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Foot Infections in the Veterans Health Administration

Posted on September 30, 2015 | Comments Off on Foot Infections in the Veterans Health Administration

by Priya P. Sundararajan DPM, FACFAS1, Barbara M. Porter DPM2, Keith A. Grant Ph.D3, Jeffrey M. Robbins DPM4pdflrg

The Foot and Ankle Online Journal 8 (3): 1

BACKGROUND: Foot infections represent a major health concern in the Veterans Health Administration as they often may lead to limb loss. A majority of these infections are associated with diabetes in the form of diabetic foot ulcers. The diabetic foot infection is associated with a substantial mortality rate and often requires amputation to fully address the nidus of infection.
METHODS: A retrospective chart analysis of all surgeries to treat foot infections in an 18-month period was conducted. Multiple variables- patient location, preventative primary care diabetic foot screenings, routine follow-up by a foot-care specialist, and pre-operative hospital admission- were reviewed and recorded. The data was analyzed using a one-tailed z-test and chi-squared tests. The one-tailed z-test provided a facility-specific data analysis highlighting areas which may benefit from education or assistance in terms of resource allocation. The chi-squared tests reveal generalizable findings regarding the association among primary care diabetic foot screenings, routine follow-up by a foot-care specialist, and the need for pre-operative admission.
RESULTS: Results show an absence of routine follow-up by a foot-care specialist is associated with a statistically higher rate of patients requiring pre-operative admission. Conversely, those patients with routine follow-up required fewer admissions. Though not significant at conventional levels, a higher percentage of patients without the primary care diabetic foot exams also lacked specialty follow-up and necessitated pre-operative hospital admission when compared to patients with the screenings.
CONCLUSION: This study provides an example of methodology reviewing pedal infection-related surgical data to perform effective limb loss prevention in the VHA setting. The generalizable results elucidate the role of the primary care and foot-care specialists in preventative medicine thereby avoiding a hospital admission. The current study suggests that a close, collaborative, patient-centered approach between primary care and podiatry results in better outcomes for patients.

Key words infection, ulcer, diabetic foot, veteran, amputation

ISSN 1941-6806
doi: 10.3827/faoj.2015.0803.0001

Address correspondence to: Priya P. Sundararajan DPM, FACFAS
[1] Director of Podiatry, Wilmington VA Medical Center, Department of Surgery, 302-994-2511, 1601 Kirkwood Highway Wilmington, DE 19805, Priya.Sundararajan@va.gov
[2] Podiatric Surgeon, Wilmington VA Medical Center, Department of Surgery,  302-994-2511, 1601 Kirkwood Highway Wilmington, DE 19805, Barbara.Porter3@va.gov
[3] Assistant Professor, James Madison University Department of Political Science, 540-568-4336, 91 E Grace St., MSC 7705 Harrisonburg, VA 22807, GrantKA@jmu.edu
[4] Director, Podiatry Service Veterans Affairs Central Office; Professor of Podiatric Medicine, Kent State University College of Podiatric Medicine; Clinical Assistant Professor, Case Western Reserve University School of Medicine; 216-791-3800, Louis Stokes VA Medical Center, 10701 East Boulevard Cleveland, OH 44106, Jeffrey.Robbins@va.gov

Foot infections are a major health issue in the Veterans Health Administration as they often jeopardize limb preservation and shorten the patient’s lifespan. A majority of these infections are associated with diabetes in the form of diabetic foot ulcers (DFU). The excessively high 5-year mortality rate associated with patients with diabetic ulcers reaches upwards of 55% [1]. With chronicity, the DFU transitions to bone infection. A festering oste-omyelitis further propagates the pedal nidus of infec-tion resulting in a statistically higher rate of fatal sys-temic disease such as heart attack or stroke [2,3,4]. Consequently, 45% of all patients with a diabetic ulcer require surgery, often times a pedal amputation, to address the nidus of infection and reach resolution of symptoms [5]. Effective preventative care can maximize limb preservation and improve life expectancy.

As the single largest health care system in the United States, the Veterans Health Administration (VHA) is working to meet the complex needs of this dramatically increasing pathology [6]. Primary care providers, podiatric surgeons, general surgeons, vascular surgeons, infectious disease physicians, and wound care nurses are integrated in the treatment of the diabetic foot infection.  In the enormity of the VHA system, providers can be oblivious to the amputation-related statistics that may improve patient outcomes.  A facility-specific assessment allows providers to better understand the events leading up to the amputation and prevent long-term loss of follow-up. Such evidence can inform future strategies to effect better prevention and management of the DFU pathology. The aim of this study is two-fold: 1) to provide an example of a retrospective statistical analysis assessing facility-specific data regarding preventative care and patient outcomes for the benefit of other VHA facilities and 2) to understand the associations among preventative primary care diabetic (PC DM) foot exams, routine follow-up by a foot-care specialist, and pre-operative hospital admission in the VHA setting.

Methods

A retrospective analysis of all surgeries to address pedal ulceration infections between January 1, 2013 and June 30, 2014 were analyzed using one-tailed z-tests and chi-squared tests. The following data was collected for each infection-related pedal surgery: chronological surgery number, chronological patient number, location following the patient, whether a preventative PC DM foot exam was performed, whether the patient’s condition required pre-operative hospital admission, if so the date of admission and the reason necessitating admission, dates of podiatric/surgical/wound care follow-ups the patient had prior to admission or surgery (in the case of no admission), whether the patient was routinely followed or not followed by a foot-care specialist prior to surgery, the date of surgery, and an update regarding the patient’s condition.  Patients who went on to have further limb amputation or endured further complication related to the pedal infection were classified as “poor prognosis.” On the contrary, patients who healed the surgical sites were classified as “healed surgical site.” A description of the data collected is detailed and summarized in Table 1 (see supplement within PDF). Table 1 was analyzed using both one-tailed z-tests (Table 2) to understand facility-specific trends and chi-squared tests (Table 3-5) to examine the association between PC DM foot screenings, routine follow-up by a foot-care specialist, and pre-operative hospital admissions.

The locations from which the patient was referred included the main medical center: Wilmington, surrounding community based outpatient clinics (CBOC) A, B, C, and D, and a nursing home: Community Living Center (CLC). The CBOC facility location was withheld for this publication. Some patients were also referred from the neighboring Coatesville VA medical center.  Patient follow-up data was not readily available from this facility, leading to the exclusion of patients originating from this location from the analysis. The variables (PC DM foot screening, specialty follow-up, admission, and surgery) measured in each facility were compared against each location’s outpatient population share as the base value (Table 2). Additional analysis was also performed to test for dependencies between the variables: preventative PC DM foot exams, specialty follow-up prior to surgery, and pre-operative hospital admissions (Tables 3-5).

The PC DM foot exam is a clinical reminder to be completed by the primary care provider as required by “VA/DoD Clinical Practice Guidelines for the Management of Diabetes Mellitus in Primary Care“ [7]. This reminder ensures that DFU prevention is performed in the primary care sector. This alert is only activated at the anniversary of the patient’s last exam. The alert remains active until the test is performed by the provider at which point the test is de-activated for another calendar year.  If the PC DM foot exam was either not performed or performed within a week of admission or surgery, the exam was considered non-preventative as it served no preventative use once the patient required surgical intervention.

table2

Table 2 One-tailed test comparing the variables measured in each location. Statistical significant findings are in bold.  Down-arrow: Findings are statistically lower than expected. Up-arrow: Findings are statistically higher than expected.

table3

Table 3 Χ2 = 9.9676, p = 0.008.  A statistically significant relationship was found between patients who were not followed by a foot-care specialist and those who were admitted.

The specialty follow-up dates, (as listed in column 5 in Table 1), dictated if the patient was adequately followed by a foot-care specialist (as noted in the adjacent column, column 6). By recording the patients’ last 3 podiatry, surgery, or wound care visits, the investigators were able to assess if the patient had regular follow-ups prior to surgery.  At these visits, all components of the diabetic foot exam were assessed. ADA guidelines suggest that a high-risk patient with a history of amputation or ulceration be seen by a specialist every 1-2 months [8]. To give the patients and providers some leeway, the patient was considered “not followed” if he/she was not seen within 3 months preceding admission or surgery.

table4

Table 4 Χ2 = 2.0563, p=0.152. No statistically significant association was found between patients who did not have a PC DM foot screening and those who were not followed by a foot-care specialist. However a higher percentage of patients who had a PC DM foot exam were also followed by a foot-care specialist. The converse also held true.

 table5

Table 5 Χ2 = 1.6067, p=0.205. No statistically significant association was found between patients who did not have a PC DM foot screening and those who were admitted. However a higher percentage of patients with no PC DM foot exam were admitted compared to patients with a PC DM foot exam. Similarly, most of the patients who were not admitted had a prior PC DM foot screening.

Results

Over the 18-month period, 53 surgeries were performed to treat foot infections on 44 patients. Of these surgeries, 92% were amputations (n=49). Fifty-six percent of the surgeries (n=30) required pre-operative admission. Of the admissions, 95.8% occurred secondary to a foot infection. Only 3.7% of the surgeries were performed on non-diabetic patients (n=2). Forty-four percent of the surgeries were performed on patients who were not followed regularly (<3 months). As a result of foot infection, 7.5% of the pedal surgeries (n=4) were associated with further limb amputation. Five of the surgeries were classified as “poor prognosis”, i.e. the patient was expected to or did lose limb or life and was associated with an unresolved pedal infection. One of these patients, healed the surgical site but subsequently developed severe hypotension, multiple bodily pressure lesions, and died from septic shock.

The one-tailed z-test was used to identify patterns within the variables that were disproportionate to that facility’s population share.  For example, a CBOC serving 15% of the population would be expected to account for 15% of the performed surgeries.  This location-specific analysis demonstrates significantly fewer infection-related pedal surgeries, missing PC DM foot exams, and pre-operative admissions out of the Wilmington facility than would be expected relative to its population share alone (table 1).  In contrast, CBOC A has a significantly higher rate of surgeries, missing PC DM foot exams, and admissions than its population share would suggest.  CBOC C also has more admissions than would be expected, but the number of surgeries and missing PC DM foot exams are not overly disproportionate to its population. Additionally, a higher than expected number of patients were regularly followed in CBOC C prior to surgery. As expected with the typical nursing home population, the CLC has a higher rate of surgery, specialty follow-up, pre-operative admissions, and poor prognosis (60%).  No significant findings were noted in CBOC B and D.

Although the above results are idiosyncratic to the Wilmington medical center and surrounding CBOCs, patterns identified in the aggregate data are generalizable to other VHA systems. Chi-squared tests were used to assess bivariate statistical dependencies in which the presence or absence of one factor influences the rate with which another factor occurs. Analysis confirmed a significant relationship (p=0.008) between patients who were not followed by a foot-care specialist to those who necessitate pre-operative admission (table 2). The observed relationship suggests that high-risk patients who are not routinely followed by a foot-care specialist are more likely to require admission than those who are routinely followed. In fact, the odds of a patient without routine specialty follow-up requiring pre-operative admission is roughly 7.5 times higher than for a followed patient.  No statistically significant relationship was found between patients without PC DM foot screenings and those followed (p=0.152) and admitted (p=0.205) at conventional levels (table 3, 4). However based on percentages, certain trends among these variables seem apparent.  Patients without the preventative PC DM foot screenings tended to also lack follow-up by a foot-care specialist (table 3). The converse also held true. Similarly, a higher percentage of the patients without the PC DM foot exam required pre-operative hospital admission when compared to patients with the screening (Table 4).

The Wilmington facility was associated with statistically fewer infection-related pedal surgeries, fewer missing PC DM foot exams, and fewer admissions than its population share would suggest. This site had fewer adverse events preceding the patient’s surgery and overall fared better in the preventative arena than its CBOC counterparts. These comparatively better outcomes coincided with the most resource-intensive location. As a result, the Wilmington facility assisted in the evaluation in slow or non-healing ulcer patients from the CBOC facilities.

The overlap between CBOC C patients who required surgery and those were admitted was 100%. Moreover, 85% of these surgeries were associated with routine follow-up prior to surgery. These clinical outcomes are suggestive of a lack of efficacy in preventative care in this location.  In CBOC A, 87.5% of surgeries required pre-operative admission, which is significantly higher than would be expected based on its population share. Our solution was to request the foot-care specialists in both CBOC A and C to send all non-healing ulcers with a duration greater than 3 months to Wilmington for evaluation and possible treatment.  In terms of resource allocation, funds for part-time nail technician were requested for CBOC A and C to allow the providers to focus on the higher risk patient population. Additionally, 75% of surgeries out of CBOC A did not have preventative PC DM foot evaluations in the year prior to surgery. Our remedy was to present a facility-wide educational lecture discussing these results and the importance of preventative care in the treatment of DFU.

As expected, patients residing in the CLC were associated with a higher rate of pedal surgery with subsequent limb amputation. With its census of patients who are elderly, immobilized, poorly-vascularized, non-responsive, or systemically complicated, a proper treatment addressing the nidus of infection is often not accomplished. We advised the dedicated CLC wound care nurse who performs weekly wound assessments to consult podiatric or general surgery for new wounds in a timely manner. In addition, the Wilmington wound care nurses have assisted in CLC management and prevention of ulcers.

Discussion

The current study demonstrates the value of collaboration between primary care and specialty care for the treatment of diabetic foot infections in the VHA setting. It is the first in its class to present an example of methodology reviewing pedal amputation and infection-related surgical data for limb loss prevention in the integrated VHA system. This facility-specific research focusing on the circumstances surrounding surgery was conducted to assess the efficacy of preventative measures and effect change to better patient outcomes. As it stands today, data collection and analysis for the purpose of limb preservation is not a routine occurrence in the VHA. The present study uses the data collected to highlight areas of concern and allow implementation of minor changes to effectively manage high-risk diabetic patients.  This methodology can be applied in any facility and may directly impact departmental reorganization, resource allocation, and provider or patient education. The present research is also suggestive of a collaborative relationship between of primary care and foot-care specialists in the management and mitigation of diabetic pedal infections. Prior to this study, the associations of these variables and the need for pre-operative hospital admission were not evident. Our results encourage a partnership between primary care providers and foot-care specialists, including podiatrists, general surgeons, and wound care specialists for early detection of pedal infections, thereby minimizing the need for pre-operative hospital admissions in VHA facilities.

Results indicate CBOC A was associated with a higher rate of surgical interventions for foot infections as well as a lower rate of completed preventative PC DM foot exams. One explanation suggests that fewer providers examining the diabetic foot may lead to undetected foot ulcers, propagate the infection, and result in an amputation. Previous studies have indicated that an increased number of providers examining the diabetic foot resulted in fewer infection-related surgeries [9,10]. A study originating in Sweden demonstrates a lower amputation rate in a region in which patients were referred by a variety of providers in contrast to only referrals from general practitioners, suggesting that the more providers examine the diabetic foot, the earlier infection is treated [9]. Another analysis documents the reduced rate of amputation with early detection of DFU [11]. With the addition of nail technicians, we increase the number of providers examining the diabetic foot. Along with the current study, these investigations illustrate the importance of cross-collaboration between specialties for the early detection and subsequent referral to a specialized diabetic wound care team.

Patients originating from CBOC C were routinely followed prior to surgery but nonetheless required admission prior to surgical intervention. This finding questions the efficacy of preventative treatment received in this facility and is suggestive of the need for education, resources, or further referral to a more specialized team. Similarly, CBOC A was associated with a significantly higher than expected rate of surgeries and admissions. As a hospital admission rather than an outpatient consult usually confers a more serious infection, the presumption that superficial infections are permitted to devolve into deeper more consequential infections is suggested. One plausible hypothesis to explain the higher rate of amputations is that care may not be adequately appropriated for the higher risk patients. Often times, VA podiatric providers are inundated with the lower risk routine nail patients leaving limited resources available for the higher risk patients with ulcers.  The American Diabetes Association task force recommends that high-risk patients (history of ulceration/amputation) be evaluated by a foot-care specialist every 1-2 months, whereas low risk diabetic patients may be evaluated annually by a primary care provider or specialist when necessary [8,12-14]. The addition of a nail technician in CBOC A and C could offload the low-risk patients allowing the providers to focus on the patients at a higher risk for amputation. Moreover, the request for the CBOC facilities to refer their long-standing DFU (> 3months) to the Wilmington facility benefits the CBOC patients. With the Wilmington facility having statistically lower rates of infection-related surgeries and admissions, the patients in the lesser performing facilities are likely to have more positive clinical outcomes with an earlier referral.

The purpose of the study was not necessarily to avoid pedal amputation but to maintain optimal compliance in the events preceding the surgery. Many providers have associated the word “amputation” with a negative connotation as in the case of “amputation prevention.” However evidence-based medicine suggests that patients who avoid amputation and live with chronic osteomyelitis generate a chronic inflammatory response by triggering vascular atherosclerosis [3,15]. A population-based study in a cohort of 23 million studied the relationship between chronic osteomyelitis and coronary heart disease [15]. Once the researchers controlled for age, gender, hypertension, diabetes, hyperlipidemia, and stroke between the control and chronic osteomyelitis cohorts, they found a significantly elevated risk of heart disease- a 95% increase- as compared to the control population [15]. Similar findings were supported in a meta-analysis study evaluating the association of the DFU and cardiovascular mortality [3]. Results showed a substantially increased risk of all-cause mortality, fatal myocardial infarction, and fatal stroke in patients with DFU [3]. These studies are among the growing number of studies that support a timely resolution of the DFU thereby preventing limb loss and increasing life expectancy [3,15-20]. The 30-day mortality rate, cardiovascular outcomes, and pulmonary events associated with a pedal amputation is substantially lower (4x) than below-knee or above knee amputations [17-20]. The goal is not simply to avoid amputation but to recognize the time-sensitivity of reaching a permanent resolution, thereby broadening our perspective to prioritize limb and life preservation.

Results derived from the full dataset suggest that the more high risk patients are followed by foot-care specialists, the less likely the infection will progress to a degree that necessitates admission (table 2). On the patient-level, routine follow-up generally translates to earlier detection of infection or vascular impairment, fewer systemic complications, and lower potential for nosocomial infections. From the facility standpoint, a substantial financial and economic burden can be obviated for each avoidable hospitalization.  Studies show that on average each hospital admission for a pedal amputation costs the facility is approximately $32,000 [21]. This confirms the role of foot-care specialists in the treatment of diabetic foot infection and limb loss prevention as documented in previous studies [22,23]. The present study also demonstrates a positive trend between PC DM foot screenings and follow-up by a foot-care specialist in the VHA setting (table 3). Thus the domino effect between the absence of PC DM foot screening and patients necessitating pre-operative admission is evident. The direct impact of fewer PC DM foot screenings and a higher rate of admission follows a negative trend, though not statistically significant at a conventional level (table 4). The current study, specific to the VHA system, is among the increasing evidence supporting the interdepartmental collaboration to improve patient outcomes and reduce complications [23-25].

Limitations to this study are inherent to any retrospective analysis in that all variables cannot be examined. Regarding the one-tailed z-test, extraneous variables such a provider methodology, patient non-compliance, reason for lacking specialty follow-up, or location-specific resources such as casts, grafts, or personnel assistance were not assessed. However, these extrinsic factors do not diminish current results highlighting areas that may benefit from assistance or modification. This study provides perspective in regards to the number of surgeries rather than the number of patients. Therefore, some patients had repeat infection-related surgeries; this variable was not assessed.  In regards to the chi-squared tests, the variables studied (specialty follow-up, PC DM foot assessments, and pre-operative admission) are generalizable among the VHA facilities nationwide. However, small sample size biases against statistically significant results. For example, the findings regarding PC DM foot screenings and specialty follow-up or admissions are likely to be significant by conventional standards with a larger sample following the current trends. Future research specific to the treatment of pedal infections or DFU may help determine which strategies and wound therapies will improve amputation prevention in this high-risk population. We encourage all VHA facilities to retrospectively assess the variables affecting patient outcomes and study the associations between these variables to better patient outcomes.

In summary, by focusing on the situations surrounding the surgical treatment of pedal infections or amputation, each facility is able to perform self-assessments to improve patient care. We believe that only with a self-investigative approach can limb preservation be legitimately pursued. By assessing relevant variables we demonstrate the value of foot-care specialists and primary care providers in the treatment of diabetic foot infections in a VHA facility. This patient-centered approach facilitates earlier detection of infection, mitigates systemic complications, decreases the economic burden to the facility, and ultimately minimizes limb loss.  With interdepartmental collaboration, we are able to prioritize limb preservation for veterans who have already sacrificed so much.

References

  1. Moulik PK, Mtonga R, Gill GV: Amputation and morality in new-onset diabetic foot ulcers stratified by etiology. Diabetes Care 26(2): 491-4, 2003. (PubMed)
  2. Bortoletto MS, de Andrade SM, Matsuo T, Haddad MC, González AD, Silva AM: Risk factors for foot ulcers- a cross sectional survey from a primary care setting in Brazil. Prim Care Diabetes 8(1):71-6, 2014. (PubMed)
  3. Brownrigg JRW, Davey J, Holt PJ, Davis WA, Thompson MM, Ray KK, Hinchliffe RJ: The association of ulceration of the foot with cardiovascular and all-cause mortality in patients with diabetes: a meta-analysis. Diabetologia 55(11):2906-2912, 2012. (PubMed)
  4. Subramaniam B, Pomposelli F, Talmor D, Park KW: Perioperative and Long term morbidity and mortality of above-knee and below-knee amputation in Diabetics and Nondiabetics. Anesth Analg 100:1241-7, 2005. (PubMed)
  5. Apelqvist J, Larsson J, Agardh CD: Long term prognosis for diabetic patients with foot ulcers. J Intern Med 233(6):485-91, 1993. (PubMed)
  6. Miller DR, Safford MM, Pogach LM: Who has diabetes? Best estimates of diabetes prevalence in the Department of Veterans Affairs based on computerized patient data. Diabetes Care 27 (Suppl. 2):B10–B21, 2004. (PubMed)
  7. VA/DoD Clinical Practice Guideline for the Management of Diabetes Mellitus in Primary Care 102-114, 2003. (Link)
  8. American Diabetes Association: Consensus Development Conference on Diabetic Foot Wound Care. Diabetes Care 22(8): 1354-60, 1999. (PubMed)
  9. Apelqvist J, Larsson J. What is the most effective way to reduce incidence of amputation in the diabetic foot?. Diabetes Metab Res Rev 16(Suppl 1):S75–S83, 2000. (PubMed)
  10. Larsson J, Apelqvist J, Agardh CD, Stenström A. Decreasing incidence of major amputation in diabetic patients: a consequence of a multidisciplinary foot care team approach?. Diabet Med 12(9):770-6, 1995. (PubMed)
  11. McCabe CJ, Stevenson RC, Dolan AM. Evaluation of a diabetic foot screening and protection programme. Diab Med 15:80–84, 1998. (PubMed)
  12. Apelqvist J, Bakker K, Van Houtum WH, Nabuurs-Franssen MH, Schaper NC. International consensus and practical guidelines on the management and the prevention of the diabetic foot. Diabetes Metab Res Rev 16: S84-92, 2000. (PubMed)
  13. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care 31(8): 1679-85, 2008. (PubMed)
  14. Frykberg RG, Armstrong DG, Giurini J, Edwards A, Kravette M, Kravitz S, Ross C, Stavosky, Stuck R, Vanore J. Diabetic foot disorders: a clinical practice guidelines. J Foot Ankle Surg 45(5 Suppl):S1-66, 2006. (PubMed)
  15. Hsiao LC, Muo CH, Chen YC, Chou CY, Tseng CH, Chang KC. Increased risk of coronary heart disease in patients with chronic osteomyelitis: a population-based study in a cohort of 23 million. Heart 100:1450-1454, 2014. (PubMed)
  16. Schofield CJ, Libby G, Brennan GM, MacAlpine RR, Morris AD, Leese GP. Mortality and Hospitalization in Patients After Amputation: A comparison between patients with and without diabetes. Diabetes Care 29(10):2252-2256, 2006. (PubMed)
  17. Lavery LA, Van Houtum W, Armstrong DG, Harkless LB, Ashry HR, Walker SC. Mortality following lower extremity amputation in minorities with diabetes mellitus. Diabetes Res Clin Pract 37:41–47, 1997. (PubMed)
  18. Lavery LA, Hunt NA, Ndip A, Lavery DC, Van Houtum W, Boulton AJ. Impact of chronic kidney disease on survival after amputation in individuals with diabetes. Diabetes Care 33(11):2365-2369, 2010. (PubMed)
  19. Mayfield JA, Reiber GE, Maynard C, Czerniecki JM, Caps MT, Sangeorzan BJ. Survival following lower-limb amputation in a veteran population. J Rehabil Res Dev 38:341-5, 2001. (PubMed)
  20. Mwipatayi BP, Naidoo NG, Jeffery PC, Maraspini CD, Adams MZ, Cloete N. Transmetatarsal amputation: three-year experience at Groote Schuur Hospital. World J Surg 29(2):245-8, 2005. (PubMed)
  21. Peacock JM, Keo HH, Duval S, Baumgartner I, Oldenburg NC, Jaff MR, Henry TD, Yu X, Hirsch AT. The Incidence and Health Economic Burden of Ischemic Amputation in Minnesota, 2005-2008. Prev Chronic Dis 8(6):A141, 2011. (PubMed)
  22. Kim PJ, Attinger CE, Evans KK, Steinberg JS. Role of the podiatrist in diabetic limb salvage. J Vasc Surg 56(4):1168-72, 2012. (PubMed)
  23. Driver VR, Fabbi M, Lavery LA, Gibbons G. The costs of diabetic foot: the economic case for the limb salvage team. J Vasc Surg 52(3):17S-22S, 2010. (PubMed)
  24. Boulton AJ, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. Lancet 366(9498):1719-24, 2005. (PubMed)
  25. Singh N, Armstrong DM, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA 293(2):217-28, 2005. (PubMed)

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Infected Gouty Tophous at the Posterior Ankle, Leg, and Achilles Tendon in a Diabetic Patient: A Case Report

Posted on May 1, 2013 | Comments Off on Infected Gouty Tophous at the Posterior Ankle, Leg, and Achilles Tendon in a Diabetic Patient: A Case Report

by Sutpal Singh, DPM, FACFAS, FAPWCA1, Long K. Truong, DPM2, pdflrgMaria Mejia, DPM3, W. Scott Davis, DPM4, Jennifer Chen, DPM5, Kamran Chaudhary, MD6, Marie Cleto-Quiaoit, MD7

The Foot and Ankle Online Journal 6 (5): 1

The clinical presentation of a diabetic patient with an open infected lesion and concomitant chronic tophaceous gout of the Achilles tendon is evaluated and treatment is described. The 42-year-old man suffered from chronic tophaceous gout with multilobular, solid, tender, enlarged subcutaneous nodules affecting the right hand and both feet. The patient was neuropathic and wearing tight shoes which resulted in laceration of the posterior skin near the soft tissue mass. This resulted in an infected ulcer and cellulitis. He was treated by incision and drainage with removal of the tophaceous mass from the Achilles tendon, sural nerve decompression, as well as debridement of the Achilles tendon.

Keywords: Achilles tendon, Gout, Diabetic foot, surgical debridement

Accepted: April, 2013
Published: May, 2013

ISSN 1941-6806
doi: 10.3827/faoj.2013.0605.001

Address correspondence to: Sutpal Singh, DPM, FACFAS, FAPWCA,
Currently at St. Alexius Medical Center, Hoffman Estates, IL

1Chief Ilizarov Surgical Instructor at Doctors Hospital West Covina, California.
2,3,4,5Residency, Doctors Hospital of West Covina, California. (PM&S 36).
6Greater Chicago Rheumatology, Chicago, Illinois.
7Pathologist, St Alexius Medical Center, Hoffman Estates, Illinois.

Gout is a condition characterized by deposition of monosodium urate crystals in tissues. Acute gout is preceded by elevated serum uric acid levels, although hyperuricemia is often not present during a gouty attack.[4] It is also important to note that most patients with hyperuricemia never experience a gout flare.[1]

As crystal deposition favors areas of the body with lower temperatures, and therefore further from the heart, it has a high tendency to affect the foot, particularly the first metatarsal-phalangeal joint, in about 56-78% of patients.[10] This is known as podagra. An acute gout flare is often characterized by a red, hot, and swollen joint that is very painful to touch, representing a similar clinical presentation as cellulitis.[4]

InfGtFig1a InfGtFig1b

Figure 1 Infected right posterior ankle and lower leg area.

Definitive diagnosis of acute gout is made by observation of negatively birefringent crystals in fluid aspirated from the affected joint. Joint aspirate analysis has been shown to have sensitivity of 85 percent and specificity of 100 percent.[2,13] In the absence of joint aspirate analysis, clinical diagnosis may be made based on meeting certain criteria which include podagra, hyperuricemia, history of monoarticular arthritis followed by asymptomatic periods, palpable tophi and knowledge of certain known co-morbidities associated with gout.[15]

Gout is a multifactorial condition, and as such, must be treated in a multifactorial manner. Gout is caused by altered purine metabolism, but other factors, including high purine diet, alcohol intake, and reduced renal clearance may also contribute. Therefore, lifestyle modification must be a part of any treatment regimen.[4] Acute gout attacks usually resolve without treatment within days to weeks. However, treatment can decrease the duration of an attack and decrease frequency of future attacks. NSAIDs (i.e. indomethacin), corticosteroids (i.e. Prednisone) and colchicine are first-line therapies in cases of acute gout. Colchicine is less commonly used due to the potential side effects.[4] Uric acid lowering agents are often used to treat chronic hyperuricemia.

InfGtMRIFig2a

Figure 2 Magnetic resonance image (MRI) of the right lower extremity shows a large mass engulfing the Achilles Tendon.

These agents are not started during an acute gouty attack, as they can exacerbate the symptoms. These include allopurinol, which is the most commonly prescribed, as well as probenecid and febuxistat (Uloric®, Takeda Pharmaceuticals U.S.A., Inc).[4] The primary treatment for tophaceous gout is to lower the uric acid level with dietary and medical therapy but this may not be easy to achieve therefore, surgical treatment maybe indicated. Surgical intervention has been shown to have a high incidence of complications6, therefore it is mainly recommended when tophi cause pain, skin necrosis, ulcerations, sinuses, nerve compression, interference with tendon function, or when joints are being destroyed and painful.[12]

InfGtFig3

Figure 3 Right hand.

It is important to distinguish gout from other conditions, as symptoms of acute gout may mimic those of other conditions, and vice versa. Septic arthritis may display the involvement of a single joint, with leukocytosis and elevated erythrocyte sedimentation rate (ESR). Septic arthritis and acute gout may even occur simultaneously.[1] This report describes a case of lower extremity infection in the presence of gouty tophi in a diabetic neuropathic patient with infiltration into the sural nerve.

Case Report

A 42-year-old diabetic patient was seen in the hospital for pus draining from the ankle and back of the leg. He said that he was wearing boots and that it may have cut the back of the leg several weeks ago. He noticed large amounts of pus draining from the posterior ankle and lower leg. He was subsequently admitted. His past medical history was significant for gout and insulin diabetes mellitus. Physical examination showed an infected abscess at the posterior ankle and leg on the right, with pus draining from the ulcerated area. (Fig 1) magnetic resonance imaging (MRI) shows the extent of infiltration of the tophus on the right lower extremity. (Fig 2)

InfGtFig4

Figure 4 Left posterior ankle without any infection.

On the right hand (Fig 3) as well as the left posterior ankle (Fig 4), there were indurated soft tissue masses for which the patient denied any pain. He had a large non-infected tophi on the left lower extremity.

Surgical Technique

The patient was placed in a prone position under general anesthesia with a thigh tourniquet. A curvilinear incision was made from the middle of the leg on the medial side, going inferiorly across the open wound and ulcer and then crossing over onto the inferior lateral heel area. The incision was deepened down to the subcutaneous tissue and then down to the deep tissue. There was a tremendous amount of brown pus draining from the wound area. Culture and sensitivity for gram positive, gram negative, anaerobic and aerobic organisms were performed. There was a large amount of adhesions noted at the subcutaneous and deep tissue. There was also a large soft tissue mass engulfing the Achilles tendon and sural nerve (Fig. 5 and Fig. 6). Neuroplasty of the sural nerve with surgical loupes was performed.

InfGtFig5 InfGtFig5b

Figure 5 Infiltration of the soft tissue mass engulfing the Achilles tendon.

The entire mass from the posterior, medial, lateral and anterior aspect of the Achilles tendon was removed. The Achilles tendon was also debrided of any degenerative tissue (Fig. 7 and Fig. 8). The necrotic skin was debrided and the skin edges were approximated using 3-0 ProleneTM, Ethicon Inc in simple as well as horizontal mattresses. The open wound area was loosely approximated and packed with Iodoform gauze. The surgical site was dressed with XeroformTM, Covidien, gauze, and KerlixTM, Covidien.

Discussion

Gout, a common metabolic disorder has increased in prevalence worldwide and is estimated to have doubled in the US alone within the last three decades.[9] Though gouty tophi are typically found in joints, it may also be present in tendons and soft tissue such as Achilles tendon, ear helices, sclera, and sub conjunctivae.[2] Despite many studies which report that gout may be found in these places, there are currently little to no studies reporting the epidemiology of gout present in places like the soft tissue or rearfoot.

InfGtFig6

Figure 6 Sural nerve entrapment (forceps) with the soft tissue mass.

In this case study, we reported on an infected tophaceous wound. (Fig 7) Histology of the mass is shown in Fig 9-12. Culture and sensitivity revealed infiltration by Streptococcus agalactiae, also known as Group B streptococcus or GBS, which is a beta-hemolytic Gram-positive streptococcus. Though rare, it is important to note that tophi, when left untreated for a long duration, may accumulate and can lead to ulceration which can become infected. A 2011 case study reported a patient who was noncompliant with his allopurinol regimen, and resulted in a tophaceous ulcerated nodule overlying the dorsal first and second metatarsophalangeal joint of the left foot.[5]

InfGtFig7

Figure 7 Removal of the soft tissue mass. Gross description: 17.2 gm of dark brown to pale yellow soft tissue mass. Sectioning reveals cystic mass with chalky white substance.

The nodule and resulting ulceration were so large that amputation of the left foot was strongly considered.[5] Though bacterial cultures were negative for septic arthritis in this case, ciprofloxacin was given as prophylaxis and the patient healed well with adequate surgical debridement. [5]

It is important to monitor gout, especially in manifestations at the Achilles tendon because if left untreated it may exhibit traumatic effects. Though not as common as in the joints, tophi have been known to be found in the Achilles tendon. A 1981 case study of an acute Achilles rupture alluded to the rupture possibly being caused by gout with deposits consistent with tophi found throughout the tendon, especially at the rupture site.[14]

Often times when assessing the aspirate of a red, hot, swollen joint, if synovial crystals are found a diagnosis of a crystal arthritis such as gout or CPPD is automatically assumed. However, a retrospective study based at a US urban medical center looked at records of all the joint synovial crystal aspirates from a seven year span, containing a total of 265 synovial crystal joint aspirates.[11]

InfGtFig8

Figure 8 Surgical appearance after removal of the mass from the Achilles tendon as well as debridement of the Achilles tendon.

Of those 265 aspirates, 4, or 1.5%, came back positive for bacterial cultures confirming concomitant septic arthritis with crystal arthritis.[11] While this may seem a small amount, if left untreated may have deleterious effects on the patient.

Another study of 30 cases of concomitant septic and gouty arthritis in 2003 from Taiwan stated that wounds as the result of subcutaneous tophi rupture were the most common source of concomitant septic and gouty arthritis, with the most common infectious organism being Staphylococcus aureus.[14] Fourteen went on to receive surgical debridement with 9 having no reported complications.[14]

InfGtFig9

Figure 9 Low power of chronic gouty inflammatory reaction with foreign body giant cell proliferation.

InfGtFig10

Figure 10 Formalin Fixation has destroyed the uric acid crystals to leave amorphous eosinophilic material. Note the multinucleated giant cells indicating chronic inflammatory process (upper right).

With the degeneration in Western diet consisting of increased intake of fast food, soft drinks, and meat it is no surprise that gout and diabetes are common co morbidities. A 2008 study based at the University of Pennsylvania Medical Centre expanded on the notion that hyperuricemia, gout, and metabolic syndrome are associated with each other. This suggests that gout in men with a high cardiovascular risk profile is at a higher risk of developing type 2 diabetes.[3]

InfGtFig11

Figure 11 Low power of acute gouty inflammation showing gouty casts.

InfGtFig12

Figure 12 Note the inflammatory neutrophils.

When dealing with diabetic patients, wounds and resulting infection can lead to limb loss or even death.[9] Therefore it is pertinent to monitor both gout and diabetes, because gout left untreated could be a means for ulceration.

InfGtFig13

Figure 13 Several months after surgery shows complete healing with good Achilles tendon strength.

The case study presented in this article highlighted the significance of the necessity of a thorough examination for patients with numerous risk factors. While our outcome was positive (Fig 13), without a thorough debridement and attentive follow up, this case had the potential to result in a below the knee amputation. This is especially true with the known potentially poor healing capacity of diabetics. Moreover, it vital that in order to prevent recurrence patients with gout must be tightly controlled.

Conclusion

As discussed before, infected gouty tophus of the Achilles tendon is a rare finding even though gout commonly affects the foot and ankle. A thorough history and physical examination with assistance of advanced diagnostic tools and laboratory studies is essential to properly diagnose this condition. Differential diagnosis of gout should always be considered in patients with a history of hyperuricemia even if symptoms are masked by cardinal signs of infection. Medical and surgical therapy has been reported to successfully treat this condition. Our case report demonstrates good prognosis with early recognition and successful surgical debridement.

References

1. Becker M. Clinical manifestations and diagnosis of gout. In: UpToDate. Basow DS (Ed), Waltham, MA, 2012.
2. Chen LX, Schumacher HR. Current trends in crystal identification. Current Opinion  Rheum 2006 18: 171-73. [PubMed]
3. Choi HK, De Vera MA, Kishnan E. (2008). Gout and risk of type 2 diabetes among men with a high cardiovascular risk profile. Rheumatology 2008  47: 1567-1570. [PubMed]
4. Eggebeen AT. Gout: an update. American family Physician 2007 76: 801-808. [PubMed]
5. Falidas E, Rallis E, Bournia V, Mathioulakis S, Pavlakis E, Villas C. Multiarticular chronic tophaceous gout with severe and multiple ulcerations: a case report. J Medical Case Reports 2011 5: 1-4. [PubMed]
6. Kumar S, Gow P. A Survey of indications, results, and complications of surgery for tophaceous gout. J New Zealand MedAssoc 2002 23: 115(1160). [PubMed]
7. Larmon WA,  Kurtz JF. The surgical management of chronic tophaceous gout. JBJS 195840 :743-772. [PubMed]
8. Mahoney PG, James PD, Howell CJ, Swannell AJ.  Spontaneous rupture of the Achilles tendon in a patient with gout. Annals Rheumatic Dis 1981 40: 416-418. [PubMed]
9. Ramsey SD, Newton K, Blough D, McCullouch DK, Sandhu NS, Reiber GE, Wagner EH. Incidence, outcomes, and cost of foot ulcers in patients with diabetes. Diabetes Care 1999 22: 382-387. [PubMed]
10. Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot? JFAR 2011 4:13. [PubMed]
11. Shah K, SpearJ, Nathanson LA, McCauley J, Edlow JA.  Does the presence of crystal arthritis rule out septic arthritis? J Emergency Med 2007 32: 23-26. [PubMed]
12. Terkeltaub R. (2010). Update on gout: New therapeutic strategies. Nature Reviews: Rheumatology 2010 6: 30-38.[PubMed]
13. Wallace SL, Robinson H, Masi AT,  Decker JL, McCarty DJ, Yü T. Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheumatism 1977 20:  895-900. [PubMed]
14. Yu KH, Luo SF, Liou LB, Wu YJJ, Tsai WP, Chen JY, Ho HH. Concomitant septic and gouty arthritis—an analysis of 30 cases. Rheumatology 2003 42: 1062-1066. [PubMed]
15. Zhang W. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the standing committee for international clinical ctudies including Therapeutics (ESCISIT). Annals Rheumatic Dis (2006) 65: 1301-311.  

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Staphylococcus simulans Osteomyelitis of the Foot: A case report

Posted on January 1, 2010 | Comments Off on Staphylococcus simulans Osteomyelitis of the Foot: A case report

by Al Kline, DPM1

The Foot and Ankle Online Journal 3 (1): 4

Staphylococcus simulans, a coagulase-negative pathogen is not commonly seen in the foot. The pathogen has been isolated in chronic osteomyelitis and infected internal fixation. This case describes a 65 year-old, diabetic male with recalcitrant osteomyelitis following partial metatarsal head resection. Staphylococcus simulans was the primary pathogen isolated. This may be the first reported case of Staphylococcus simulans osteomyelitis of the foot.

Key words : Osteomyelitis, Diabetic foot infection, Staphylococcus infection.

Accepted: December, 2009
Published: January, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0301.0004

Staphylococcus simulans is a common, coagulase-negative (CoNS) pathogen linked to animals, including cattle. [1] The pathogen is common in normal flora and is primarily acquired through contact with domestic animals. In animals, the pathogen has been isolated and implicated in a condition called “bumble foot”. [2,4] Bumble foot, or ulcerative pododermatitis, has been described in both rats and birds. [2,3,5] In humans, the pathogen has been isolated in intravascular and indwelling catheters and conditions including urinary tract infections, septicemia, conjunctivitis, and endocarditis. [1,6,7,8] In the past 15 years, the organism has been isolated in cases of osteomyelitis, prosthetic joint infections, and infected internal fixation devices. [1,7,8] The author has found no reported cases of Staphylococcus simulans osteomyelitis of the foot. This report describes a patient who presented with a draining wound after having a previous partial metatarsal resection for acute osteomyelitis.

Case Report

A 65 year-old diabetic male presented to our office with a draining dorsal abscess of the right foot. In May 2006, he underwent a partial metatarsal resection of the 3rd right metatarsal by another podiatrist. Unfortunately, the area became infected. He states the surgery was performed through the ‘top of the foot’ and the ulcer was left to close on the bottom. He reports the dorsal incision, which was primarily closed, opened just days after surgery and began to drain. The plantar ulcer did not close. The patient reports he had a dog. It appeared that hair from the dog constantly adhered to his wound because of walking bare foot on the carpet. His treatment included antibiotic therapy and local wound care. He was on an oral Ciprofloxacin He continued on local wound care and oral antibiotics until he presented to our office in January, 2007. He has had a draining sinus for the past eight months. Radiographic evaluation revealed reactive bone changes to the base of the 3rd proximal phalanx consistent with recalcitrant osteomyelitis. (Fig. 1)

Figure 1  Radiographs of the foot revealed a previous metatarsal resection.  Reactive, osteolytic changes were seen of the 3rd proximal phalanx base consistent with chronic osteomyelitis.

Magnetic resonance imaging (MRI) was performed using high field 1.5 Tesla without contrast. Multiplanar, multisequence images were obtained through the previous partial amputation of the distal right third metatarsal bone and proximal phalanx. On T1 coronal and axial views abnormal bone marrow signal intensity was seen involving the proximal phalanx of the third toe and third metatarsal at the distal shaft. On the respective STIR coronal images and T2WI, there was diffuse high signal intensity. MRI confirmed osteomyelitis to the base of the 3rd proximal phalanx as well as the 3rd end of the remaining metatarsal stump. (Fig. 2A and 2B)

 

Figure 2A and 2B   MRI axial (a), coronal (b) images revealed abnormal image intensity to the base of the 3rd proximal phalanx and 3rd metatarsal bone.

The patient was admitted to the hospital and scheduled for incision and drainage of the wound with deep tissue and bone cultures with partial resection of the metatarsal stump and base of the proximal 3rd digital phalanx. At surgery, the patient had significant scarring with chronic osteomyelitis of the 3rd metatarsophalangeal joint (MPJ) space. Deep tissue cultures were performed around the base of the 3rd proximal phalanx. Bone was then resected from the base of the 3rd phalanx and 3rd metatarsal stump. Bone was then sent for culture and sensitivity. The wound was left open and packed with plain gauze and saline.

Surgical Culture Report

Surgical culture results revealed Staphylococcus simulans as the primary organism. Bone cultures were also consistent with the same organism. Culture sensitivities reported resistance to Ampicillin, Ciprofloxacin, Clindamycin, Erythromoycin, Oxacillin, Penicillin, Primaxin, Cefazolin and Ceftriaxone. The organism was susceptible to Gentamycin, Tetracylcine, Vancomycin and Bactrim.

Discussion

Osteomyelitis associated with Staphylococcus simulans is rarely reported. This appears to be the first documented case of Staphylococcus simulans osteomyelitis from a chronic plantar foot ulcer. In 1985, Males, et al., documented a case of fibular, malleolar osteomyelitis after removal of a syndesmotic screw that led to Staphylococcus simulans septic ankle arthritis and septicemia. [8] Before 1985, many species of staphylococcus, including S. simulans, were not identified as a separate strain of staphylococcus and were often labeled Staphylococcus epidermidis. This may explain the lack of reported cases from this pathogen. Staphylococcus simulans is also known to produce a strong slime layer. The production of a strong slime layer and its adherence to smooth surfaces, is linked to the organisms ability to colonize, especially in prosthetic devices, shunts and catheters. [8,9,10] In cases of chronic osteomyelitis, this slime layer is also observed in grossly colonized abscesses. In this case, we also observed a mucoid, slime layer adherent to the packing material. We lavaged and repacked the wound daily. It has also been shown that the encapulated forms of Staphylococcus simulans (i.e. slime layer), as compared to unencapsulated forms of the pathogen, have a antiphagocytic effect on human PMN’s. Little phagocytosis was observed during a 2 hour incubation of PMN’s , even when the ratio of PMN’s to bacteria was increased from 1:1 to 10:1.11 This would explain the virulence of this organism and its ability to colonize wounds and prosthetic devices.

Conclusion

The patient responded well to intravenous (IV) Vancomycin during his hospital course. He remained in the hospital setting for 16 days on IV antibiotic therapy until the dorsal incision closed. This patient returned to a diabetic shoe without further complication. To date, no signs of recurrent osteomyelitis have been reported.

References

1. Razonable RR, Lewallen DG, Patel R, Osmon DR: Vertebral osteomyelitis and prosthetic joint infection due to staphylococcus simulans. Mayo Clinic Proc. 76 (10): 1067 – 1070, 2001.
2. McArthur J: Bumble Foot, ulcerative pododermatitis. [Online] Unable to find complete reference – the website address has been closedown.
3. McLeod L: Bumblefoot in Rats. About: Exotic Pets, [Online] Unable to find complete reference – the website address has been closedown.
4. Vorgelgt V, Pfanzelt D: Epidemiologie boviner staphylococcus epidermidis isolate: Pravalenz Virulenz-assoziierter Gene und klonale Verwandtschaft mit humanen Isolaten. Hannover, 2006 [Online] Unable to find complete reference.
5. Clauer PJ: Leg and Foot Disorders in Domestic Fowl. Small Flock Factsheet No 35. Virginia Cooperative Extension [Online] Unable to find complete reference – website unavailable.
6. Marrie TJ, Kwan C, Noble MA, West A, Duffield L: Staphylococcus saprophyticus as a cause of urinary tract infections. J Clin Microbiology 16: 427 – 431, 1987.
7. Wilson M: Microbial inhabitants of skin, their ecology and role in health and disease. Cambridge Press, November, 2004.
8. Males BM, Bartholomew WR, Amsterdam D: Staphylococcus simulans Septicemia in a Patient with Chronic Osteomyelitis and Pyarthrosis. J Clin Microbiology 21 (2): 255 – 257, 1985.
9. Byston R, Penny SR: Excessive production of mucoid substance in Staphylococcus IIA: a possible factor in colonization of Holter shunts. Dev Med Child Neurol 14 (suppl 27): 25 – 28, 1972.
10. Christensen GD, Simpson WA, Bisno AL, Beachey EH: Experimental foreign body infections in mice challenged with slime-producing staphylococcus epidermidis. Infect. Immun. 40: 407 – 410, 1982.
11. Ohshima Y, Schumacher-Perdreau F, Peters G, Quie PG, Pulverer G: Antiphagocytic effect of the capsule of staphylococcus simulans. Infection and Immunity, 58 (5), 1350 – 1354, 1990.

Address correspondence to: Al Kline, DPM
3130 South Alameda, Corpus Christi, Texas 78404.
Email: alklinedpm@gmail.com.

1  Adjunct Clinical Faculty, Temple University School of Podiatric Medicine, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot and Ankle Online Journal, 2010

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EBMR: Comparison of Negative Pressure Wound Therapy using Vacuum-Assisted Closure with Advanced Moist Wound Therapy in the Treatment of Diabetic Foot Ulcers

Posted on December 1, 2008 | Comments Off on EBMR: Comparison of Negative Pressure Wound Therapy using Vacuum-Assisted Closure with Advanced Moist Wound Therapy in the Treatment of Diabetic Foot Ulcers

Evidence Based Medicine Review

Authors:
Blume P., Walters J., Payne W., Ayala J., and Lantis J.

Publication:
Diabetes Care 31:631-636, 2008

Reviewer:
Michael Turlik, DPM

The Foot & Ankle Journal 1 (12): 5

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Methods

This was a multi-center randomized controlled efficacy trial of 342 diabetic subjects who were followed for a minimum of 112 days. The study was performed across 37 diabetic foot clinics and hospitals principally in the United States. The primary outcome was complete ulcer closure. There was a thorough description of the method of randomization as well as, concealment allocation. Subjects and investigators were not blinded and it was unclear if data collectors and analysts were blinded. Safety and effectiveness analysis was conducted by the company sponsoring the study.

Results

A sample size calculation was carried out with the expectation of a 20% difference between groups (Absolute Risk Reduction). Enough subjects were enrolled in the study to satisfy the sample size calculation. Baseline data examination reveals no difference between groups. Data from the primary outcome were analyzed as intention to treat as well as, per protocol. Efficacy of the intervention was reported as statistically significant both for intention to treat and per protocol analysis favoring the vacuum assisted closure method. Point estimates were reported for the primary outcome but 95% confidence intervals were not reported.

Funding

The manufacturer of the wound closure vacuum assisted device (KCI) supported the study. It was not indicated if the study was registered. The primary author has received payments from the manufacturer for speaking engagements. No other disclosures were noted for other authors or investigators. The article has been marked as an advertisement by the publisher.

Comment

The study contains several well described methodological techniques to limit bias, randomization, concealment allocation, and intention to treat analysis. However, due to the nature of the study investigators and subjects were unable to be blinded.

Although unblinded studies are associated with an increased treatment effect this is less likely when the primary outcome is objective such as resolution of an ulcer as opposed to soft measurements such as patient reported outcomes. [1] However, no mention was made regarding blinding of data collectors and analyzers.

The data from the study was analyzed by the company funding the study. This may be perceived as a potential source of bias, it is more reassuring to the reader when the data is analyzed by a neutral third party. The results of the primary outcome were presented as intention to treat and per protocol. It appears the author chose to assign the worst case scenario for the data lost to follow-up for the ITT analysis. Both methods were statistically significant however differed in their point estimate. Was this study clinically significant? The authors expected a 20% difference (ARR) between groups when they calculated their sample size. If the 20% difference is to be accepted as a clinically significant result then the result of the primary outcome using the intention to treat analysis was not clinically significant but only statistically significant. The per protocol analysis was both clinically and statistically significant. Furthermore, it is difficult to analyze the results with only point estimates and not 95% confidence intervals (CI). Why 95% CI were reported for secondary measures and not the primary outcome was unclear.

There appears to be a fairly high loss to follow-up in both arms of the study (approximately 30% per treatment arm). The prognosis for subjects lost to follow-up is thought to be different than the patients who remain in the study. [2] This loss of data may compromise the randomization sequence. Did the loss of follow-up effect the results of the study? The strength of the inference drawn from the study is modified by the magnitude of the difference between the intention to treat and per protocol analysis. It would have been instructive for the reader if the authors addressed this point during their discussion of the results.

Interpretation the study’s results would be better understood with a clear clinically important difference stated by the authors and with 95% CI reported about the point estimate of the primary outcome.

Using the data from this study 95% CI can be calculated for the Absolute Risk Reduction (ARR) and Number Needed to Treat (NNT) for both the intention to treat and per protocol analysis. [3] (table 1)

Table 1

The ARR only exceeds 20% during the per protocol analysis. The lower end of the 95% CI for both ITT and PP is greater than 0 which is consistent with a statistically significant result. Although the point estimate (ARR) for the intention to treat analysis is less than 20% , a risk reduction of more than 20% cannot be ruled out by evaluating the upper end of the 95% CI and would suggest a larger study is necessary or less loss of follow-up.

The NNT is a more clinician friendly metric to access efficacy in studies with dichotomous outcomes. The NNT for both are similar 5 (PP) and 8 (ITT) however, the upper limit of the 95% CI or worse case scenario is 12 (PP) and 24 (ITT). This appears to be a large difference.

Although the use of the vacuum assisted closure appears to be more efficacious the magnitude of the effect is unclear and the inference reduced. It is up to the reader to determine if the loss to follow-up, lack of blinding and lack of clinical significance reduces the inference of the results of this study.

In addition, since the study was designed as an efficacy rather than an effectiveness study, generalizing the results to clinical practice should be undertaking with caution.

The safety data were presented as treatment related rates at six months. However, the trial evaluated treatment until day 112 or ulcer closure by any means. It would be informative to the reader to review the data on safety prior and post intervention termination. There have been two meta-analysis published this year for vacuum assisted closure and diabetic foot ulcers this year. [4,5]

References

1. Woods L, Egger M, Lotte Gluud L, Schulz KF, Jüni P, Altman DG, Gluud C, Martin RM, et al. Empirical evidence of bias in treatment effect estimates in controlled trials with different interventions and outcomes: meta-epidemiological study. BMJ 336 (March): 601 – 605, 2008.
2. Montori VM, Guyatt GH. Intention-to-treat principle. Can Med Assoc J 165 (10): 1339 – 1341, 2001.
3. Graphpad. http://www.graphpad.com/quickcalcs/NNT1.cfm Accessed 11/3/2008.
4. Gregor S, Maegle M, Sauerland S, Krahn JF, Peinemann F, Lange S. Negative pressure wound therapy a vacuum of evidence? Arch Surg 143 (2): 189 – 196, 2008.
5. Bell G, Forbes A. A systematic review of the effectiveness of negative pressure wound therapy in the management of diabetes foot ulcers. Int Wound J 5 (2): 233 – 242, 2008.

© The Foot & Ankle Journal, 2008

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Necrotizing Soft Tissue Infection of the Foot: A Case Report

Posted on April 1, 2008 | Comments Off on Necrotizing Soft Tissue Infection of the Foot: A Case Report

by Shelly A.M. Wipf, B.M.1, Robert M. Greenhagen, B.S.2, Denise M. Mandi, DPM3, Nicholas J. Bevilacqua, DPM4 , Lee C. Rogers, DPM5

The Foot & Ankle Journal 1 (4): 2

We report a rapidly spreading necrotizing foot infection in a healthy 37 year old male with associated sepsis and no identifiable portal of entry. Multiple debridements were required to control this infection which eventually necessitated a LisFranc’s amputation. We review the current literature of the diagnosis and treatment of necrotizing soft tissue infections in the foot. Early diagnosis and appropriate treatment can preserve life and limb.

Key words:Necrotizing soft tissue infection, diabetic foot infection, LRINEC score

This is an Open Access article distributed under the terms of the Creative Commons Attribution License. It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Published: April 1, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0104.0002

Necrotizing soft tissue infection or (NSTI) is a broad term that comprises a rare group of limb and life-threatening surgical emergencies. We report on an unusual case of a 37 year old, otherwise healthy male, who presented with a NSTI without a portal of entry. First described by Confederate army surgeon Joseph Jones in 1871 as “hospital gangrene,” [1] this condition is caused by a variety of organisms. These infections require operative debridement and appropriate antibiotic therapy, as well as fluid resuscitation and other supportive care.

The term “necrotizing fasciitis” was coined by Wilson in 1952. [2] Today, most authors prefer the term “necrotizing soft tissue infection,” or NSTI.

Case Report

A 37-year-old white male presented to the Emergency Department complaining of a very painful and swollen right foot. The patient noted that the swelling and pain had been increasing to the lower leg and up to the knee. There had been increasing redness and some clear drainage from the right foot. The patient had been evaluated at an urgent care clinic five days earlier with a complaint of severe pain to the arch. At that time, there was no evidence of an infectious process and the patient was diagnosed with plantar fasciitis. He was given a non-steroidal, anti-inflammatory and a narcotic for pain.

The patient denied a history of trauma or laceration to the foot, as well as any illicit drug use. The patient had a negative history of recent respiratory or genitourinary infections, although he had noticeably poor dentition. His past medical history was unremarkable. The patient reported allergy to penicillin. Significant vital signs included a temperature of 38.1oC/100.6oF, and tachycardia at a rate of 124. Examination of the right lower extremity revealed non-palpable pedal pulses secondary to edema, although capillary refill was normal. No lacerations, punctures, or abrasions were observed. There were hemorrhagic blisters on the dorsal and plantar forefoot that exuded no purulence. (Fig 1)

Figure 1  The initial presentation of the foot.  There is extensive cyanotic skin changes and bullae formation.

Ecchymosis was observed at the medial plantar arch and the lateral sub-fibular region. Radiographs failed to reveal any bony pathology or subcutaneous gas. Admission laboratory studies were performed. Results included a white blood cell count of 14,700 with 18% bands, hemoglobin and hematocrit of 13.8 and 39.3 respectively, sodium of 131, potassium of 3.3, and blood glucose of 197. C-reactive protein was markedly elevated at 23.6. Blood cultures were drawn and Gram stain revealed Gram positive cocci in chains (later identified as Streptococcus Group A).

The patient was taken to the operating room for incision and drainage, at which time seropurulence was expressed from all major compartments of the foot. (Fig 2)

Figure 2  Intra-operative photo of the plantar incision and drainage showing extensive myonecrosis with minimal bleeding.

Lack of resistance of fascial planes to blunt dissection was noted. Multiple coagulated veins were present in the subcutaneous tissue. No bleeding occurred. Following hydroscapel debridement and irrigation with pulse lavage, the wound was packed open with Iodoform gauze. The patient was placed on Linezolid, Clindamycin, and Aztreonam.

On hospital day three, it was discovered that the cultures from the foot revealed Group A Streptococcus. The antibiotic spectrum was narrowed to Clindamycin. Over the next six days the patient underwent two subsequent debridements involving the removal of digits 2, 3, and 4 which had become necrotic. (Figs. 3,4)

Figures 3,4   Appearance of the foot after amputation of the fourth toe prior to the fourth surgical debridement.  There is continued necrosis of soft tissue and loss of tissue viability to toes 1-3.

Negative pressure wound therapy was employed after the amputations. On hospital day nine, the infection was controlled and no further necrosis was observed. Attention was focused on limb salvage and creation of a functional foot. On day sixteen, the patient underwent a LisFranc disarticulation amputation with primary closure utilizing local tissue transfer. (Figs. 5,6)

Figure 5  After four surgical debridements with amputation of toes 2, 3, and 4, there is now viable bleeding tissue that is free from infection and necrosis.

Figure 6  The forefoot was disarticulated at the LisFranc joint and the medial and lateral forefoot skin was used as a fasciocutanous flap to cover the defect.

Discussion

NSTIs are characterized by bacterial invasion leading to thrombosis and suppuration of the subcutaneous vasculature. The angiothrombosis effectively decreases blood supply, causing liquefactive necrosis of the subcutaneous tissue, fascia, and eventually the musculature. The angiothrombosis renders the delivery of parenteral antibiotic therapy ineffective, necessitating emergent operative debridement of gangrenous fascia, fat, and blood vessels to the extent of healthy, bleeding and viable tissue.

Debridement reveals gray necrotic fascia, lack of bleeding during dissection, muscle fascia that gives way to blunt dissection, and foul-smelling “dish-water” purulence. [3] The clinical course of NSTI is often not as rapid as would be expected from the media reports of “flesh-eating bacteria.” Although fever and tachycardia may begin at 24 hours, the pathognomonic features of skin sloughing, bullae, and cutaneous gangrene do not usually occur until the fourth or fifth day. [4,5,6] Our patient demonstrated this course of disease.

The bacteriologic isolates of necrotizing soft tissue infection have evolved since early descriptions. Giuliano and colleagues [7] classified NSTI into two groups: Type I is a polymicrobial infection consisting of anaerobic bacteria and facultative anaerobic bacteria; and Type II is a monomicrobial infection of Group A Streptococcus. However, in their original report Giuliano, et al, describe one Type II infection with Group A Streptococcus in combination with Staphylococcus aureus. Recent reports have isolated non-Group A Streptococcus in monomicrobial infections, including Staphylococcus aureus, Clostridium, Pseudomonas aeruginosa, Escherichia coli, and Serratia marscesans. [8,9]

The exact microbiological etiology of NSTI is a moot point, however, when the patient presents in the fulminant phase of disease. At that most critical period only two types of NSTI must be differentiated: pure clostridial myonecrosis and non-clostridial infection. [11] Clostridial infection invades muscle tissue and carries a four-fold risk of mortality and limb loss. [22] NTSI are associated with several co-morbidities. The most common factors predisposing patients to NSTI are diabetes mellitus, peripheral vascular disease, obesity, alcohol abuse/hepatic disease, malignancy, immunosuppressant therapy, and intravenous drug abuse. [3,8,10,11] Portals of entry for NTSI include sites of pre-existing ulcerations, recent surgical wounds, traumatic wounds, sites of subcutaneous insulin injection or illicit drug injection, and minor abrasions, burns, lacerations, or insect bites. [8,11] In urban hospital settings, the incidence of NSTI secondary to intravenous injection of illicit drugs has been increasing in recent years, necessitating the need to question the patient’s social history. The physician must be aware of the practice of “skin popping,” in which a substance such as heroin is injected directly into the subcutaneous tissues. Infections associated with intravenous drug abuse are caused by skin flora and anaerobic bacteria. Oropharyngeal bacteria such as Streptococcus viridans and Eikenella corrodens can also cause NSTI. This is due to the practice of abusers licking their needles to avoid wasting any drug. [12] Rapid differentiation between NSTI and cellulitis or abscess is paramount in reducing morbidity and mortality. The most common presenting signs of NSTI are nonspecific signs of inflammation such as erythema, edema, and pain. Wong, et al, [3] describe a “triad” of exquisite pain (97.8% of patients), swelling (92.1%), and fever (79.8%). In their matched consecutive case series of 21 NSTI cases and 21 non-NSTI controls, Wall and colleagues [13] identified tense edema (38% vs 0%, p=0.003) and bullae (24% vs 0%; p=0.049) as the most specific physical findings. Present in four-fifths of patients with document NSTI, the three most specific “hard” clinical signs of NSTI are bullae formation, skin necrosis, and crepitance. [11]

Some patients do not possess any of these signs at presentation. Imaging, such as plain radiography [20] ultrasound, [14,15] CT scans, [16] and MRI [17,18] show non-specific changes and are often not significant until late in the course of the disease. Near-infrared spectroscopy is a newer, less available modality that can diagnose NSTI in the lower limbs by measuring tissue hypoxia secondary to microvascular thrombosis and necrosis. At a tissue oxygen saturation reading of less than 70%, the test is 100% sensitive and 97% specific for NSTI. [19]

McHenry reported the cumulative mortality of NSTI to be 34%. [8] Death can result from disseminated intravascular coagulation, acute respiratory distress syndrome, or multiple organ failure in response to overwhelming sepsis. [20] Anaya, et al, [21] found the most significant predictors of mortality to be white blood cell count greater than 30,000×103/μL and creatinine greater than 2 mg/dL. The single most important determinant of survival and limb preservation in NSTI is the amount of time elapsed between initial presentation and surgical debridement. McHenry reported the average time from admission to operation in non-survivors to be 90 hours, while in survivors the elapsed time was only 25 hours (p = 0.0002). [8] In a retrospective review of 68 patients, Bilton, et al, [22] reported 4.2% mortality for patients undergoing early surgical debridement and 38.0% mortality for those with delayed treatment (p=0.0007).

Wong and colleagues [23] developed the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) scoring system for accurately identifying NSTI based on lab values at time of hospital admission (Table 1).

Table 1: Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score

This scoring system was derived using univariate and multivariate logistic regression analysis of 89 patients with surgically confirmed NSTI and 225 control patients with cellulitis or subcutaneous abscess. The LRINEC score considers the lab values for C-reactive protein, total white cell count, hemoglobin, sodium, serum creatinine, and glucose.

For patients whose score was greater than 6 points (range 0-13), the LRINEC score had a positive predictive value of 92.0% and a negative predictive value of 96.0%. Patients were stratified into risk categories: low risk for a score of ≤5, moderate risk for a score of 6-7, and high risk for a score ≥8. The authors’ suggested algorithm for patients in the low risk category is intravenous antibiotics and continued monitoring of CBC and CRP. For intermediate risk patients, they suggest urgent MRI, frozen section biopsy, or “finger test,” a bedside procedure in which a 2-cm incision is made down to deep fascia and the wound inspected for lack of bleeding, presence of “dishwater pus,” and lack of resistance to blunt dissection. For patients at high risk with a score of 8 or higher, the recommendation is emergent operative debridement. Our patient presented to the Emergency Department with a LRINEC score of 7, placing him in the moderate risk category.

The mainstay of treatment for necrotizing soft tissue infections is rapid surgical debridement followed by appropriate antibiotic therapy after initial resuscitation with fluid and electrolyte replacement and/or blood transfusion. Often multiple debridements are necessary. In the report by Wong, et al, [23] survivors underwent a mean of 2.7 debridements (range, 0-9) to control the infective process. While amputation was not found to reduce mortality, patients who underwent amputation had to undergo fewer operations to control the infection and to achieve wound coverage (2.59 compared with 3.45; p<0.05). [3] Before cultures are available, empiric antibiotic therapy that is effective against gram positive, gram negative, and anaerobic bacteria should be initiated early. McHenry and colleagues [8] suggest using single antibiotics such as imipenem-cilastin, ticarcillin-clavulanate, ampicillin-sulbactam, or piperacillin-tazobactam.

In their series, Bosshardt, et al, [12] employed triple antibiotic therapy consisting of ampicillin or high dose penicillin G, an aminoglycoside, and clindamycin or metronidazole.

They suggested the combination of ampicillin-sulbactam and high dose penicillin G for drug abusers due to the higher percentage of infections caused by oropharyngeal flora and Clostridial species.

The use of hyperbaric oxygen to treat NSTI may be beneficial. Wilkinson, et al, [24] reported a study of 44 patients with NSTI. Thirty-three patients received HBO2 in addition to standard care and eleven patients received only standard care. They found a significant reduction in the incidence of amputation (p=0.05) and an 83% reduction in the relative risk of death for the HBO2 group, which corresponds to a number needed to treat (NNT) of 3.

The diagnosis of necrotizing soft tissue infection can be elusive and requires an astute clinician to recognize it in its early stages. This will help to increase the patient’s chance of survival and limb preservation. The clinician must realize that the pathognomonic skin changes do not appear until four or five days after initial presentation of pain, swelling and erythema. Though unconfirmed, we speculate that our case of NTSI was initiated by bacteremia from poor dentition. (Fig 7).

Figure 7  A view of the patient’s oropharyngeal cavity exhibiting severe tooth decay and ginigivitis.

In our case, rapid identification of the NSTI and septicemia contributed to our ability to preserve life and limb, through a foot sparing amputation. The patient underwent a dental consultation immediately following surgery to evaluate necrotizing gingivitis and severe tooth decay.

References

1. Jones J. Investigation upon the nature, causes and treatment of hospital gangrene as it prevailed in the Confederate armies, 1861-1965. In: Surgical Memories of the War of Rebellion New York: United States Sanitary Commission, 1871.
2. Wilson B: Necrotizing fasciitis. Am Surg. 18 :416-431, 1952.
3. Wong CH et al: Necrotizing Fasciitis: Clinical Presentation, Microbiology, and Determinants of Mortality. JBJS. 85-A(8): 1454-1460, 2003.
4. Beathard GA: Necrotizing Fasciitis Due to Group A β-hemolytic Streptococci. Arch Intern Med. 120:63-67, 1967.
5. Janevicius RV et al: Necrotizing fasciitis. Surg Gynecol Obstet. 154:97-102, 1982.
6. Koehn GC: Necrotizing fasciitis. Arch Dermatol. 114:581-583, 1978.
7. Giuliano, A et al: Bacteriology of necrotizing fasciitis. Am. J Surg. 134: 52-56, 1977.
8. McHenry CR et al: Determinants of Mortality for Necrotizing Soft-Tissue Infections. Annals of Surgery. 221(5): 558-565, 1995.
9. Singh G et al: Bacteriology of Necrotizing Infections of Soft Tissues. Aust N.Z. J. Surg. 66: 747-750, 1996.
10. Wang KC et al: Necrotizing Fasciitis of the Extremities. J Trauma. 32: 179-182, 1992.
11. Elliott D et al: Necrotizing Soft Tissue Infections: Risk factors for mortality and strategies for management. Ann Surg. 224: 672-683, 1996.
12. Bosshardt TL et al: Necrotizing soft-tissue infections. Arch Surg. 131: 846-854, 1996.
13. Wall DB; et al: Objective criteria may assist in distinguishing necrotizing fasciitis from nonnecrotizing soft tissue infection. Am J Surg. 179: 17-21, 2000.
14. Tsai CC et al: Early diagnosis of necrotizing fasciitis by utilization of ultrasonography. Kaohsiung J Med Sci. 12:235-240, 1996.
15. Yen ZS et al: Ultrasonographic screening of clinically-suspected necrotizing fasciitis. Acad Emerg Med. 9(12): 1448-1451, 2002.
16. Wysoki MG et al: Necrotizing Fasciitis: CT Characteristics. Radiology. 203: 859-863, 1997.
17. Brothers TE et al: Magnetic resonance imaging differentiates between necrotizing and non-necrotizing fasciitis of the lower extremity. J Am Coll Surg. 187: 416-421, 1998.
18. Schmid MR et al: Differentiation of necrotizing fasciitis and cellulitis using MR imaging. Am J Roentgenol. 70: 615-620, 1998.
19. Wang TL et al: Role of Tissue Oxygen Saturation Monitoring in Diagnosing Necrotizing Fasciitis of the Lower Limbs. Ann Emerg Med. 44: 222-228, 2004.
20. Fontes RA et al: Necrotizing Soft Tissue Infections. J Am Acad Orthop Surg. 8(3): 151-158, 2000.
21. Anaya DA et al: Predictors of Mortality and Limb Loss in Necrotizing Soft Tissue Infections. Arch Surg. 140: 151-157, 2005.
22. Bilton BD et al: Aggressive surgical management of necrotizing fasciitis serves to decrease mortality: a retrospective study. Am Surg. 64(5): 397-401, 1998.
23. Wong CH et al: The LRINEC( Laboratory Risk Indicator for Necrotizing Fasciitis) score: A tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 32(7): 1535-1541, 2004.
24. Wilkinson D et al: Hyperbaric Oxygen Treatment and Survival From Necrotizing Soft Tissue Infection. Arch Surg. 139: 1339-1345, 2004.

Address correspondence to: Lee C. Rogers, DPM. Director, Amputation Prevention Center, Broadlawns Medical Center, 1801 Hickman Road, Des Moines, IA 50314. Email: Lee.C.Rogers@gmail.com

1Submitted while a 3rd Year Podiatric Medical Student at Des Moines University – College of Podiatric Medicine and Surgery, 3200 Grand Avenue, Des Moines, IA 50312

2Submitted while a 4th Year Podiatric Medical Student at Des Moines University – College of Podiatric Medicine and Surgery, 3200 Grand Avenue, Des Moines, IA 50312

3Chairman; Department of Surgery, Broadlawns Medical Center, 1801 Hickman Road, Des Moines, IA 50314

4Amputation Prevention Center at Broadlawns Medical Center, 1801 Hickman Road, Des Moines, IA 50314

5Director; Amputation Prevention Center at Broadlawns Medical Center, 1801 Hickman Road, Des Moines, IA 50314

© The Foot & Ankle Journal, 2008

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