting after acute occlusions. For booting to be effective there has to be some inflow down or connected to the occluded system. One does not squeeze an empty sponge and expect to clean it; one squeezes out at least a partially wet sponge. Here the "leg sponge" proved to be empty. Still the boot can be applied and removed quickly as the clinical situation of the patient dictates. The improvement in facial color and strength was an important observation suggesting if needed the Long-Boot might be used later in her case to support her cardiovascular system. In the discussion of her options with the patient and her husband, the material in the article of Ouriel et al and the editorial of Porter were quoted. See our library (Angioplasty, Bypass and Invasive Procedures). One wonders if her HMO had allowed vascular testing and booting in June if her occlusion might have been avoided.

Sunday night admission.Emergency room laboratory data included Hgb 11.8 G/dl, BUN 36 mg/dl, creatinine 1.7 mg/dl, albumen 3.9 G/dl and proteinuria 2+. The vascular surgeon examined the patient at 8PM and agreed an immediate arteriogram and Urokinase therapy was indicated. The roentgenologist shortly thereafter performed the arteriogram (below). At 11:30 PM he summarized his findings: Using a left femoral approach, he found thrombus in the femoral-popliteal bypass graft and popliteal. He was able to demonstrate no runoff in the calf. He placed a 65 cm 5 French infusion catheter in the graft and started Urokinse (2000 units/ml) at 120 ml per hour. He wrote for the infusion to be slowed to 60 ml per hour at 12:30 AM and transferred her to our Intensive Care Unit. In view of her dependence on prednisone for her rheumatoid arthritis, the endocrinologist wrote for supporting steroids (which were tapered over the next few days) and began insulin to control her obvious hyperglycemia. Her blood pressures through the evening varied 154 to 196 mm Hg.

At 22:14 on July 26th, her arteriogram showed some flow in the deep femoral but no flow in the superficial femoral, her graft, the popliteal or distal vessels The red arrow is placed at the origin of the occluded superficial femoral at the level of her greater trochanter The large branch in the deep femoral is at the level of her pubic ramus.

Day #2(7/27):Overnight intake and urine output 904 ml vs 1547ml. Laboratory values for 7/27: Hgb's 11.1-11.3 G/dl, BUN 28-29 mg/dl, creatinine 1.4-1.6 mg/dl. At 6:30 AM the surgeons found Doppler flow down the graft but no distal flow. The foot remained cold, paralyzed and "threatened". At 10 AM the roentgenologist reported his films showed now 90% lysis of the graft but no flow below the knee. He noted, "The right foot has no motor or sensory function. I'm concerned about re-perfusion phenomena (hyperkalemia, acidosis and myoglobinuria) if we proceed." He commented that leg amputation might be the safest immediate course for her and a likely eventual requirement anyhow.

At 09:06 on July 27th, the urokinase catheter had been advanced to the popliteal but little contrast media found its way down the vessel and no runoff was visible below the knee.

Day#2 continued. The patient returned to ICU and a Circulator Long-Boot was applied to the right leg to help disseminate the Urokinase and hopefully to help restore blood flow throughout the leg. The patient returned to X-ray at 3:30PM. The roentgenologist reported, "Graft is 95% lysed + there is tibial runoff to the foot! But the foot looks no better to me clinically. No evidence of acidosis or " increased "K+ as of 11AM labs." The boot service placed a oxygen catheter around her foot, placed a plastic bag over the foot to trap the oxygen and reinserted her leg in the Long Boot to run all night.

At 15:16 on July 27th, her popliteal and tibial vessels were demonstrated to be patent. The arrow points to a stenotic area at the origin of the posterior tibial.

While the peroneal faded in the distal leg, the anterior tibial and posterior tibial were patent to the ankle.

The anterior tibial ended in a few collaterals above the ankle and the posterior ended in a few collaterals behind the internal malleolus.

The The vessels at the ankle are better seen here on the subtraction films.

Comments: It is thought that a compartment pressure of 30mm Hg over 8 hours will produce a compartment syndrome. One can measure the pressure with a manometer to help in the fasciotomy decision. But a fasciotomy does not prevent rhabdomyolysis and renal failure (see preceding case). Further the incisions may be painful and make booting more difficult. The Long-Boot generally pumps with a pressure of 55-60 mm Hg, sufficient to soften the leg and hopefully to prevent the compartment syndrome. In the many ischemic legs we have pumped, we have never seen a compartment syndrome problem. For more on the fasciotomy and its advocates see Lang EK in our library on Clotting Factors. The Kendall boot is less bulky than the Circulator Boot but is not cardiosynchronous and not designed for arterial insufficiency or cardiac support. It was used here as part of our anti-swelling program. All of her physicians had great concern for her kidneys also. Her initial proteinuria, modest azotemia, her intravenous contrast dye load, her periodic hypotension, the myoglobinuria, her transfusions, her bleeding and her compromised heart function were all major risk factors for renal failure. As seen elsewhere in these case reports, Long-Boot therapy is helpful in supporting the kidney.

Day #3, continued. Her systolic blood pressures varied from 96-135 mm Hg through the day. She had been hypotensive in X-ray and returned with some chest heaviness. The intensive care specialist noted a "resolving hematoma in the left groin" and deep T-wave inversions in her anterior-lateral chest EKG leads; he ordered supplemental oxygen, topical nitrates and reduction of her Beta blocker dosage. The boot service returned and restarted her Long-Boots. She quickly forgot her chest discomfort. A central line was placed to allow infusions of protein and lipids. See Corti et al in our Epidemiology library for significance of the albumen level).

The admission EKG was read as showing left ventricular hypertrophy with a repolarization abnormality and a possible septal infarct. The chest leads are shown here.

The marked T-wave inversions found by the intensive care specialist are seen here.

In the CAT scan of the pelvis, the mass cradled above the white "figure-eight" on the right is the pelvic hematoma.

The white in the upper left is her gallbladder while the speckled organs to the right and left of the vertebral column are her kidneys.

Day #4 (7/29) continued. Her intake and urinary output for day #3 were noted to have been 3064 vs 1044ml. The laboratory data for the day included Hgb's 10.2-10.7, BUN 36, creatinine 2.3, CPK 11144-14816, CKMB 133.2-146.9, CKMB index 1.0-1.2% (N<2.0%). The high values for the CPK's were thought to represent leg muscle breakdown. Intravenous heparin was started . She was started on a full liquid diet. Bronchodilators (Abuterol 2.5 and Atrovent 0.5) were ordered every 4 hrs. Circulator Long-Boot therapy was administered at 10AM and 3PM. The radiologist and the intensive care specialist again questioned the desirability of a fasciotomy.

At 02:54AM, the R-wave was gone in V3 and the voltage was diminished in the limb leads and V3-V6.

At 09.55 AM, the voltage was restored and the tracing appeared much like that on admission. Part of her hospital identification stamp is seen in the upper right.

Day #5 continued. Serial cardiac enzymes were drawn. She was comfortable in the supine position in the morning. Her fluid intake for the previous 24 hours was then noted to be 3123 ml and her urine output 2805 ml. Her medications now included renal dose Dopamine, intravenous nitroglycerin, heparin and Lopressor. Tilting her bed, however, resulted in syncope and a systolic BP of 60mm Hg. Laboratory studies for the day included Hgb's 9.7-11.6 G/dl, BUN 26-31 mg/dl, creatinine 2.0-2.1 mg/dl, albumen 1.9 G/dl, serial CPK's 6579-9750, CKMB's 36-49[N 0-4.9], Troponin I 0.3-0.5 [N 0.1-0.6]. Two units of packed cells were administered and intravenous fluids continued (5%G/ 0.5 PSS and an amp of bicarbonate at 80 ml/hr) A consultation with a cardiologist was requested. The latter read her ECHOcardiogram and noted her history of 60-pack years of smoking. He reported that the ECHO showed anteroseptal and apical wall hypokinesis with an estimated ejection fraction of 40-45% and the possibility of an apical mural thrombus.

The upper tracing is the EKG and the lower tracing the dZ/dT waveform of the Renaissance IQ electrical impedance apparatus. Her baseline cardiac output was 5.50L/minute and stroke volume 82.1 ml.

These tracings were made during 1:1 booting of both legs. The dZ/dT waveform is obviously larger. Her cardiac output had risen to 7.12 L/minute and her stroke volume had increased to 111.3 ml.

Here both legs were booted on alternate beats. On the bottom line, 3 dZ/dT complexes are seen: the first and 3rd occurred after beats in which the leg had been released immediately before the QRS complex. The middle beat was unassisted but is seen to be slightly larger than the baseline.

Day #14(8/9) Her hemoglobin again dropped suggesting continued blood loss (Hgb 10.7). Her BUN (48mg/dL) and creatinine (2.1mg/dl) remained stable while her low albumen (2.6G/dl) pointed to her need for nutritional support. Again, her systolic blood pressures remained variable 118-136 suggesting continued need to observe her for bleeding. Instruction in insulin administration and self determination of blood sugars (AccuCheks) was begun. Her right leg was still swollen (29.7 cm vs left 24.6 cm circumference) suggesting a persistence of some increased compartment pressures in her calf; her boot therapies were continued.

Comments: She was unable to get the prothrombin time on 8/17. Her HMO required that she go to one of their approved sites. The test was accomplished 8/18 and reported to be greatly prolonged at 80 seconds. Such excessive "thinning of her blood" put her at risk of new hemorrhage and might have been avoided by keeping her in the hospital (or obtaining prothrombin times over the weekend) until her dosage was stable. Again the problem would have been identified a day earlier if her HMO did not have restrictions as to where she could obtain the prothrombin time. This case history is presented on a day by day basis as her HMO would like to deny a significant number of her hospital days. The reader might attempt to determine when a proper discharge should have been made. Again, this HMO, unlike Medicare and US Healthcare, makes every effort to refuse coverage for boot therapy. In this lady's case, boot therapy seemed to restore her vitality prior to admission, helped with Urokinase to open her right leg, provided a therapy to avoid fasciotomies, supported her heart and head during episodes of angina and faintness, opened and maintained the left leg, supported her kidneys helping to avoid potential dialysis, prevented swelling of the left leg and potential chronic lymphedema and has opened her feet which are well on the way to healing. Her thrombolytic therapy was complicated by bleeding at her catheter site. In other patients with thrombosed native arteries, we have given the Urokinase in a peripheral vein and begun boot therapy immediately restoring blood flow to the leg with no complications.