A Tri-Corder for your Smart Phone? (27 Jan, 2012)

This device could prove to be the ultimate theragnostic tool of the future.

New device will detect infections, cancer in minutes

Posted: Jan 26, 2012 11:00 AM ET 

Last Updated: Jan 26, 2012 8:02 PM ET

This is the prototype of the new detection device developed by Dr. Shana Kelley at the University of Toronto. This is the prototype of the new detection device developed by Dr. Shana Kelley at the University of Toronto. (CBC)

Toronto's medical community is buzzing about an invention that could change the way health professionals screen for infectious disease and cancer.

"We've been working on this, really, for about a decade," said Dr. Shana Kelley, a scientist at the University of Toronto.

Kelley spoke as she held a small black device her hand, shaped like a smartphone but bulkier, with a microchip inside that Kelley says can determine in 15 minutes if you have cancer or an infectious disease.

The device works with a blood sample or swab placed on a microchip. It then reads — and recognizes — certain types of cells.

Kelley says eventually there will be a disposable cartridge that contains the sample.

Instead of days, or sometimes weeks, before patients get their results, with the new machine they're ready in minutes.

For those on health care's front-lines, the promise of an early diagnosis means more lives can be saved.

"Infectious disease is the medical condition where rapid turnaround is maybe most critical and our chip, coupled with portable instrumentation, are good at providing very fast answers," Kelley said.

It could also save the health care system millions. In the case of detecting prostate cancer it means no more lengthy, costly and uncomfortable biopsies.

"I think it's superb and very exciting," said Dr. Robert Nam, an uro-oncologist at Sunnybrook Hospital, who believes Kelley and her team's invention will transform the medical community in Canada and abroad.

"We can identify patients with most lethal cancer…and, secondly, how about avoiding a biopsy?" he said.

Canada and the United States have invested millions and there's a European company that's jumped on board with more cash for this invention, which they hope will be in use in a couple of years.

Expectations are high.

"It will allow physicians out in the field, and I'm thinking public health physicians, to be able to assess patients right then and there," said Dr. Frances Jamieson, a medical microbiologist with Public Health Ontario. She highlighted tuberculosis as one possible disease the new device could diagnose faster.



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Posted by: PV Mayer at 08:34 am 0 comments - Add a Comment Category: Theragnostics


TMI Team Sends Patients on Road Trip to Revascularization (13 Jan, 2012)

Joanna Frketich's brilliant Spec article about what needs to be done to save our patient's limbs.

    • Joanna Frketich 
    • Sat Jan 14 2012 

    Diabetes patients head to Toronto or lose a limb

    Dr. Perry Mayer treats patients with diabetic foot and wound issues in his Railway Street clinic. Many of his patients are on such a long wait list for surgery that they run the risk of loosing a limb. Mayer sends these patients to Toronto for surgery even though the surgery could be done here in Hamilton.
    Dr Perry Mayer Dr. Perry Mayer treats patients with diabetic foot and wound issues in his Railway Street clinic. Many of his patients are on such a long wait list for surgery that they run the risk of loosing a limb. Mayer sends these patients to Toronto for surgery even though the surgery could be done here in Hamilton.
    Cathie Coward/The Hamilton Spectator

    Diabetes patients in danger of losing limbs are being sent to Toronto for treatment because Hamilton’s waits are too long.

    The Mayer Institute, which specializes in diabetes wound care, sends patients needing urgent treatment, within 30 days, to vascular surgeons at Sunnybrook Health Sciences Centre instead of waiting for diagnostics and surgery at Hamilton Health Sciences or St. Joseph’s Healthcare.

    “In my world, I wait an inordinate amount of time,” said the institute’s medical director, Dr. Perry Mayer. “It’s a ridiculous situation in Hamilton. We have brilliant, gifted surgeons here, they’re second to none. But their hands are tied.”

    Hamilton’s lead vascular surgeon says the problem is that 90 per cent of patients referred to them are urgent, so it can be difficult to determine who gets the care first.

    “A lot of us feel overwhelmed with the sheer volume of disease,” said Dr. David Szalay, division head of vascular surgery at HHS, St. Joseph’s and McMaster University. “The challenge can be to try to work through your list and make sure nobody dies of a ruptured aneurysm waiting for you, nobody has a stroke waiting and you can intervene on the leg quick enough to prevent limb loss.”

    Szalay says the delays occur when patients are referred and waiting for their first appointment and again when surgeons order diagnostic tests. In contrast, Toronto has more vascular surgeons to share the load, so patients get their first appointment faster. The doctors at Sunnybrook also have access to their own angioplasty suite so they do the diagnostics themselves and immediately do the treatment.

    “Their model is ideal but pretty unique,” Szalay said of Sunnybrook.

    Angelo Maletta says he would have lost his foot if he’d waited any longer for treatment. The 61-year-old Welland maintenance worker was told in August his right foot would have to be amputated because of a diabetic wound.

    His cousin knew someone whose leg was saved by Mayer and recommended the clinic on Railway Street. Many of Mayer’s patients tell the same story of finding the institute by chance from friends or family after being told they’d need an amputation.

    “My cousin, who I hadn’t seen in months, happened to be at my house the day they told me they wanted to amputate,” said Maletta, who shudders to think what would have happened otherwise. “It would have been terrible for me.”

    Maletta saw Mayer at the end of August. Tests showed there was not enough blood flow in his foot, so he was referred to Sunnybrook in October and had surgery on Nov. 9.

    “Everything was just boom, boom, boom,” said Maletta, commenting on the speed of treatment.

    His foot is now healing well.

    Getting treatment fast is significant considering Wound Care Canada reports there is a “small window of opportunity” for therapies. More than 50 per cent of lower extremity amputations are due to non-healing foot ulcers and the long-term prognosis isn’t good for amputees. The death rate is 39 per cent to 68 per cent over a five-year period.

    There is hope that waits will ease a bit in Hamilton as another vascular surgeon is being recruited — the equivalent of three fewer surgeons are practising in this area compared to seven years ago. A second vascular ultrasound opened last week to double diagnostic capacity, and other health professionals such as physician assistants are being added to the vascular team.

    But until then, Mayer says he will continue to send patients to Toronto: “These people can’t wait. The patients who don’t get to me lose their limbs. They lose their limbs at an astonishing rate.”

    jfrketich@thespec.com

    905-526-3349 | @Jfrketich



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Posted by: PV Mayer at 09:34 pm 0 comments - Add a Comment Category: Limb Salvage Teams


Part 1 on Infection by Frykberg (3 Jan, 2012)

The Challenges of Diabetic Foot Infections:
Part 1 

I’ve had a particularly difficult (and frustrating) week caring for several patients with very severe diabetic foot infections. I’ve been at this for about 35 years now, but it doesn’t seem to be getting any easier. Perhaps the patients are just getting more complex and sicker or perhaps the pathogens are getting more virulent. Regardless, the infections just seem to be getting more difficult to control. While we have many more antimicrobial agents than we did years ago, antibiotics are only part of the solution to managing foot infections in the diabetic patient. We certainly need to have a very good understanding of the spectrum of coverage (and gaps in coverage) for a number of different agents. But the reality is, antibiotics alone can most often NOT be relied on to be the “magic bullet” for managing such complications. In fact, a good friend of mine who specializes in such matters is known to advocate that “draino” is the best (and perhaps the most important) agent for treating diabetic foot infections (DFI). Others can do a better job than I of discussing the multitude of antimicrobial therapies available for treating such infections (and perhaps it might be the subject of a future discussion). 
 Infections just seem to be getting more difficult to control
Hence, I will focus here on the non-pharmacologic principles of assessment and management that are critical to success in this regard. For the purposes of our discussion, we will concentrate primarily on limb threatening (moderate or severe) infections.

The Physical Exam

A systematic and thorough evaluation is absolutely essential to detect associated abnormalities that either directly lead to the infection or contribute to its severity. Medical history and evaluation is obviously important for antecedent injuries, comorbidities such as kidney disease, peripheral arterial disease, heart disease, diabetes control and medications, allergies, etc.

A diabetic foot ulcer (DFU) is rarely caused by an infection but is perhaps the most frequent causal factor leading to diabetic foot infections. Sometimes it is just a blister or a burn (especially in the Summer heat of Arizona) or a puncture wound that breaks the skin envelope and opens the portal to infection. In the most severe presentations (necrotizing soft tissue infections) signs will include secondary blisters, bullae, or necrosis proximal to open wounds or gangrenous toes.

Figure1.jpg

Fig. 1. Necrotizing soft tissue infection- no gas on x-rays but note the severe cellulitis, edema, and necrotic dorsal skin. The portal of entry was in the webspace at the base of the second toe.

Palpation of the foot might not only express purulence, but subcutaneous crepitance might be palpable as well. Ulcers of long duration or with bone exposure are at high risk for developing infections. Therefore, it is important to carefully examine such lesions - or to look for them when they might be between the toes. A sterile probe or even applicator stick can be used to examine the depths of any wounds to ascertain bone involvement or exposure or whether sinus tracts extend proximally along fascial planes or tendon sheaths. While this “probe-to-bone” test has been maligned as a good indicator for osteomyelitis, in hospitalized patients with severe infections, it actually has quite good predictive value for osteomyelitis. It is therefore a routine and essential part of my examination.

A diabetic foot ulcer (DFU) is rarely caused by an infection

While many, if not most, of hospitalized patients with DFIs have at least some degree of peripheral neuropathy and sensory loss, you must always look for underlying ischemia. I am quite impressed with the frequency of undetected peripheral arterial disease (PAD) that we first diagnose upon presentation with a rather severe DFI.  Perhaps the frequency of neuroischemic wounds has risen over the years; certainly the number of foot infections in such patients has in my clinical practice. Hence, palpation of pulses (at least from the Popliteal to pedal arteries) is a key part of the examination as well. Too often, however, the foot is so swollen that pulses- even when present- are difficult to palpate. This is why I carry a Doppler ultrasound unit in my pocket. I will routinely ascertain the presence and quality of Doppler signals in the pedal vessels. While rarely finding triphasic signals in the affected feet, we will often find biphasic or monophasic signals in the dorsalis pedis and posterior tibial arteries. Monophasic signals portend peripheral arterial disease, although when intermetatarsal artery signals are present, there is less concern for critical ischemia.  Nonetheless, we very liberally order Doppler Segmental Limb Pressures and ankle-brachial indices (ABI) or toe pressures for qualitative and quantitative evidence of peripheral perfusion. Pulse volume recordings (PVR) are also quite useful in this regard, especially in the presence of calcified arteries in this patient population. Vascular surgical consultation to assess the need for angiography and revascularization is necessary when significant abnormalities are found.

Imaging

 Palpation of pulses is a key part of the initial examination as well

X-rays, of course, must be taken to determine whether there are underlying foreign bodies, deformities (Charcot), or signs of osteomyelitis. Equally important, one must always look for the presence of subcutaneous gas. Necrotizing soft tissue infections, whether caused by anaerobes, gram negative bacilli, staphylococci, or Beta-hemolytic streptococci frequently demonstrate gas accumulations around and proximal to the original focus of infections. Accordingly, plain films of the leg must also be taken to ensure that the foot infection does not involve these fascial planes or tendon sheaths. There are obvious treatment implications –emergent treatment implications- when gas is found in the soft tissues. But air is not gas in this sense of the word- sometimes air is found in the periwound area from walking on the foot. This is called emphysema and this is really not an emergency. When undrained abscesses or osteomyelitis are suspected, MRI or other advanced imaging can assist in making the diagnosis.

Figure2.jpg

Fig. 2. Note the soft tissue defect adjacent to the first MTP joint and the gas at the lateral ankle in this other patient.

Leukocytosis or elevated core temperature does not always accompany a moderate or severe infection in the diabetic patient 
Laboratory Studies

Laboratory studies are, of course, critical in determining the patients’ response to the infection and help determine its severity. While complete blood count (CBC), differential, serum glucose, glycohemoglobin, and sedimentation rate are routine labs in this scenario, one must recognize that leukocytosis does not always accompany a moderate or severe infection in the diabetic patient.  Hence, the clinician cannot be lulled into a false sense of comfort upon not finding an elevated white blood count (or elevated temperature for that matter).  Suspicion and caution are the best attributes of the provider caring for such patients. Routine assessment of renal function is also necessary, following serum creatinine, blood urea nitrogen, and estimated glomerular filtration rate (eGFR). These values will obviously affect antimicrobial dosing as well as consideration for angiography and contrast for MRI studies.

Classification

Once the patient assessment has been completed, classification of the infection will be helpful in guiding treatment. The Infectious Disease Society of America (IDSA) has put forth a DFI Classification scheme that has been almost universally adopted here and abroad. (See Table below) This scheme is an expansion of the former non-limb threatening/ limb threatening classification used several decades ago.

Table 1

The reader is referred to the references below for an in-depth review of the points discussed in this month’s ezine. Next month, in Part II, we will discuss treatment of the infected diabetic foot.  As always, your comments are always appreciated and encouraged.

###

References are provided below that can expand upon many of the points made above. We welcome your opinions, concerns, and suggestions.  If you have an interesting case or a troubling circumstance that you would like to share with fellow PRESENT Diabetes members,  please feel free to comment on eTalk.

Best regards,

Robert Frykberg, DPM, MPH

Robert Frykberg, DPM, MPH
PRESENT Editor, 
Diabetic Limb Salvage


REFERENCES
George Liu, DPM, FACFAS

  • Eneroth M, Apelqvist J, Stenstrom A. Clinical characteristics and outcome in 223 diabetic patients with deep foot infections. Foot Ankle Int. Nov 1997;18(11):716-722.
  • Frykberg RG. An evidence-based approach to diabetic foot infections. Am J Surg. Nov 28 2003;186(5A):44S-54S; discussion 61S-64S.
  • Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg. Sep-Oct 2006;45(5 Suppl):S1-66.
  • Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections.Clin Infect Dis. Oct 1 2004;39(7):885-910.
  • Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW, Karchmer AW. Assessment and management of foot disease in patients with diabetes. N Engl J Med. Sep 29 1994;331(13):854-860.
  • Grayson ML, Balaugh K, Levin E, Karchmer AW. Probing to bone in infected pedal ulcers. A clinical sign of underlying osteomyelitis in diabetic patients. J Am Med Assoc.1995;273(9):721-723.
  • Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA. Risk factors for foot infections in individuals with diabetes. Diabetes Care. Jun 2006;29(6):1288-1293.






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    Posted by: PV mayer at 06:55 am 0 comments - Add a Comment Category: Infection


    Part 2 on DFU Infection by Frykberg (3 Jan, 2012)

    The Challenges of Diabetic Foot Infections:
    (Part 2) 

    In the last issue of FootNotes, we focused on what I consider to be the essential components in the assessment of patients presenting with diabetic foot infections. Although I concentrated on severe or limb threatening foot infections, the principles remain the same for even mild or moderate infections: always be suspicious, always look for ischemia, and always obtain appropriate laboratory tests and imaging procedures as essential parts of your evaluation. Also important, please recognize that just having a wound does not imply that it is infected; most, if not all, wounds are contaminated. Infection is a clinical diagnosis based on those classical signs we are all familiar with: rubor, tumor, dolor, and calor. Nonetheless, diabetes (like syphilis) has become the great masquerader in that typical signs and symptoms are masked – especially in the presence of neuropathy.  Hence, my exhortation that one must always be suspicious in such patients who often do not respond to treatment the way one would expect them to under normal circumstances (i.e. persistent fever after several days of ostensibly appropriate therapy).

    Essential Principles of Evaluating Diabetic Foot Infections:  Always be suspicious, always look for ischemia, and always obtain appropriate laboratory tests and imaging procedures.
    So now let us focus on the management of established diabetic foot infections that have been appropriately evaluated. Our focus will always be aimed at limb salvage, a much harder task in many cases than primary leg amputation!

    Management of Diabetic Foot Infections

    Diabetic patients cannot tolerate undrained infection - Gary Gibbons, MD.

    Antibiotics are 
    only part of the management strategies for these complicated patients, although a significant component, of course.  In most cases, however, antimicrobial therapy becomes adjunctive to non-pharmacologic (surgical) therapy. An old adage from my years of training in Boston stipulates that diabetic patients cannot tolerate undrained infection (I believe this comes from an old friend and surgeon, Gary Gibbons). This is a good point to remember, since it is painfully driven home whenever it is forgotten! As I mentioned earlier, those patients not responding to antimicrobial therapy alone likely are failing due to an undrained abscess or retained necrotic tissue. This is a very common scenario and one that is seen especially frequently in those patients with necrotizing soft tissue infections (necrotizing fasciitis, necrotizing cellulitis, clostridial myonecrosis, etc.). These patients typically require several trips to the operating room before their infection is controlled- short of doing a primary major amputation. Last month, I presented a case of necrotizing soft tissue infection. (Figure 1 )  As in this case, such patients do not always present with gas in the soft tissues – that would be too easy. Gas easily identifies those individuals requiring an urgent trip to the operating room – few would miss this clinical clue. Nonetheless, many individuals present with severe cellulitis and some soft tissue necrosis even in the absence of purulent drainage

    Figure1.jpg
    Fig. 1. Necrotizing soft tissue infection- no gas on x-rays but note the severe cellulitis, edema, and necrotic dorsal skin. The portal of entry was in the webspace at the base of the second toe. No ischemia was present.

    They may or may not be sick (IDSA Grade 4 or 3), but the severity of their infection is signified by recalcitrant hyperglycemia, leukocytosis, and failure to resolve cellulitis with broad spectrum antimicrobial therapy.  These important clinical clues should indicate that, very likely, surgical debridement or partial foot amputation is necessary. Several procedures are often required prior to eventual control of infection and definitive closure. (Figures 2-4)

    Figure2.jpg
    Fig. 2. Same patient after initial extensive debridement and toe amputations. Although infection somewhat improved, further necrosis and persistent cellulitis required further debridement.

    Figure3.jpg
    Fig. 3. After further debridement and toe amputations, the infection came under control. A large soft tissue and osseous defect remained with residual necrosis at the midfoot, placing the limb at risk.

    Figure4.jpg
    Fig. 4. Definitive closure was obtained with a Chopart amputation.

    Equally important is the necessity for detecting and treating peripheral ischemia (PAD) when present. Many patients with pre-existing PAD have a foot infection as their first presenting sign of ischemia. In the presence of neuropathy, critical limb ischemia is often silent in that the usual symptoms of claudication or rest pain are absent.  Therefore, in all patients presenting with acute foot infection it is prudent to look for underlying PAD and request appropriate vascular studies and consultations.  That being said, ischemia does not preclude appropriate surgical management for the acute infection.  It is still essential to drain abscesses or to perform emergent local amputations to control infection. Revascularization should be performed after immediate control of infection. A final, definitive procedure such as a closed amputation or skin graft should follow the revascularization and restoration of perfusion to the foot.

    Many patients with pre-existing PAD have a foot infection as their first presenting sign of ischemia.  But in the presence of neuropathy, critical limb ischemia is often silent in that the usual symptoms of claudication or rest pain are absent.

    We have previously discussed the management of osteomyelitis in Diabetic Footnotes Issue 18 - Osteomyelitis — Now What?, but it is worth mentioning again in the overall context of managing diabetic foot infections.  I am of the (biased) opinion that in the diabetic foot, osteomyelitis is best managed surgically in most instances. While this is a matter of debate around the Globe, surgical debridement or bone resection (and sometimes local amputation) with adjunctive systemic antimicrobial therapy seems to more predictably affect a cure than treatment with just antibiotics. This is the course of treatment followed by most US surgeons until prospective studies can definitively identify those sites or patients best suited to medical therapy alone.  Nonetheless, osteomyelitis very rarely, if ever, presents as an acute problem – it usually comes associated with an acute soft tissue infection.

    I am of the opinion that in the diabetic foot, osteomyelitis is best managed surgically in most instances.
    Once the acute infection has been managed, the bone infection can be definitively treated as appropriate for the circumstances. For instance, in a patient with an infected plantar ulcer of a metatarsal head without gangrene, a joint resection with a 4 to 6 week course of culture-directed oral antibiotics will most often result in a “cure”.

    I have not specifically addressed antimicrobial therapy thus far, because I think that we need to place a good deal of emphasis on the surgical management of limb threatening infections. Nonetheless, in our next issue, we will discuss my approach to antimicrobial management of diabetic foot infections – from a clinician’s viewpoint. I have been in the trenches for many years in this regard and have made many mistakes. Hopefully, I’ve learned from them and can offer some guidance to you as well. Until next time…


    ###

    References are provided below that can expand upon many of the points made above. We welcome your opinions, concerns, and suggestions.  If you have an interesting case or a troubling circumstance that you would like to share with fellow PRESENT Diabetes members,  please feel free to comment on eTalk.

    Best regards,

    Robert Frykberg, DPM, MPH

    Robert Frykberg, DPM, MPH
    PRESENT Editor, 
    Diabetic Limb Salvage


    REFERENCES
    George Liu, DPM, FACFAS

    • Eneroth M, Apelqvist J, Stenstrom A. Clinical characteristics and outcome in 223 diabetic patients with deep foot infections. Foot Ankle Int. Nov 1997;18(11):716-722.
    • Frykberg RG. An evidence-based approach to diabetic foot infections. Am J Surg.Nov 28 2003;186(5A):44S-54S; discussion 61S-64S.
    • Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg. Sep-Oct 2006;45(5 Suppl):S1-66.
    • Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. Oct 1 2004;39(7):885-910.
    • Javier Aragón-Sánchez, Yurena Quintana-Marrero, Jose L. Lázaro-Martínez, et al: Necrotizing Soft-Tissue Infections in the Feet of Patients With Diabetes: Outcome of Surgical Treatment and Factors Associated With Limb Loss and Mortality. INT J LOW EXTREM WOUNDS 2009; 8; 141
    • Javier Aragón-Sánchez: Seminar Review: A Review of the Basis of Surgical Treatment of Diabetic Foot Infections International Journal of Lower Extremity Wounds 2011 10: 33


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    Posted by: PV mayer at 06:54 am 0 comments - Add a Comment Category: Infection


    The Cost of Diabetes Keeps Rising (3 Jan, 2012)

    The Cost of NOT Doing our Job Well Escalating

    Cost of Diabetes Will Be $3.35 Trillion by 2020

    The United States of Diabetes: New report shows half the country could have diabetes or prediabetes at a cost of $3.35 trillion by 2020.

    More than 50 percent of Americans could have diabetes or prediabetes by 2020 at a cost of $3.35 trillion over the next decade if current trends continue, according to new analysis by UnitedHealth Group's Center for Health Reform & Modernization, but there are also practical solutions for slowing the trend. See this week's Tool for Your Practice.


    New estimates show diabetes and prediabetes will account for an estimated 10 percent of total health care spending by the end of the decade at an annual cost of almost $500 billion -- up from an estimated $194 billion this year.


    The report, The United States of Diabetes: Challenges and Opportunities in the Decade Ahead,produced for November's National Diabetes Awareness month, offers practical solutions that could improve health and life expectancy, while also saving up to $250 billion over the next 10 years, if programs to prevent and control diabetes are adopted broadly and scaled nationally. This figure includes $144 billion in potential savings to the federal government in Medicare, Medicaid and other public programs.

    Key solution steps include lifestyle interventions to combat obesity and prevent prediabetes from becoming diabetes and medication control programs and lifestyle intervention strategies to help improve diabetes control.

    "Our new research shows there is a diabetes time bomb ticking in America, but fortunately there are practical steps that can be taken now to defuse it," said Simon Stevens, executive vice president, UnitedHealth Group, and chairman of the UnitedHealth Center for Health Reform & Modernization. "What is now needed is concerted, national, multi-stakeholder action. Making a major impact on the prediabetes and diabetes epidemic will require health plans to engage consumers in new ways, while working to scale nationally some of the most promising preventive care models. Done right, the human and economic benefits for the nation could be substantial."

    The annual health care costs in 2009 for a person with diagnosed diabetes averaged approximately $11,700 compared to an average of $4,400 for the remainder of the population, according to new data drawn from 10 million UnitedHealthcare members. The average cost climbs to $20,700 for a person with complications related to diabetes. The report also provides estimates on the prevalence and costs of diabetes based on health insurance status and payer, and evaluates the impact on worker productivity and costs to employers.

    Diabetes currently affects about 27 million Americans and is one of the fastest-growing diseases in the nation. Another 67 million Americans are estimated to have prediabetes. There are often no symptoms, and many people do not even know they have the disease. In fact, more than 60 million Americans do not know that they have prediabetes. Experts predict that one out of three children born in the year 2000 will develop diabetes in their lifetimes, putting them at grave risk for heart and kidney disease, nerve damage, blindness and limb amputation.

    Estimates in the report were calculated using the same model as the widely-cited 2007 study on the national cost burden of diabetes commissioned by the American Diabetes Association (ADA).

    The report also focuses on obesity and its relationship to diabetes. Being overweight or obese is one of the primary risk factors for diabetes, and with more than two-thirds of American adults and 17 percent of children overweight or obese, the risk is clearly rising. In fact, over half of adults in the U.S. who are overweight or obese have either prediabetes or diabetes, and studies have shown that gaining just 11-16 pounds doubles the risk of type 2 diabetes and gaining 17-24 pounds nearly triples the risk.

    "Because diabetes follows a progressive course, often starting with obesity and then moving to prediabetes, there are multiple opportunities to intervene early and prevent this devastating disease before it's too late," said Deneen Vojta, M.D., senior vice president of the UnitedHealth Center for Health Reform & Modernization, who helped develop UnitedHealth Group's Diabetes Prevention and Control Alliance.


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    Posted by: PV mayer at 06:46 am 0 comments - Add a Comment Category: Economics


    Tackling Diabetic Foot Disease in China (20 Oct, 2011)

    Outstanding work by Professor Xu.

    Diabetic foot care in mainland China

    Diabetic foot ulcersService delivery | Zhangrong Xu

    Diabetic foot care in mainland ChinaDiabetes is a major non-communicable disease worldwide. There are now some 40 million people with diabetes – and a similar number with impaired fasting glucose or impaired glucose tolerance – in mainland China alone (China News, 2008). Among those with diabetes, diabetic foot disease is becoming a serious health burden, impacting negatively both on peoples’ quality of life and on healthcare budgets.


    The First and Second Diabetic Foot Groups of the Chinese Diabetes Society were founded in 1996 and 2002, respectively. The groups aimed to establish a campaign to improve diabetic foot care in China. This included the participation of the Second Diabetic Foot Group in the International Consensus on the Diabetic Foot, which was published by the International Diabetes Federation (International Working Group on the Diabetic Foot, 2003).

    The Third Diabetic Foot Group of the Chinese Diabetes Society was founded in October 2008 and is currently active. This group aims to recruit new members from fields not specifically diabetes related, such as orthopaedic and vascular surgery, but whose contribution to diabetic foot care is essential.

    Over the past 5 years, various national meetings on diabetic foot disease and its management and prevention have been held at both local and national levels in China. A number of international experts in the field of diabetic foot care have been invited to China for lectures and clinical visits.
     
    The International Forum on Diabetic Foot and Related Diseases was held in Beijing in 2005 and 2006, in Kunming in 2007, and in Chengdu in 2008. Some 400-500 delegates attended each of these 3-day meetings. Workshops where held, during which approximately 100 participants were divided into groups to learn how to conduct basic examinations of the diabetic foot and investigations for peripheral vascular disease.
     
    A range of topics were covered, including taking an ankle-brachial pressure index and ulcer dressing choice. The workshops were mostly attended by physicians and nurses from teaching hospitals. Many attendees asked the Diabetic Foot Group to hold similar workshops in the future. To date, more than 1500 healthcare professionals have participated in diabetic foot care training provided by the group.

    In August of this year, the 5th International Forum on Diabetic Foot and Related Diseases  was held simultaneously with the 6th Asia-Pacific Diabetic Limb Problems Meeting in Beijing. More than 500 participants from 16 countries took part. Speakers included Professors Robert Frykberg, Andrew Boulton, David Amstrong, Bejamin Lipsky and Dennis Yue, as well as Marg McGill, Senior Vice-President of the International Diabetes Federation.

    There are now more diabetic foot clinics in China than ever before, with seven new centres established in the past 5 years. However, relative to the size of the population with diabetes, there remains too few diabetic foot centres. The clinic at which I work has treated more than 350 people with diabetic foot problems over 5 years. We have been able to achieve a reduction in the amputation rate from 11.5% 5 years ago to 7.2% (mostly minor amputations) today.


    Some newer techniques for the management of diabetic foot disease have been used in Chinese clinics. These include vascular intervention (stents, Figure 1), and the transplantation of autologous peripheral blood stem-cells for the treatment of peripheral vascular disease. Autologous platelet-rich gels and negative pressure therapy have also been used for the treatment of hard-to-heal ulcers, with some diabetic foot centres achieving positive results. Some Chinese physicians treat foot problems with a combination of Western medicine and traditional Chinese medicine.

    Figure 1. Ischaemic ulcer (a) upon admission to hospital and (b) shortly after. Reperfusion was undertaken, the vascular supply is shown (c) before and (d) after intervention. The ulcer (e) 2 weeks after the intervention, and (f) 2 months after the intervention.

     

     
    In an effort to increase the amount of literature available to healthcare professionals with an interest in the diabetic foot working in China, the Diabetic Foot Group has undertaken a number of initiatives. The International Consensus on the Diabetic Foot (International Working Group on the Diabetic Foot, 2003) has been translated into Chinese and is now in its second print run, with 6000 copies distributed to-date. The group has worked with experts from a range of fields to produce books that introduced topics on the care of the diabetic foot. The output of literature from China has likewise increased. The number of scientific articles published by practitioners working in diabetic foot care in China has risen dramatically, from 6 in 1996 to 360 in 2006.

    In 2004, the Diabetic Foot Group organised research involving 14 teaching hospitals located in cities around China. A range of topics were investigated, including the classification and pathogenesis of diabetic foot disease and peripheral arterial disease, and the cost of diabetic foot disease to hospitals. People (n=634) with diabetes and foot problems or peripheral arterial disease admitted from 1 January to 31 December 2004 were included in this research.
     
    Neuropathy was present in 68.0% of participants, hypertension in 57.4%, peripheral arterial disease in 28.7%, coronary heart disease in 28.5%, cerebral vascular disease in 24.3%, and 38.8% were smokers. Foot ulcers were, in the majority (82.2%) of cases, at Wagner stage 1 or 2. In 42.7% of cases, more than one ulcer was present, and 67.9% of ulcers were complicated by infection. Ulcers were commonly neuroischemic. The average direct medical cost to the hospital attributable to diabetic foot disease or peripheral arterial disease in people with diabetes was ¥RMB 14906/person ($US 1850/person). Our results were presented at the 5th International Symposium on the Diabetic Foot held in The Netherlands (Xu, 2007).

    Diabetic foot disease is becoming a serious health and economic burden in China and around the world. The First, Second and Third Diabetic Foot Groups of the Chinese Diabetes Society have looked to provide healthcare professionals working in China with more information on, and clinical skills in, the management of diabetic foot disease. Practitioners in China look forward to increasing national and international cooperation between those with an interest in the care of the diabetic foot, through knowledge-sharing and participation in research.

     

    REFERENCES

    China News (2008) [Rapidly increasing prevalence of diabetes in China.] (In Chinese) Available from: http://tinyurl.com/yfnwsfz (accessed 26.10.09) 
    International Working Group on the Diabetic Foot (2003) International Consensus on the Diabetic Foot and Practical Guidelines on the Management and the Prevention of the Diabetic Foot. International Diabetes Federation, Amsterdam
    Xu Z (2007) The diabetic foot in China. 5th International Symposium on the Diabetic Foot, 9-12 May 2007, Noordwijkerhout, The Netherlands



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    Posted by: PV Mayer at 10:02 am 2 comments - Add a Comment Category: Limb Salvage Teams


    Theragnostics on Steriods (20 Oct, 2011)

    Next Up for Artificial Intelligence: Real Biology

    by  on  • 5:46 pm

    First, artificial intelligence trumped expert chess players at their own game. Then came Watson, a computer system that famously beat Jeopardy! champions Brad Rutter and Ken Jennings. Now, researchers are putting artificial intelligence to work to automate biological research—-specifically the reverse engineering of metabolic networks from experimental data.

    A team of scientists from Vanderbilt University, Cornell University, and CFD Research Corp. have shown that a computer can take raw experimental numbers from a biological data and derive equations from it that describe how the system functions. The modelling used in the research is said to be one of the most complex scientific modeling problems that artificial intelligence has solved completely from scratch.

    Check out the announcement from Vanderbilt University:

    The “brains” of the system, which [Vanderbilt professor John P. Wikswo] has christened the Automated Biology Explorer (ABE), is a unique piece of software called Eureqa developed at Cornell and released in 2009. [Michael Schmidt and Hod Lipson at the Creative Machines Lab at Cornell University] originally created Eureqa to design robots without going through the normal trial and error stage that is both slow and expensive. After it succeeded, they realized it could also be applied to solving science problems.

    One of Eureqa’s initial achievements was identifying the basic laws of motion by analyzing the motion of a double pendulum. What took Sir Isaac Newton years to discover, Eureqa did in a few hours when running on a personal computer.

    In 2006, Wikswo heard Lipson lecture about his research. “I had a ‘eureka moment’ of my own when I realized the system Hod had developed could be used to solve biological problems and even control them,” Wikswo said. So he started talking to Lipson immediately after the lecture and they began a collaboration to adapt Eureqa to analyze biological problems.

    “Biology is the area where the gap between theory and data is growing the most rapidly,” said Lipson. “So it is the area in greatest need of automation.”

    Wikswo believes that artificial intelligence could potentially be harnessed to generate and analyze biological data to such a degree that it could predict the behavior of biological systems under a variety of conditions.

    [Wikswo also] maintains that this approach will give scientists the ability to control biological systems even if [the researchers] can’t completely explain how they work, and this capability can provide the basis for the development of significantly improved drugs and other therapies.

    According to Cornell professor Hod Lipson, the researchers might need to create another program to translate the meaning of the equations that the Eureqa program comes up with.

    This this video from a couple of years ago explains how the Eureqa software derived the fundamental equations of motion from observations of a double pendulum.

    Top image: The microformulator pictured enables the biological experiments to be performed without human intervention. Image credit: Wikswo Lab.

    Abstract in Physical BiologyAutomated refinement and inference of analytical models for metabolic networks

    Press release: Robot biologist solves complex problem from scratch



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    Posted by: PV Mayer at 10:01 am 2 comments - Add a Comment Category: Theragnostics


    Amputation Rates Vary Widely Across US (30 Sep, 2011)

    It matters where you live.

    Location, Location, Location: Geographic Clustering of Lower-Extremity Amputation Among Medicare Beneficiaries With Diabetes

    1. David J. Margolis, MD, PHD
    2. Ole Hoffstad, MA
    3. Jeffrey Nafash, BA,
    4. Charles E. Leonard, PHARMD, MSCE
    5. Cristin P. Freeman, MPH,
    6. Sean Hennessy, PHARMD, PHD and 
    7. Douglas J. Wiebe, PHD

    +Author Affiliations

    1. Department of Biostatistics and Epidemiology and the Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
    1. Corresponding author: David J. Margolis, margo@mail.med.upenn.edu.

    Abstract

    OBJECTIVE Lower-extremity amputation (LEA) is common among persons with diabetes. The goal of this study was to identify geographic variation and the influence of location on the incidence of LEA among U.S. Medicare beneficiaries with diabetes.

    RESEARCH DESIGN AND METHODS We conducted a cohort study of beneficiaries of Medicare. The geographic unit of analysis was hospital referral regions (HRRs). Tests of spatial autocorrelation and geographically weighted regression were used to evaluate the incidence of LEA by HRRs as a function of geographic location in the U.S. Evaluated covariates covered sociodemographic factors, risk factors for LEA, diabetes severity, provider access, and cost of care.

    RESULTS Among persons with diabetes, the annual incidence per 1,000 of LEA was 5.0 in 2006, 4.6 in 2007, and 4.5 in 2008 and varied by the HRR. The incidence of LEA was highly concentrated in neighboring HRRs. High rates of LEA clustered in contiguous portions of Texas, Oklahoma, Louisiana, Arkansas, and Mississippi. Accounting for geographic location greatly improved our ability to understand the variability in LEA. Additionally, covariates associated with LEA per HRR included socioeconomic status, prevalence of African Americans, age, diabetes, and mortality rate associated with having a foot ulcer.

    CONCLUSIONS There is profound “region-correlated” variation in the rate of LEA among Medicare beneficiaries with diabetes. In other words, location matters and whereas the likelihood of an amputation varies dramatically across the U.S. overall, neighboring locations have unexpectedly similar amputation rates, some being uniformly high and others uniformly low.

    • Received April 29, 2011.
    • Accepted July 28, 2011.


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    Posted by: PV Mayer at 02:48 pm 2 comments - Add a Comment Category: Prevention


    Early Insulin Use in the Progression of Diabetes by the Master, Dr Aaron Vinik (29 Sep, 2011)

    Dr. Aaron I. Vinik on Early Insulin Use in the Progression of Diabetes

    VinikOne of the leading diabetes researchers in the world, Dr. Aaron I. Vinik, Director of Research and Neuroendocrine Unit, EVMS Strelitz Diabetes Research Center, shares his views on early insulin initiation.

    The natural history of type 2 Diabetes (T2DM) is a progressive worsening of glycemic control as a consequence of progressive beta cell failure so that ultimately all patients with T2DM are equivalent to patients with type 1 DM and are insulin deficient. In addition the clock starts ticking for macrovascular complications such as heart attacks, strokes and peripheral vascular diseases before the advent of fasting or postprandial hyperglycemia indicating that there are, in addition to hyperglycemia, a host of risk factors conducive to macrovascular disease. In contrast, the glycemia milieu is the single most important determinant of microvascular complications 

    Major studies in T2DM have indubitably shown a reduction of microvascular complications by good glycemic control and the effect persists despite failure to maintain A1c's near normal. This is in stark contrast with the recent attempts to show that intensive glycemic control in the ACCORD, ADVANCE and VADT studies reduce macrovascular events: somewhat disconcerting was the finding in the ACCORD study of an increase in sudden death by 22% in the intensively treated group. Thus, the window of opportunity to aggressively treat T2DM is early and patients can enjoy a 'legacy effect' or what has been reported as metabolic memory. Why then did we not see this benefit in the three studies above and what have we learned? The lessons were invaluable and suggest that there can be a bad metabolic memory or legacy effect in certain situations:

    1. If the diabetes has been there for > 12-15 years;
    2. Older people and African Americans;
    3. Significant impairment of renal function;
    4. The presence of coronary calcification;
    5. The history of peripheral neuropathy and the findings of autonomic neuropathy.

    So the window of opportunity has to be early in the absence of kidney, somatic and autonomic dysfunction, established cardiovascular disease and there are gender and ethnic group sensitivities. Perhaps the only protective factor appears to be obesity but that is almost contrary to everything we are trying to achieve in T2DM.

    So armed with this information, why is it that we have developed a treat-for-failure approach trying several medications, diet and exercise and only when we have failed to reach goal do we make adjustments? The median delay of adjusting a sulfonylurea is 24 months and metformin is 36 months. Titration is a tardy task and treating for failure is doomed to failure. A fundamental change in physicians' management of T2DM is required and the traditional treatment algorithm should emphasize treatment for success not failure.

    Traditional oral hypoglycemic agents such as sulfonylurea, metformin, the glitazones and the Incretins and Gliptins are able to lower A1c's about 0.5 to 2.0 %. Combinations of these agents can under optimum conditions achieve an A1c reduction of 3%. Thus in people close to goal of 6.5% (AACE) or 7.0% (ADA) then exercise, diet and a single agent are appropriate. If the A1c is between 7.5% and 9.0%, combinations of oral agents are an appropriate first choice. When A1c is > 9.0 we need the unlimited capacity of insulin to achieve goal. This can be accomplished in a number of ways which include addition to the oral regimen, use of a single long acting insulin analog, use of combinations of different forms of insulin and finally a basal long acting insulin together with a short acting bolus based upon the prevailing blood glucose and the anticipated carbohydrate intake. Data from the UKPDS indicate that after insulin is introduced either alone or in combination with oral therapy, the long term outcome is improved glycemic control. There is however a clinical inertia amongst generalists and even endocrinologists to make these change.

    The barriers to initiation of insulin therapy are legion. Physicians have a fear of hypoglycemia and imagine there are adverse health consequences of the insulin itself. They have misconceptions of the regimens as being too complex and that it should be the therapy of last resort or limited efficacy. They are indeed major contributors to the fear patients have of the needle. This is a paradox when the needle per se is more benevolent than, for example, a finger stick. Patient-related behaviors are fear of hypoglycemia, adverse health outcomes, medication errors, needles and pain, weight gain and the complicated regimens and scheduling of injections. Unfortunately patients have been brainwashed into thinking that use of insulin is a personal failure, their disease is too advanced, it is the therapy of last resort and it greatly increases cost. Our own studies comparing insulin with oral agents have shown that insulin is associated with improved quality of life, less fatigue, increase in energy and enhanced state of emotion. Patient education along with the use of insulin formulations that reduce risk of hypoglycemia and weight gain, simplified treatment regimens and easy to use insulin delivery systems, should help to reduce the barriers to early aggressive insulin use when the window of opportunity presents itself and clinicians need to overcome inertia and not allow the window to close upon them. Every day here at the EVMS Strelitz Diabetes Center we see patients who are grateful for the restoration of their quality of life as well as the anticipated reduction of the burden of diabetes complications.

    Dr. Aaron I. Vinik has written five books, published more than 250 papers in medical journals, and is recognized as a pioneer and scholar. Dr. Vinik has received research funding for his studies from the National Institutes of Health, the National Cancer Institute, the Kroc Foundation and the American Diabetes Association.  He is a leader in research on the diagnosis and treatment of diabetic neuropathy with a particular expertise in the area of autonomic diabetic neuropathy, a complex and challenging condition. Dr. Vinik has also been a leader in research on new approaches to generate islet cell tissue from pancreatic duct tissue which may one day lead to a true cure for diabetes.

    For more information on Dr. Vinik and his groundbreaking work at the Strelitz Diabetes Center, just follow this link, Eastern Virginia Medical School Strelitz Diabetes Center.



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    Posted by: PV Mayer at 04:23 pm 2 comments - Add a Comment Category: Diabetes Management


    Primer in Wound Preparation by Rogers (26 Sep, 2011)

      

    Current Concepts In Wound Bed Preparation

    Author(s): 
     Lee C. Rogers, DPM

    Proper preparation of the wound bed is essential to priming the wound for effective healing. Accordingly, this author discusses key principles from the literature and shares insights from his clinical experience in employing debridement and adjunctive modalities to help facilitate better wound healing and eventual wound closure.

    Wound bed preparation is a term that describes making the wound ready for closure by advanced means. If the wound is not properly prepared, even the most expensive products or devices are unlikely to produce a positive outcome. One does not usually perform wound bed preparation in a single visit. There is more of a process to prepare the wound to be closed. In addition to the wound itself, one must ensure the patient is prepared for wound closure.

       Podiatric physicians must manage infection, ensure adequate vascularity and remove external pressure from the wound.1 One can confirm the patient’s vascular status via noninvasive testing since pedal pulses alone are not a good indicator of sufficient perfusion. If there is vascular impairment, podiatrists should consider an appropriate referral for an intervention to improve circulation.

       In regard to infection, patients with diabetes do not often mount systemic responses to infection. Therefore, clinicians must rely upon local signs. Is there erythema, purulent drainage or odor present? As infection is purely a clinical diagnosis, a culture cannot determine if the wound is infected. Cultures can only help to discern which bacteria are pathogens in that infection. Uninfected wounds should not be cultured.

       One can mitigate external pressure either by surgical intervention or by using devices such as a total contact cast or removable cast walker.2

       Completing the above process and creating a good wound healing environment is considered the standard of practice in most communities. One monitors the wound over four weeks. If the wound area does not reduce by at least 50 percent in that time period, the wound is unlikely to heal in 12 weeks and one should employ advanced therapies.3 There are many advanced therapies, ranging from skin grafts and flaps to bioengineered tissues, but they all require the wound to be adequately prepared.

    A Closer Look At Key Factors That Can Affect Wound Healing

    Wound bed preparation consists of far more than just a debridement and, in some cases, may take weeks to accomplish. The goal is to optimize the wound in order to promote healing with advanced means and remove the barriers to healing. Let us first consider the inherent factors that are detrimental to wound healing like bacteria, senescent cells and hyperkeratotic tissue.

       Bacteria. A wound is a break in the dermal envelope. It is usually contaminated by bacteria and may even have a biofilm present. Just because a wound is colonized does not mean that it is infected. If the wound becomes critically colonized with bacteria, an infection may develop. Researchers suggest that bacterial loads between 105 and 106 per gram of tissue in the wound bed may cause infection.4 
     However, more virulent organisms may cause infection at lower concentrations. Biofilm itself is detrimental to wound healing and will hinder the process, but infection causes tissue destruction. Biofilm is difficult to treat. At this time, only thorough debridement has proven to be a definitive treatment.

       Senescent cells. Cellular dysfunction is common in diabetic foot ulcers and other chronic ulcers. Somatic cells can only divide 50 times before their DNA telomeres have shortened and they can no longer replicate full copies of the DNA. At that point, there should be apoptosis or programmed cell death.

       In some diabetic wound healing models, researchers have shown that the apoptotic mechanism is impaired. They note that these old (senescent) cells continue to live in the wound but do not replicate or produce growth factors.5 The senescent cells impair the ability of the wound to heal.

       Hyperkeratotic tissue. This hardened tissue forms along the wound periphery and its formation is accelerated by pressure, either direct forces or shearing forces. Bearing weight on the hardened tissue causes subdermal tissue trauma and hemorrhage. Hyperkeratotic tissue acts as a barrier to epithelialization. This tissue can also undermine and collect fluid and debris, thus increasing the risk for infection.

    Using Debridement And Adjunctive Modalities To Prepare The Wound Bed

    The main goal of preparing the wound bed is to provide a healing surface, which would accept a graft. While wound bed preparation involves debridement, this is more than just debridement. It also includes consideration of the aforementioned factors such as bacteria, cell senescence and hyperkeratotic tissue. Debridement removes devitalized or contaminated material from within or surrounding the wound. Selective debridement stimulates the repair process. There are various methods of debridement including surgical (scalpel), hydrosurgical (Versajet, Smith and Nephew), biosurgical (maggots), enzymatic or mechanical (wet to dry dressings).6

       I have heard the axiom that debridement converts a chronic wound into an acute wound. However, acute and chronic are specifically terms that describe time. One cannot take a chronic wound that has been open for four months and convert it into an acute wound present for one day. However, I believe debridement can put an acute injury into a chronic wound, which may provide growth factors and speed healing.

       For the purposes of wound bed preparation, surgical or hydrosurgical debridement is preferred. It can occur at the same time as grafting or precede grafting by up to a week. Use a scalpel to remove the wound margins, saucerizing the tissue, and then use a curette or hydroscalpel to debride the wound bed. The goal is to obtain a bleeding granular wound. If you are preparing a wound in the operating room for grafting, ensure that bleeding is under control prior to applying the graft in order to avoid a hematoma. Hematoma between the wound bed and the graft is a leading cause of graft failure. One should avoid electric cautery, if possible, and employ pressure, epinephrine or thrombin if needed

      If the wound is not completely granular, one should consider using either platelet-derived growth factor (PDGF, Regranex, Healthpoint Biotherapeutics) or negative pressure wound therapy (NPWT, VAC therapy, KCI) to make the wound granular and level with the surrounding tissue. The VAC therapy works well in combination with debridement to prepare the wound for grafting. VAC therapy can also assist in managing wound exudate. If one uses VAC therapy in the OR setting, ensure that bleeding is under control before applying NPWT.

     

       Armstrong and Lavery studied 162 patients as part of a 16-week randomized clinical trial.7 As part of the study, 77 patients received NPWT while 85 received standard moist wound care. They found that VAC therapy had a faster rate of developing granulation tissue in comparison to standard moist wound therapy.

       When choosing a biomaterial, foam is more effective than gauze at producing granulation tissue. Foam also compresses and contracts better than gauze, enhancing the wound’s ability to contract. Employing a silver impregnated foam can help manage bioburden.

       When performing wound bed preparation a week prior to applying bioengineered tissue, one should perform an adequate debridement, saucerize the margins and promote a good wound healing environment with regular dressing changes until applying the tissue.

       The first photo on page 1 shows two wounds on the lateral surface of a foot that are fibrotic but uninfected. We performed debridement with a scalpel and curette, which uncovered a healthy bleeding base (see the second photo on page 1). The use of bioengineered tissue prepared the wound for grafting. This preparation occurred in a single stage. One can apply a silver dressing to the wound to manage bacterial load and prevent infection until the application of bioengineered tissue.

       Often, the wound requires a maintenance debridement at the time of grafting and during subsequent applications. Cardinal and colleagues retrospectively analyzed the results from two controlled, prospective, randomized trials of topical wound treatments on 366 venous leg ulcers and 310 diabetic foot ulcers over 12 weeks.8 The study results suggest that frequent debridement of diabetic foot and venous leg ulcers may increase wound healing rates. Maintenance debridements usually involve removing any obvious debris, fibrosis or hyperkeratotic margins.

       In some cases, the purpose of bioengineered tissue application might be to aid wound bed preparation because the cellular therapy provides the wound with multiple growth factors.

    Case Study: When There Is An Ankle Wound With Exposed Tendon

    A 71-year-old male with diabetes presents to the clinic with a small, painful, undermining wound on the anterior ankle with an exposed extensor digitorum longus tendon. The wound was caused by direct trauma from a water sprinkler head. The tendon was visibly moving in the wound when the patient dorsiflexed and plantarflexed the ankle. This is problematic because bacteria has access to the tendon and can spread to adjacent compartments. The moving tendon also prevents granulation tissue from adhering.

       The patient went to the operating room for a wide debridement and I removed all undermining tissue. The patient was admitted to the hospital

      We started the patient on a VAC Ulta, a new product by KCI that instills a fluid into the wound. In this case, I infused one-quarter strength Dakin’s solution for the anti-infective and anti-inflammatory properties. With the VAC Ulta, one can tightly control the infusion/suction rate. I set this to instill 50 mL of Dakin’s solution, hold for five minutes, then resume suction and repeat the process every two hours.

       After three days, the wound appeared to improve but the tendon was still exposed. The patient went back to the OR, where we performed debridement with a Versajet. I placed Integra (Integra Life Sciences) on the wound and used traditional VAC therapy with the Granufoam Bridge Dressing as a bolster. The patient wore a total contact cast (TCC-EZ, MedEfficiency) to keep the tendon from moving under the graft. I changed the TCC-EZ and VAC therapy twice per week. After two weeks of treatment, the wound became granular and the tendon was covered.

       The aforementioned process describes wound bed preparation. I debrided the margins with a scalpel and performed light debridement of the wound bed with a Versajet. A split thickness skin graft was harvested from the anterolateral ipsilateral thigh at a thickness of 0.020 inches. I meshed this at 1:1.5 ratio, placed it on the wound and stapled it in place. I used a Mepitel silicone dressing (Molnlycke) as an interface. I placed VAC therapy on the graft as a bolster dressing and set this to -125 mmHg continuous pressure for five days.

       After VAC therapy removal, I covered the wound with Mepilex Ag (Molnlycke) at that point. The graft interstices healed in about 10 days. I covered the donor site with a Mepilex Border (Molnlycke) and changed it as needed. The wound healed uneventfully.

    Final Words

    Proper preparation of the wound bed is vital to graft or tissue success. Wound bed preparation is much more than just a debridement and takes into account factors that impede wound healing.

       By creating a recipient wound bed that is well vascularized, free from infection and granular with even sloping margins, we can increase the chance of graft take and facilitate more reliable wound healing.

       Dr. Rogers is the Associate Director of the Amputation Prevention Center at Valley Presbyterian Hospital in Los Angeles

    1. Rogers LC, Bevilacqua NJ. Organized programs to reduce lower-extremity amputations. J Am Podiatr Med Assoc. 2010;100(2):101-104.
    2. Armstrong DG, Boulton AJ. Pressure offloading and “advanced” wound healing: isn’t it finally time for an arranged marriage? Int J Low Extrem Wounds. 2004; 3(4):184-187.
    3. Snyder RJ, Kirsner RS, Warriner RA, Lavery LA, Hanft JR, Sheehan P. Consensus recommendations on advancing the standard of care for treating neuropathic foot ulcers in patients with diabetes. Ostomy Wound Manage. 2010; 56(4 Suppl):S1-24.
    4. Sen RK, Murthy N, Gill SS, Nagi ON. Bacterial load in tissues and its predictive value for infection in open fractures. J Orthop Surg. 2000; 8(2):1-5.
    5. Rogers LC, Bevilacqua NJ, Armstrong DG. The use of marrow-derived stem cells to accelerate healing in chronic wounds. Int Wound J. 2008; 51(1):20-25.
    6. Attinger CE, Bulan E, Blume PA. Surgical debridement: the key to successful wound healing and reconstruction. Clin Podiatr Med Surg. 2000; 17(4):599-630.
    7. Armstrong DG, Lavery LA. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet. 2005; 366:1704-1710.
    8. Cardinal M, Eisenbud DE, Armstrong DG, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Rep Regen. 2009; 17(3):306-311.


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    Posted by: PV Mayer at 11:08 am 2 comments - Add a Comment Category: Debridement


    Suture-less Vascular Anastomosis:Entering a New Era in Limb Salvage (25 Sep, 2011)

    Researchers Develop Method of Joining Blood Vessels Without Sutures

    by  on  • 
    3:08 pmNo Comments

    For 100 years, the process of vascular anastomosis has largely been the same. Surgeons take a needle and thread and delicately suture together the walls of the blood vessel. Though literally sewing together blood vessels is a widely utilized surgical procedure, it isn’t without its issues. Intimal hyperplasia, a cell response to the trauma of the needle and thread, causes blood vessels to narrow which increases the risk of a blood clot or localized turbulence. Sutures may trigger an immune response that causes dangerous inflammation. Moreover, suturing becomes extremely challenging on blood vessels that are less than one millimeter in diameter.

    Microsurgeons at Stanford University have developed a new method of vascular anastomosis that is safer and faster. The key ingredient in this new process is Poloxamer 407, a unique, FDA-approved polymer whose properties can be reversed by heating. In the case of vascular anastomosis, Poloxamer 407 is injected at the site where the blood vessels are to be joined, and the area is heated. The unique properties of Poloxamer 407 cause it to become elastic and solid when heated above body temperature. This causes both openings of a severed blood vessel to become distended, allowing surgeons to precisely join the openings together with Dermabond, a commonly used surgical sealant. After the blood vessels have been joined, a decrease in temperature causes Poloxamer 407 to dissolve harmlessly into the bloodstream.

    The process has been successfully demonstrated on blood vessels as small as 0.2 millimeters. If successful, the process could ultimately improve patient care by decreasing amputations, strokes and heart attacks while reducing health-care costs.

    Press release from Stanford University: Stanford researchers invent sutureless method for joining blood vessels

    Journal abstract in Nature MedicineVascular anastomosis using controlled phase transitions in poloxamer gels



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    Posted by: PV Mayer at 04:38 pm 2 comments - Add a Comment Category: Vascular Support


    Oxygen MicroGenerators to Treat Ischemic Wounds? (25 Sep, 2011)

    Implantable Oxygen Generators Help Fight Cancer

    by  on  • 
    12:47 pm1 Commen

    A couple of days ago, we ran a blog post on an implantable oxygen sensor for monitoring tumor growth. In related news, researchers at Purdue University are developing an implantable device using a similar approach to treat tumors. But instead of monitoring oxygen, the device generates the gas in order to boost the effectiveness of chemotherapy and radiation treatment. The technology generates oxygen through water electrolysis.

    The device targets tumors that are hypoxic, meaning having low levels of oxygen. Hypoxic tumors are difficult to treat using radiation therapy because oxygen amplifies the effectiveness of radiation by helping to form free radicals, which damage a tumor’s genetic material. “So the hypoxic areas [of tumors] are hard to kill,” says Babak Ziaie, a Purdue professor who led the research. “Pancreatic and cervical cancers are notoriously hypoxic. If you generate oxygen you can increase the effectiveness of radiation therapy and also chemotherapy,” he adds.

    Ziaie reports that his father is a cancer survivor, who went through many rounds of painful chemotherapy treatment. “This is a new technology that has the potential to improve the effectiveness of such therapy,” he says.

    In testing on mice, the research group showed the oxygen generators are effective in treating pancreatic tumors. Measuring less than one centimeter in length, the generators were inserted into tumors using a hypodermic biopsy needle.

    Press release: Tiny oxygen generators boost effectiveness of anticancer treatment

    Abstract in IEEE Transactions on Biomedical EngineeringAn Ultrasonically-Powered Implantable Micro Oxygen Generator (IMOG).



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    Posted by: PV Mayer at 04:34 pm 2 comments - Add a Comment Category: Diabetic Foot Ulcer Treatment


    Who Says That Wound Care Isn't Sexy: Wounds Get Wet Before They Get Hot (25 Sep, 2011)

    Is Moisture the New Heat?

    2 Comments

    Bruin Biometrics’ Sub-Epidermal Moisture Scanner Might Detect Decubitus Ulcers Before They Show Up

    Bruin Biometrics' Sub-Epidermal Moisture Scanner Might Detect Decubitus Ulcers Before They Show Up

    Bruin Biometrics, LLC,  a wireless health technology company, and researchers at UCLA have developed a device for measuring the risk of pressure ulcer formation. The Sub-Epidermal Moisture (SEM) scanner is a handheld device which measures the dielectric properties of the tissue being assessed and provides an estimation of the sub-epidermal moisture which is indicative of risk of decub ulcer formation. The SEM scanner is designed to overcome current difficulties with visual pressure ulcer assessments by detecting early pressure damage before it becomes visible on the skin surface.

    The scanner is intended for use in a point of care environment and can wirelessly transmit measured data for storage and analysis on Bruin Biometrics’ proprietary back end system. The video below gives a nice overview of the early clinical work on SEM that led to the development of the system. It also has some nice technical info and shots of the device itself (techies scroll to 3:30). The SEM scanner was officially unveiled in April of this year and is expected to be commercially launched in the coming months.

    Product pageBruin Biometrics SEM Scanner…



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    Posted by: PV Mayer at 12:29 pm 2 comments - Add a Comment Category: Prevention


    FREMS as a Novel Therapy for treatment of DFU (25 Sep, 2011)

    Case Presentation and Conclusion: 
    A Novel Therapy for Treatment of a Diabetic Ulceration
    by Conway T. McLean, DPM

     
    Jay Lieberman, DPM, FACFAS
    Conway T. McLean, DPM
    Director of Podiatric Surgery
    Cottage Clinics
    Chicago, IL 

    A diabetic patient presented to the office with a common presenting complaint, a non-healing wound. Like so many individuals with diabetes, this particular patient's level of self-care (as well as their understanding of the disease) was somewhat lacking. A limb-threatening infection had developed of the left foot, due, at least in part, to inappropriate care. Relevant medical history included a five year history of a charcot foot deformity of the right tarsus.

    The motor changes associated with this patient's neuropathy manifested in hammertoe deformities, which predictably led to a distal digit ulceration. A better informed diabetic would have sought care sooner, well before the ulcer had developed into osteomyelitis. Thus, a primary causative agent, it might be argued, was a lack of education.

    The patient presented to the office three weeks after the development of the digital ulceration. He had received minimal care prior to his arrival, consisting of simple wet-to-dry guaze dressing changes.

    click image set to enlarge
    Ulceration at first post-op check following debridement of infected bone and non-viable soft tissue, appropriate wound care.

    Physical Exam

    Initial assessment naturally included evaluation of the wound, vascular status and neurological function, and radiographs. Arterial doppler studies revealed patent pedal vessels, although skin perfusion was reduced, likely due in part to excessive edema with induration of soft tissues. The ulceration itself was fairly typical for the clinical situation, with surrounding hyperkeratosis, the presence of mild amounts of purulence, and gross enlargment of the digit. No actual pain was reported by the patient secondary to neuropathy, nor were systemic signs of infection evident, as is so often the case with a localized diabetic infection.

    Musculoskeletal exam revealed contracture of the lesser digits with increased pressures to the distal aspect of the 3rd digit left. As is the pathogenesis of this condition, mild, non-infectious erythema led to the development of hyperkeratosis. The insensate patient will experience minimal to no symptoms, and only attuned health care specialists will be aware of impending events.

    Plain film radiographs revealed osseous changes consistent with osteomyelitis, including cystic changes, fragmentation and osteolysis.

    click image set to enlarge
    Digit after debridement and excision of osteomyelitic bone and one FREMS treatment.

    Treatment Considerations

    Unfortunately for many diabetics, the terrible triad of immunopathy, neuropathy and vasculopathy combine to create very real and formidable obstacles to healing. "We are held captive by the blood flow" is a very apt saying, and though this individual had sufficient large vessel flow, signs of inadequate perfusion due to microvasculopathy were noted, included hair loss and atrophic epithelium.. The most obvious and accepted therapies, which were utilized here, include debridement of necrotic bone and soft tissue, moist wound healing, and appropriate antibiosis.

    click image set to enlarge
    Ulcerated digit demonstrating progressive healing following seven FREMS treatments

    Unique Treatment

    Utilized in this case was a very new, unique form of electrical stimulation, which employs high negative potential, single-phase electric current pulses, with suitably modulated frequencies and very short durations. These pulses are regulated in frequency, intensity, duration and potential, and act on the surface as well as the deep tissues. FREMS (Frequency Rhythmic Electrically Modulated Stimulation) was designed to take advantage of the belief that the summation of sub-threshold electrical stimuli, conveyed through the skin proximal to a motor nerve in a non-invasive system, would induce composite motor action potentials in excitable tissues.

    This is in stark contrast to a single, low-intensity impulse of brief duration, such as the one delivered by TENS. This is unable to overcome the dielectric skin barrier and thus will not excite the underlying nervous and/or muscle to elicit a recordable motor action potential (MAP). The signal of the FREMS is quite different. Through a specific sequence of weak impulses, with a rapid increase and decrease in pulse frequency and duration, there is a gradual recruitment of MAP in the stimulated tissues.

    The patient's wound closed quickly and progressively, without interruption. An additional benefit to this patient was the associated improvement in sensorium. Because the therapy was utilized to treat the ulceration, it was performed unilaterally. The increase in sensation, as compared to the untreated side, was reported by the patient with signs including improved two point discrimination, vibratory sensation, monofilament detection. Also importantly, this benefit continued, with minimal loss, for eleven months.

    The science and art of wound care has developed rapidly as a field of study in the last few decades. This is evidenced by the explosion of new products and materials now available. Many adjunctive treatments have been developed, with more recent advances including negative pressure wound therapy, hyperbaric oxygen therapy and biological living skin equivalents.

    The FREMS device has been shown through numerous double-blind studies to have several significant and important effects. For example, there are changes in the perfusion velocity in the microcirculation, as well as inducing a long-acting increase in vasomotor activity (with significant changes noted at four months post treatment).

    Some other effects are an increase in the release of growth factors including VEGF, increased blood flow and capillary density encouraging the formation of new granulation tissue. Additionally, there is a significant increase in nerve conduction velocity(MNCV) and a statistically significant reduction of pain after FREMS. On average, at the end of active treatment, MNCV was increased by almost 5 m/s; vibration perception threshold was reduced by more than 2 V; and the number of foot points insensitive to the Semmes–Weinstein monofilament was decreased.

    In this case, healing progressed rapidly upon initiating the FREMS, while the usual armamentarium of antibiosis, appropriate debridement and proper wound care were employed. Osteomyelitic bone was resected during the course of FREMS treatments (typically consists of ten sessions). The presence of infection is not a contraindication to its use, and it seems likely that FREMS aids the process of bacterial eradication by increasing perfusion.

    click image set to enlarge
    Osteomyelitic metatarsal head excision site healing via secondary intention.

    Immunopathy is an important component of the lower extremity problems experienced so frequently by people with diabetes. Yet vasculopathy and neuropathy may be considered the more devastating mechanisms, which lead so often to limb loss, disability, and a drastic reduction in quality of life. Those studies performed to date appear to indicate that we have a new and powerful tool that may significantly alter the natural history of this condition, leading to morbidity and mortality. No side effects or complications from it's use have been experienced, and though perhaps not all will experience such dramatic effects as this patient did, it appears certain that this modality has the potential to drastically change the outcomes of diabetic patient care and maintanence.

    Sincerely,

    Conway McLean

    ###

    REFERENCES:

    • Barrella M, Toscano R, Goldoni M, Bevilacqua. Frequency rhythmic electrical modulation system (FREMS) on H-reflex amplitudes in healthy subjects. Eura Medicophys 2007, 43: 37-47.
    • Bevilacqua M, Barrella M, Toscano R et al (2004) Disturbances of vasomotion in diabetic (type 2) neuropathy: increase of vascular endothelial growth factor, elicitation of sympathetic efflux and synchronization of vascular flow (vasomotion) during frequency modulated neural stimulation (FREMS). 86th Annual Meeting of the Endocrine Society, p 321, P 2–61 (abstract)
    • Bevilacqua M., Baruffaldi L., Foddis L., Toscano R., Vago. Increase of  Vascular Endothelial Growth Factor by Electrical Stimulation with High Varialbility in Frequency and Amplitude: a clinical study in non-insulin dependent diabetics with limb ischemia. 85th International Congress of Endocrine Society, Philadelphia, June 2003
    • Bevilacqua M. et al. – Increase of Vascular Endothelial Growth Factor (VEGF) by FREMS. A clinical study in Non-Insulin Dependent Diabetics with Limb Ischemia. Presented at ENDO 2003 – Endocrinology Society’s 85th annual meeting – Philadelphia.
    • Bosi E, Conti M, Vermigli C, et al. Effectiveness of a novel frequency modulated electro-magnetic neural stimulation in the treatment of painful diabetic neuropathy. Diabetologia 2005, 48: 817-23
    • Ciancia, et al. Diabetic plantar ulcer treated with an innovative thearpy - FREMS (frequency modulated  electro-magnetic neural stimulation).  Italian Society of Gerontology and Geriatics, Florence; Palazzo Congressi 9-13 November 2005
    • Combi F. Application of novel neuromodulation for skeletal muscle regeneration following chronic fobrosis process. The Rehabiliation of Sports Muscle and Tendon Injuries-Milano April 2004
    • Conti M., Peretti E., Cazzetta G., Folini L., Vermigli C., Galimberti G. Frequency modualted electromagnetic neural stimulation enhances cutaneous microvascular perfusion in patients with diabetic neuropathy. 42nd Annual Meeting of the European Association for the Study of Diabetes, Copenhagen Sept. 2006
    • Da Ros R., C. Vitale, R. Assaloni, A. Ceriello  Neuromodulation FREMS in the treatment  of diabetic peripheral arterial disease. 42nd Annual Meeting of the European Association for the Study of Diabetes, Copenhagen Sept. 2006
    • Facchini M.G., Mambelli E., Checchia G., Gaggi R., Santoro A., The Lorenz Therapy: a new tool in the treatment of uremic neuropathy. European Dialysis and Transplant Association, Lisbona May 2004.
    • Farina S., Casarotto M., Benelle M., Tinazzi M., Fiaschi A., A randomized controlled study on the effect of two different treatments (FREMS and TENS) in myofascial pain syndrome. EUR MED PHYS 2004; 40:293-301
    • Guggi S, Cavina U. Experience of a novel transcutaenous neuromaodulation as first approach to muscle injuries. XIV International Congress on Sports Rehabilitation and Traumatology, Bologna 2005
    • Kumar D, Marshall HJ (1997) Diabetic peripheral neuropathy: amelioration of pain with transcutaneous electrostimulation. Diabetes Care 20:1702–1705
    • Scionti L., Conti M., Vermigli C., Cazzetta G., Galimberti G., Bosi E. A new treatment for painful diabetic neuropathy: the Frequency Modulated Neural Stimulation (FREMS). NEURODIAB, Resensburg, Germany
    • Zhao M. Bai H, Wang E, Forrester J.V., McCaig CD. Electrical stimulation directly induces pre-angiogentic responses in vascular endothelial cells by signaling through VEGF receptors. J Cell Sci 2003:117.395-405.


    Lorenz NeuroVasc is a Canadian company operating as the exclusive supplier of FREMS™ technology to the North American healthcare industry.

    FREMS™ technology is the product of Lorenz Biotech S.p.A. of Modena, Italy, and is rapidly being adopted as a preferred treatment option in the European markets.

     

    — Products —
    FREMS™ is a composition of electrical signals characterized by negative and multi-modulated pulses which mimic different electrophysiological processes.
    Aptiva™ Ballet is the ideal device for the treatment and clinical research of peripheral nervous and vascular systems diseases.
    Aptiva™ Move is the portable and flexible choice in rehabilitation.
    To learn more about Lorenz Neurovasc and its products and services, 
    visit www.lorenzneurovasc.ca or call toll free at 1.866.443.8567.


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    Posted by: PV Mayer at 12:18 pm 2 comments - Add a Comment Category: FREMS


    You Can't Manage What You Can't Measure (2 Sep, 2011)

    Wouldn't this be a great application for the treatment of the diabetic foot!

    A partnership between the Mayo Clinic and the minds behind IBM's Watson technology is close to completing development of tools to mine data from electronic health records that speak different digital languages.

    The goal is to "safely and securely convert stores of electronic health records into a bottomless pool of real-world clinical knowledge," the Mayo Clinic says in a news release. Reaching that goal requires the ability to glean information from a variety of EHRs that tag and store clinical information in different, often proprietary, digital formats.

    So far, investigators with the Mayo-led team have used "natural language processing tools" to pull information from the records of 30 patients with diabetes and run it through computing systems developed with IBM's Watson Research Center, a process that transforms the data into 134 billion pieces of information, according to the clinic. (Watson is the language-recognition computer that recently won a Jeopardy! challenge against two of the game show's best human players.)

    HHS believes that mining EHRs for clinical information can lead to improved care by allowing researchers to learn from trends and treatment successes across the country.

    "This gets to the heart of meaningful use," says Lacey Hart, Mayo's SHARP administrator, in the news release. "It's one thing to meet the government requirement that you should have an electronic record, but it's another thing, once you have that record, to make meaning out of it."

    The project is one of four funded by the $60 million Strategic Health ITAdvance Research Project (SHARP) program, an initiative of the U.S. Department of Health and Human Services through its Office of the National Coordinator for Health IT.



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    Posted by: PV Mayer at 06:48 am 2 comments - Add a Comment Category: Research


    An Excellent Case Study on the Diabetic Heel Ulcer by Dr. Jay Lieberman (2 Sep, 2011)

    Case Presentation: Decubitus Ulcer at Its Worst

     
    Jay Lieberman, DPM, FACFAS
    by Jay Lieberman
    DPM, FACFAS

     

    Decubitus ulcers are caused by pressure, sheer, and friction.  The patient presented here had compromised blood flow.  The additional pressure on the heel deformed the vascular bed and precipitated the necrosis/ischemia.  If a decubitus ulcer is stable, my protocol is to evaluate the vascular status, hydrate anhydrotic skin, address any potential infections, optimize nutrition, offload the area (preventing friction and sheer), and have the patient ambulate if possible.

    This 54-year-old insulin dependent diabetic was initially treated for a sterile bullae on the posterior aspect of the left heel.  There was no precipitating acute trauma or thermal injury. 

    PAST MEDICAL HISTORY:   This includes hypertension, diabetes, peptic ulcer and osteoarthritis.

    MEDICATIONS:  Catapres, Lovenox, Insulin, Zestril, Lisinopril and Reglan.

    ALLERGIES:  Percocet

    FAMILY HISTORY:  Diabetes, history of GI bleed.

    SOCIAL HISTORY:  Previous history of smoking, ceased more than ten years ago.

    SURGICAL HISTORY:  The patient has had left toe amputation, right ankle surgery times two, cholecystectomy and trigger finger release.


    Activity Level

    TREATMENT AND COURSE

    After two weeks, the bullae dried into a gangrenous eschar with minimal moist necrosis in the deeper layers.  The eschar was loosely adhered to the heel.  The patient was seen weekly for debridement of devitalized tissue. 

    A L’Nard splint was utilized to offload the area.  Home healthcare did daily assessments and applied enzymatic debridement agents with dressing changes.

    This patient slowly developed a poor quality granulating base.  Although there was some evidence of improvement, new areas of necrosis were seen.  After some time, a component of the Achilles tendon could be visualized.  Her pain level was between a 5 or 6 out of 10, giving a high suspicion that ischemia was a larger component of the problem than originally thought.

    The patient was sent for a vascular evaluation.  Peripheral flow to her leg was marginal at best.  Stent placement would be considered, only if the wound would not heal, as patient was not an ideal candidate for surgical intervention.  The arterial Doppler suggested partial occlusion of the femoral artery with calcifications in the distal branches. 

    Two months after the initial presentation, the patient came to the office with large bullae formation along the medial and lateral walls of the calcaneus.

    Infectious Bullae Medial Wall  
    Bullae Lateral Wall (post debridement)
    Moist necrosis Heel with MRSA
    Infectious Bullae Medial Wall 
    (post debridement)
    Bullae Lateral Wall (post debridement)
    Moist necrosis Heel with MRSA

    Erythema, fluctulance and drainage were readily apparent.  Cellulitis and lymphangitis were noted.  Cultures taken at that time indicated a MRSA infection. 

    The patient was admitted to the hospital and started on Vancomycin.  An MRI indicated marrow signal changes in the posterior calcaneus compatible with osteomyelitis. 

     

    Standard x-rays showed loss of normal cortical structure. 

    MRI Standard Radiograph
    MRI
     
    Standard Radiograph

    Hospital Admission

    Upon admission, the patient’s WBC was 22, 000.  Blood glucose was 360.  Blood cultures were negative.  After 48 hours, a partial calcanectomy was performed with wound debridement. 

    Upon admission, the patient’s WBC was 22, 000. Blood glucose was 360. Blood cultures were negative. After 48 hours, a partial calcanectomy was performed with wound debridement. 

    Postoperatively negative pressure wound therapy was initiated.

    VAC in place  
    VAC in place
    VAC in place

    2nd Hospital Admission

    During a subsequent hospitalization, stents were placed in the left leg.  The quality of the granular bed improved markedly over the next two to three weeks. 

    Ultimately, a GRAFTJACKET® t was applied to the heel to further promote healing.  Below is the most recent photograph showing the patient at one month status post surgery.

    Graft Jacket AppliedOne month post-opOne month post-op
    GRAFTJACKET® Applied
    GRAFTJACKET® from KCI
    One month post-op

    Two Month Post-op 
    10 weeks post-op
    Two month post-op
     
    10 weeks post-op

    At this point the options available to us are:

    1. Hyperbaric Oxygen Therapy to promote further neovascularization
    2. Debridement of undermined tissue with second application of synthetic skin
    3. Debridement of undermined tissue with direct application of split thickness skin graft
    4. Application of silver dressing to decrease bacterial load


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    Posted by: PV Mayer at 06:20 am 2 comments - Add a Comment Category: Diabetic Foot Ulcer Treatment


    A Tribute to the Master: Dr. Paul Brand (2 Sep, 2011)

    Paul Brand – Missionary and Pioneer

    At this year's Desert Foot Multidisciplinary High Risk Foot Seminar (Nov 16- 18, AZ Grand Resort in Phoenix) we will be honoring a true legend with the inauguration of our Annual Paul Brand Memorial Lectureship. Some of you may have no idea who this remarkable man was (even though you all practice with the principles that he taught us). If you treat a neuropathic foot, you are approaching that high risk foot with the guidance that Dr Brand offered over his many years of practice and writings.

    Paul Brand, MD (July 17, 1914 - July 8, 2003)
    Paul Brand, MD
    7/17/1914 - 7/8/2003
    Paul Brand, MD (July 17, 1914 - July 8, 2003)was a Christian Missionary working in Vellore, India at a Leprosy Mission for many years (1946-1966). A trained Orthopaedic Surgeon, Dr. Brand, who grew up the son of English missionaries to South India, achieved world renown for his research on leprosy and related research on the dynamics of pain. He was a pioneer in developing tendon transfer techniques for use in the hands of those with leprosy (Hansen's Disease). He was the first physician to appreciate that leprosy did not cause the rotting away of tissues, but that it was the loss of the sensation of pain which made sufferers susceptible to injury. 
    If you treat a neuropathic foot, you are guided by Dr. Brand's seminal work
    Brand contributed extensively to the fields of hand surgery and hand therapy through his publications and lectures, and wrote popular autobiographical books about his childhood, his parents' missionary work, and his philosophy about the valuable properties of pain.

    His book, Pain: The Gift Nobody Wants, one of several of his reflections on physiology, combines autobiography, stories of research, and reflections on pain and pain management. Indeed, still today we hear renowned lecturers use that same term to describe the affliction of diabetic persons with neuropathy — and how that loss of protective sensation robs them of the "gift of pain" that can protect their limbs from injury.

    He wrote the book and coined the phrase, Pain: The Gift Nobody Wants

    In 1966, after 19 years of service in India, he moved to the U.S.A. to become the Chief of Rehabilitation Branch at the National Hansen’s Disease Center at Carville, Louisiana. He worked there for 20 years and established a well-equipped and well-staffed research unit to study the complications of insensitive hands and feet, their prevention and management. During his time in Carville, he trained a number of podiatrists, physicians, and physical therapists and became well known for his understanding of neuropathic injuries to the lower extremities in leprosy as well as diabetic patients. He also introduced the concept of moderate repetitive stress (through his experiments on the footpads of mice) as the underlying etiology for the majority of neuropathic foot lesions.
    Brand introduced the concept of moderate repetitive stress as the underlying etiology for the majority of neuropathic foot lesions.

    His methods for prevention and management of plantar ulcers have subsequently been widely adopted for treatment of patients with diabetes mellitus. Brand reintroduced and popularized the Indian technique of total contact casting for effective offloading of the ulcerated neuropathic foot.

    I first met Dr. Brand in 1978 as a new practitioner when I visited him in Carville to learn of his theories and principles. When he retired in 1986 from the U.S. Public Health Service, he moved to Seattle and continued his teaching as  Emeritus Professor of Orthopaedics at the University of Washington. I again met him in Atlanta in 1996 at the American Diabetes Association Meeting, where he was awarded the prestigious Roger Pecoraro Award from the Foot Care Council, which I had the great honor to receive this year.  His lecture on the Biomechanics of the Insensitive Foot was a stirring account of his life and research on neuropathic deformities and injuries. The lecture certainly warranted the standing ovation that he received after its delivery!  My final encounter with Dr Brand was at the APMA National Meeting in Seattle in 2002, where he also was a guest speaker.  The photo attached was taken at that meeting where you can see Paul Brand flanked by a much younger me (right) and the world renowned diabetic foot expert, Professor Andrew Boulton of Manchester, U.K.

    Professor Andrew Boulton, Paul Brand and yours truly, Robert Frykberg at the APMA National Meeting in Seattle in 2002

    Professor Andrew Boulton, Paul Brand and yours truly, Robert Frykberg at the APMA National Meeting in Seattle in 2002