Linda A. Westra, R.N., B.S.N.

        Supervisor

Medical Policy Department

Highmark, Inc.

P.O. Box 890169

                                                                        August 25, 2002

Dear Ms. Westra:

            Thank you for bringing to our attention your proposed Bulletin for end-diastolic pumping. May I make the following observations and comments as to how the Bulletin may affect our ability to best serve the public and contain health costs?

LMRP Description: …(Historically immediate) "Therapeutic effects from the treatment regimen" (was) "is thought to decrease venous pressure, interstitial fluid pressure, vasoconstriction, and viscosity, and increase cardiac output, pulse pressure, and fibrinolysis in the treated extremity…" Additional immediate effects include the generation of nitric oxide, prostacyclin  and vascular endothelial growth factor by the endothelium. Beneficial effects appreciated after multiple treatments include improvement in most non-invasive vascular tests and healing of ischemic lesions. Mechanisms for the latter involve neovascularization, dilatation of patent vasculature, and rechannelization of obstructed arteries….

Indications and Limitations of Coverage and/or Medical Necessity: First, it has always been a general guideline in medicine that initial therapy should entail the least risk and cost. There is, of course, no comparison in either risk or cost between hospital revascularization procedures and outpatient booting. Need for inpatient booting has usually resulted from deterioration of the leg while other therapies and/or surgeries were attempted. Again, for a successful bypass to be accomplished, there needs to be a healthy segment of proximal vessel to initiate the bypass, a healthy segment of artery to receive the bypass, some runoff from the distal site and a suitable vein (for distal bypasses) for the procedure. The healthier each of these variables is, the more likely is the success of a bypass and the less need for one. The more diseased each variable is, the likelihood for a successful bypass is lessened and the need for some form of therapy is increased. Common sense would suggest that most arterial problems in the leg might first be treated with boot therapy to obviate need for hospitalization and more risky procedures and to improve the condition of the leg should such procedures be required. In those legs not showing a response to therapy over the course to a few days (patients in severe straights) to a few weeks, appropriate studies might then be done to evaluate the potential success of invasive procedures. Finally, should studies show that invasive procedures are not likely to succeed, boot therapy might then be undertaken for longer periods of time. The current proposed policy, "Arterial ulcers of the lower extremity may be covered in limited situations where the ulcer(s) are not clinically amenable to revascularization and/or skin grafting or surgical intervention is contraindicated," makes booting a therapy of last resort, promotes hospitalization and expensive procedures and provides potential malpractice protection for a surgeon attempting ill-advised surgery in lieu of boot therapy. The vascular laboratory and/or appropriate clinical observations might provide more helpful guides for therapy. Low transcutaneous PO2 levels, an absence of Doppler sounds below the ankle and low-to-flat pulse volume curves, for example, signify that healing is unlikely. An absence of palpable pulses, pallor on elevation, an absence of capillary refilling, cyanosis, coldness and areas of focal necrosis/gangrene are worrisome physical findings. Complaints of pain and numbness call for immediate attention. In such patients, the "conventional" therapies described as desirable prior to instituting booting are not indicated and may allow deterioration of the foot, thus prolonging the illness and increasing the risk for loss of limb. Moist dressings may macerate ischemic tissue. Compression bandages impede arterial inflow. Exercise may be impossible. Blood does not run uphill in the absence of appropriate arterial pressure; ischemic tissue is blanched by elevation.

            An x-ray showing osteomyelitis has been a common indication for hospitalization, intravenous antibiotics, the placement of various intravenous devices for home antibiotic therapies, visiting nurses and, when failure is shown, foot resections or amputations. The foot resections in turn result in foot deformities that promote new ulcers.  Standard therapies have a dismal record here.  It is to be appreciated that bacteria do not eat calcium or dissolve bone. Bone dissolution results from attempts of bone repair and remodeling. One does not remove a fractured toe when the x-ray shows the remodeling common to healing. We have had great success in healing osteomyelitis when other measures have failed with the combination of local antibiotics and boot therapy (Dillon: Successful treatment of osteomyelitis and soft tissue infections in ischemic diabetic legs by local antibiotic injections and the end-diastolic pneumatic compression boot. Ann Surg 204(6): 643-9, 1986). We have not seen complications to justify proscribing boot therapy because of osteomyelitis. Is there a situation where osteomyelitis might be worrisome? Perhaps it is worrisome in the case of a resistant organism. Why only perhaps? Because the local injection of antibiotics produces a concentration of antibiotic far higher than that attained by high dose intravenous antibiotics allowing the bacteria to be killed when it is not otherwise possible.  And because you know the antibiotic reached the infected area when you put it there. It is true that many physicians are inexperienced in treating osteomyelitis by the described techniques, but is their inexperience reason to list osteomyelitis as a contraindication for therapy. Hopefully, the many instances of successful treatment shown on our website will add to their experience. Perhaps, the clinician should be allowed to exercise clinical judgment.

            Koch (Koch CA: External leg compression in the treatment of vascular disease. Angiology 48, Supplement, S3-S15, 1997) and I (Dillon RS: Treatment of resistant venous stasis ulcers and dermatitis with the end-diastolic pneumatic compression boot. Angiology 37-47-55, 1986) have reviewed boot devices over 190 years. I was especially interested in the Landis suction-pressure boot (1933) when I discovered Dr Landis had used it on the wards of my father at the Philadelphia General Hospital. Dr. Landis was widely lauded for his boot and recruited by Harvard where he was made Chief of Physiology. I searched out Dr. Landis in the later 1970's and found him retired in the Poconos. I asked him what happened to his boot. He replied that it did work but the benefits were just too long in coming. A more rapid boot was needed. I summarize the work in the 1950-78 period with the first abstract in the pneumatic boot section of our website library (…."Allwood (Clin Sc 16:231, 1957) pumped on the lower calf and documented an increase in blood flow in the foot with a plethysmographic method. Loan ( J Appl Physiol 14(3): 411-413, 1959) rhythmically inflated a cuff around the ankle in the seated position and noted an increase in blood flow in the foot by three methods: venous occlusion plethysmography, heat flow and calorimetry. Henry and Winsor (Am Heart J 70:79-88, 1965) pumped from the head of the fibula to the malleoli and documented increased flow in the foot by measuring falloff in counts from injected  I131. Gaskell and Parrott (Surg Gyn & Obstet 146:583-592, 1978) pumped on the foot and ankle and documented an increased clearance of 133 Xe from the dorsum of the foot."…). It is to be noted that none of this work resulted in a method of treatment that found its way into clinical practice and healing legs. In recent years, there has been a host of articles promoted by the manufacturers of the impulse pumps. Comments on these articles may likewise be found in the pneumatic boot section of our website. These articles are interesting in that they confirm with the vascular tests now in vogue that pumping does indeed improve the leg circulation. The reader is encouraged to review the severity of the lesions described in these articles and to note the experience of Vella et al at the Mayo Clinic who dealt with patients with low transcutaneous PO2 levels thought to indicate likely failure to heal with conservative care. They treated their patients with the Circulator Boot and in those with incomplete healing at discharge prescribed impulse pumps in half and found no benefit. The manufacturers of the ArtAssist list their supporting literature on their website. The articles describe the acute and long term effects of their device on vascular tests. As with the boot of Landis, obtaining long term benefits requires dedication: three treatments daily for perhaps three months. Few of the reports involve wound healing: 1) Nancy Shebel RN et al (one case report); 2) George Louridas et al (25 legs in 33 patients… 12 % died and 42% lost their legs); and 3) Paul S.Bemmelen et al (14 patients … 9 limbs salvaged and 4 amputations).  It would appear premature to recommend an impulse pump in place of the Circulator Boot Systems in the patients generally referred for Circulator Boot therapy. It is to be appreciated that the Circulator Boot differs in many significant ways from previous maneuvers, beds, boots and devices.

            The suction-pressure devices required a tight seal around the leg that itself potentially blocked blood flow into the leg and they were not cardiosynchronous. Buerger described his exercises (elevate the leg for a time interval sufficient to empty the veins and then lower it until it became ruborous and repeat the cycle as long as one's energy lasts).  The rocking bed allowed the same benefit: high reverse Trendelenburg for two minutes and Trendelenburg for 30 seconds. Both of the latter used gravity to alternately empty the veins and promote arterial inflow. The various venous pumps and impulse devices use gravity to promote arterial inflow and leg compression to force venous outflow. They are not cardiosynchronous and impede arterial inflow to some degree while they are inflated. Ischemia is thought to be a strong stimulus for angiogenic growth factors (VEGF). Why then does not the endogenous production of VEGF or the injection of such factors result in new vessels? Such studies to date have been disappointing. It appears that some pulsatile flow in likely necessary for the endothelium to respond. The Circulator Boot provides pulsatile flow. Each pulse wave is allowed to enter the leg as best it can and then the leg is squeezed disseminating the blood throughout the tissue (as one disseminates water through a half-wetted sponge when one squeezes it), while at the same time some returning the venous blood. The Circulator Boot provides considerably more energy than previous devices or the impulse devices.

            Proper use of the Circulator Boot requires knowledge of the particular pathological anatomy of the individual patient. The "Circulator Boot" is not an individual boot but a system of devices and monitors. The physician may prescribe treatment from groin to ankle, from knee to toes, from ankle to toes… on any segment of the leg that requires help. Each patient differs to some degree and treatment may be adjusted as necessary. It is to be appreciated that both neuropathy and ischemia promote breaks and fissures in the skin that allow the entrance of bacteria. The latter in turn release enzymes and toxins that digest the tissue (wet gangrene) and decrease local blood flow because of swelling, infective arteritis and local thrombi. The decrease in local blood flow may allow progression of the lesion in spite of appropriate intravenous or oral antibiotics. Circulator Boot treatment may be adapted to the patient needs. The patients may be pumped after local antibiotic injections, with medicated dressings in place or their feet immersed in antibiotic solutions. An individual treatment, hence, may benefit the patient by its cardioassist action, by improving the circulation in the leg, by reducing swelling, by debriding the lesions in the soak solutions, by bringing systemic antibiotics to the lesions and by disseminating locally injected antibiotics. The combination of these benefits helps us heal lesions commonly thought to be very difficult or impossible to heal.

Treatment of Claudication Pain and Chronic Lymphedema of the Lower Extremities: To be limited to six treatments? There is a spectrum between mild claudication and rest pain. The risk of limb loss in the former is minor while it is significant in the latter. Likewise, leg pain precipitated by walking a few hundred yards does not alter life style to a great degree while rest pain may make even a few steps difficult and limit a patient to a wheel chair. We have had inoperable patients arrive wheelchair-bound and leave us able to walk a few miles. One such lady still complained as after the two miles her leg still experienced some soreness. She required many more than six treatments, more like 60. On the other hand, we have had people with acute occlusions respond to as little as the six treatments. The number of treatments required to allow an independent life style depends on the underlying pathology. The diabetic with the acute occlusion had a normal walking capacity prior to his airplane trip; he likely had an acute thrombosis that we were able to lyse. Patients with diffuse occlusive arteriosclerosis lesions require more work. What is one to do with the patient with moderate claudication which impedes his life style and /or his ability to work? An exercise program may be tried. Whyman et al found discrete lesions suitable for angioplasty in but 10% of their 600 claudicants and little benefit for the procedure over time compared to exercise (J Vas Surg26:551-7, 1997 and European J  of Vascular & Endives Surgery12(2): 167-72, 1996).  There are several studies abstracted in the claudication section of our website showing that bypass is more effective than exercise therapy, but there is the cost of hospitalization, the loss of leg veins for future heart bypass or from past heart bypass and the questionable detrimental effect of bypass over time (see Morris et al: Surgery and the progression of the occlusive process in patients with peripheral vascular disease. Radiology 124:343-8, 1977). In my study of 2177 patient episodes, I found vascular surgery and an aggressive vascular surgeon to be significant risk factors. This observation does not stand alone. There are actually few prospective bypass studies; most report percentages of patent grafts over time with the inference that the bypass led to leg salvage. Reports suggesting that prospective vascular surgical studies might be helpful in proving benefit of invasive procedures include those of Eickhoff HJ et al (The effect of arterial reconstruction on lower limb amputation rate. Acta Chir Scand 502: 181-187, 1980), Humpfrey LL et al (The epidemiology of lower extremity amputation in diabetes; a population based study in Rochester, Minnesota. Diabetes 38; suppl 2:33A, 1989), Tunis ER et al (The use of angioplasty, bypass surgery and amputation in the management of peripheral vascular disease. N Engl J Med 325: 556-62, 1991), Sayers RD et al (Changing trends in the management of lower limb ischemia: a 17 year review. Br J Surg 80:1269-1273, 1993) and Connelly J et al (Variation in clinical decision making is a partial explanation for geographical variation in lower extremity amputation rates. Br J Surg 88(4): 529-35, 2001). It is appreciated that Medicare should attempt to curtail unnecessary booting, but is it desirable to promote more risky and expensive procedures with doubtful benefit for some patients. The boot patient must go to clinic for treatment; it is an uncommon patient who will keep going without benefit. It would appear desirable that (a) appropriate non-invasive tests be initially done to document the vascular nature of the patient's complaints; (b) the life limitations due to the vascular impairment be documented; (c) alternate therapies and risks be explained to the patient perhaps after the six allowed treatments; and (d) the patient have some choice in subsequent therapies. It would be a shame if some patients were house-bound for lack of any therapy.

            Lymphedema may be a life-long problem with a genetic basis or a condition acquired after trauma, surgery, chemotherapy, soft tissue hemorrhage etc. If edema in the leg is persistent, fibrocytes may invade the fluid space making the swollen leg firm and very difficult to reduce in size with any treatment. In studying the patient with acquired lymphedema, it is desirable to determine the level and cause of the lymphatic obstruction. Many do not appreciate that the lymphatics comprise a third circulation in the leg. Their clear fluid contents make them invisible to the eye, but they have valves like the veins which they commonly accompany. When a whole leg is swollen, for example, the lymphatic obstruction is commonly in the pelvis. Pumping on the foot in such patients is unlikely to alter the course of the disease. The inflation of a Circulator Boot bag, however, enclosing the whole leg up to the groin, sends a fluid wave like a water-hammer at the obstruction potentially dilating it. Such therapy is most effective early before scarring due iron deposits (the trauma or hemorrhage patient) occurs and may be curative. Patients have preferred Circulator Boot therapy, which leaves their legs soft and pliable, to other lymphedema boots, which deliver one compression every few minutes and leaves the leg relatively firm and stiff. Again, patients will not return to the clinic if they do not see progress. If progress seems unlikely, we have prescribed other lymphedema for home use along with support stockings. Hence, as opposed to the Medicare policy, in cases of acquired lymphedema we recommend early treatment continuing as long as progress is seen and/or a potential cure is in the offing.

Other Comments: These would seem to exclude the usage of the Circulator Boots by podiatrists.  This prohibition appears to be because of concern that the boots may promote dangerous diuresis. First, it should be noted that the Miniboot systems do not have a significant cardiac-assist action and the Miniboot (treating the area from the knee to the toes) is more commonly used in the treatment of diabetic foot ulcers than the Long Boots. Second, as the podiatrists are the foot professionals, it would appear undesirable to exclude them from the foot care team. Again, who should replace the podiatrists? Most cardiologists and internists are woefully ignorant in peripheral vascular medicine. Indeed, even specialists in peripheral vascular medicine and vascular surgery are not well versed in the differences among pneumatic boots. It would be a rare patient with a heart problem sufficiently severe to be benefited by boot therapy to a degree causing a dangerous diuresis without there being an internist or a cardiologist involved in the care of the patient. It would be reasonable in such patients to require the podiatrist to consult the appropriate medical specialist. Simply asking the patients to weigh themselves daily would identify such patients at risk.

            I hope that these explanations and comments will help you arrive at appropriate guidelines for boot therapy. I would be glad to discuss any item you may desire with you or other parties.

                                                                        Sincerely yours,

                                                                        Richard S. Dillon, M.D.

  President