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Hello and welcome to this present online learning session. My name is John S. Steinberg. I am full time faculty in the Department of Surgery at Georgetown University in Washington DC. I am representing to you on the topic of basic management of diabetic foot infections.



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Dr. Malik Sykes, a vascular surgeon in San Antonio and someone who has published extensively on the diabetic foot and vascular disease, said in one of his publications that the diabetic foot is like a forest in a drought. He stated that it is stable to superficial infection yet prone to rapid destruction if a simple spark occurs. This analogy really sets the tone for much of the discussion that we are going to have in this presentation on diabetic foot infection and really helps to give us an idea of what type of compromise and what type of high-risk we are looking at in these diabetic lower extremities that often are predisposed with peripheral vascular disease.



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In looking at the high-risk diabetic lower extremity, one of the key factors to consider in front is the patient education and awareness level. As physicians, we certainly depend on this patient intervention and the patient being aware of the early warning signs of the infection and compromised in the diabetic extremity. One of the key factors to keep in mind is sensory, motor, and autonomic neuropathy predisposing these patients to injury and ulceration. Structural deformity certainly is a key factor in the “at risk” extremity setting these patients up for pressure and other complications. Vasculopathy makes these patients poorly equipped to deal with the necessary factors of

wound healing and immunopathy certainly compromises their ability to deal with the infection and other complications that may arise in the diabetic extremity.



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As mentioned earlier, the diabetic foot certainly can be an unfortunate fertile ground for infection. We can see patients who present with cellulitis petechia and this can be rapidly ascending and certainly limb threatening. First and foremost, we have to consider bacterial infections. These can often times involve closed and open infections. Closed infections usually are in the form of a cellulitis spreading through the foot, ankle, and/or lower limb or an abscess, which is often times focal and sometimes plantar deep space. These closed infections are generally caused by a single bacterial organism and this most commonly is a staph or strep type of bacteria. We have to consider also in a diabetic foot the open wounds as a source of bacterial infection. These are often times chronic and can be much more complicated than the closed infections. Open wounds are often times draining deep plantar abscesses. They most often contain mixed bacterial flora and these can involve a combination of aerobic and/or anaerobic bacterial infections.



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Certainly, one of the most obvious warning signs of infection that the patient may detect is redness, cellulitis, erythema, or petechia. In discussing the cellulitis in a diabetic lower extremity, it is important to keep in mind two key types that may present most commonly. This is nonblanching cellulitis and blanching cellulitis. In the photo on the right you see an evidence of blanching cellulitis. This is a typical bright red erythema that can be blanched easily upon palpation. The photo on the left demonstrates a more deeper petechial and ruborous type of a cellulitis and this is really a nonblanching cellulitis which is most commonly associated with a strep infection in contrast to the blanchable cellulitis most commonly presenting with a staph infection.



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One key factor that we have become much more aware of in recent times and recent literature is the fact that lab values and typical indicators of infection can be much less sensitive in the diabetic lower extremity. Individuals who present with a significant diabetic foot infection often times have a normal white blood cell count and in fact 57.6% of patients in the study by Dr. Lavery presented with diabetic foot infection that they had a normal white blood cell count. Dr. Armstrong followed this up with additional study showing 54% of 28 diabetic patients who had osteomyelitis confirmed had a normal white blood cell count on laboratory evaluation. In addition, common tests such as sedimentation rate or ESR can also be misleading. In study and work by Dr. Lavery, the ESR was found to be normal in 36% of patient’s who had puncture wound infections and oral temperature in addition was found to be a poorly sensitive indicator of diabetic foot infection with no significant elevation in 82% of diabetic foot infection patients who present to the hospital.



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A delay in treatment certainly is a well-documented risk factor for poor outcomes and amputation in the presence of diabetic foot infection. Dr. David Armstrong studied this and published in 1997 looking in particular of the interval from the time of injury to the time of surgery for diabetic foot infections in those individuals who indeed had diabetes versus those who had foot infections without diabetes. It was found that this interval or delay was nearly twice as long in the diabetic population of 13.3 days versus 6.9 days in the nondiabetic foot infection population. This has an obvious and strong negative influence on outcomes for these patient and limb salvage. This can be closely tied to the prevalence of peripheral neuropathy as you can see here 84.4% of patients with diabetes presenting with neuropathy versus the nondiabetic population certainly having very rare incidents of sensory neuropathy at 8.7% per this study.



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It is a rather interesting case study involving a young Hispanic American male, who is a construction worker. Several weeks prior to presenting to our emergency room he recalls stepping on nail through his work boot and actually had a hard time removing this nail from his boot. When he presented he complained of some focal redness and swelling to the area underneath his third metatarsophalangeal joint and upon operative incision we found a focal abscess involving the minimal amount of soft tissue destruction right in the area of this suspected puncture wound tract. We got down to a fairly viable soft tissue bed. However, we elected to continue our dissection deeper despite the viable soft tissues because of our concern from this preoperative x-ray that you see. This cystic focal change in this radiolucency to the central distal aspect of his third metatarsal had corresponded precisely with the area that the individual complained of his puncture wound and we were suspicious that this could involve some trauma from the actual nail itself.



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Here you can see the clinical picture once we continued dissecting through these soft tissues and exposed then the third metatarsal head through the plantar incision. You can actually see this puncture in the third metatarsal head going through the cartilage centrally and deep into the bone. We elected at that time because of the significant contamination posed by this puncture wound to resect that portion of his third metatarsal head and this was confirmed to be early osteomyelitis on pathology.



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One key question that comes up often is regarding the choice of empiric antimicrobial agent for patients with diabetic foot infection. Rather certainly there is no single right or wrong protocol for how to treat your patients with antibiotics. Most institutions and individuals practice broad spectrum initial therapy until you can guide that to a more narrow spectrum therapy from your surgical cultures. Often times, the combination antibiotics such as a Piperacillin/tazo-bactam will be utilized as a front line therapy and then this eventually can be tapered down to a more specific agent guided by the cultures and the sensitivities from your surgical specimen.



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Another key question that arises in regards to diabetic foot infection is on the topic of surgical debridement when and in whom should that be performed. Some of these clinical scenarios are quite easy such as on the left-hand photo. This is an aggressive, deep, and spreading plantar foot abscess that requires emergent debridement as soon as possible. The photo on the right, however, is a bit more vague in a patient who presents with some swelling, some redness, and vague pain and in this situation you may have to put further attention at the differentiating between Charcot versus infection. However, a good general rule to follow is that if there is any doubt or concern for the possibility of infection there is very little hesitation generally to perform a simple incision and drainage and remove this possible doubt from the scenario.



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A significant complicating factor for diabetic foot infection can be peripheral arterial disease. As you can see in each of these clinical scenarios there is presence of both diabetic foot infection and critical limb ischemia and gangrene. In each of these scenarios one has to weigh the priority between dealing with the infection versus treating the critical limb ischemia. Literature tells us that if possible revascularization should be attempted prior to definitive amputation to yield better salvage and healing rates. However, again if the infection reaches a limb threatening potential and cannot be controlled with local incision or systemic antibiotics then the infection again takes priority and emergent debridement must be performed.



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As with many things in the diabetic foot, an infection should be approached systematically when possible. These key steps can include incision, exploration, culture, debridement, hemostasis, lavage, and appropriate dressings. We will review each one of these in detail in the following slides.



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When the decision is made to proceed to the operating room with a diabetic foot infection, the incision generally should be aggressive and complete. There should be no doubt that purulence extends past the incision line and additionally the surgeon should follow the tissue planes, explore the compartments, and open the adjacent areas to remove any possible doubt of adjacent or remaining infection.



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In reviewing some of the basic anatomy regarding facial planes of the foot, it is important to point out the complex nature of the plantar compartments. These compartments are multiple and extend deep into the arch and central space of the foot but there is also significant concern for the communication that occurs between the central, medial, and lateral compartments and also the communication that can occur between the plantar compartments and the dorsal compartment of the foot.



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One key clinical tool that can be utilized in incision planning for diabetic foot infection is the use of a blunt probe. This can involve a sterile stainless steal instrument or a disposable cotton tip applicator. Here you can see a patient who presented with clinical infection on the dorsum of the foot that began from an abscess and open wound at the fourth webspace. The blunt probe or cotton tip applicator is placed within the beginning of this abscess and in this picture you can see how deeply this was passed to help guide our incision planning for this individual. Finally, you see the eventual ray amputation and extensive dissection, which was guided by our blunt probe planning.



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One popular incisional approach for plantar compartment diabetic foot infections was published by Loeffler and Ballard in Foot and Ankle in 1980. This single incisional approach can expose all five central plantar spaces and involves an incision that begins at the distal aspect of the first intermetatarsal space and proceeds as necessary proximally through the medial longitudinal arch towards the medial malleolus. This follows the natural anatomy of the flexor tendons and soft tissue apparatus and follows the natural progression often times of foot infection through the facial planes proximally.



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Medial compartment infections are some of the most commonly presenting infection types in the diabetic foot. As you can see from these clinical examples, they are often times well circumscribed by the natural anatomy of the medal compartment. The three key sources for a medial compartment infection are ulceration underneath the first metatarsal head, ulceration at the medial aspect of the first metatarsal, and ulceration of the hallux.



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Central space infections can be some of the most devastating secondary to the depth and multiple layers of the plantar central spaces in the foot. You can see here some clinical examples of central space infections that are quite extensive and certainly can be limb threatening. Key sources for central space infections are ulcerations of the central metatarsal heads, web space infections which can easily contract proximally, central digital ulcerations which again contract proximally into the deep spaces, and then Charcot deformity with “Rocker Bottom” foot type ulcerations that can present at the midfoot plantarly.



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Similar to a medial compartment infection, a lateral compartment diabetic foot infection is naturally bound by the anatomy and the facial structures of that compartment. One of the most common sources for a lateral compartment infection is an ulceration on the lateral aspect of the fifth metatarsal head. In addition, a digital ulceration to the fifth digit can be the source for infection of a lateral compartment, and finally an ulcer underneath the plantar aspect of the fifth metatarsal head can be an inciting event for a lateral compartment diabetic foot infection.



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Dorsal space infections in the diabetic foot can begin from a primary source of infection dorsally or can be secondary to spread from a plantar diabetic foot infection. We should differentiate clearly between the dorsal space infections of two types. One is a subcutaneous infection, which is rather superficial in nature and the other is the subaponeurotic dorsal space infection. This is deep to the deep fascia of the dorsal foot and is located between the fascia and the dorsal interosseous membrane. Each of these infections can spread rapidly, but are noted to be at different levels of the dorsal spaces.



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Once the appropriate incision has been made, exploration is the next step to assure that all the adjacent tissues have been explored and the appropriate tissue planes have been opened. Here you must rely upon your knowledge of the compartmental anatomy and the functional anatomy in communication between each of these spaces that would necessitate additional exploration or blunt dissection. You should compress each of the suspicious compartments to assure that you have not left an abscess behind in an adjacent compartment.



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Appropriate culturing is a key and very necessary segment of treating a diabetic foot infection. Some important points to keep in mind are that tissue and bone cultures are generally preferred over a surface swab culture. Secondly, an intraoperative culture secondary to the appropriate environment and nature in which the culture was taken is generally preferred to an outpatient or bedside performed culture, and finally, there is really very little clinical value to repetitive postoperative culturing mostly because these patients most likely are already on antibiotics and their wounds are probably been treated with some type of a topical antimicrobial agent, which would definitely skew the results of a surface culture.



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Once the incision has been made, the wound has been explored and the appropriate cultures have been obtained. The next general step in diabetic foot infection treatment is appropriate debridement. This is generally performed utilizing a blade and/or scissors for sharp dissection and it is important to remove all obviously necrotic soft tissue and skin edges and also bone, if it was exposed and suspect for infection is generally removed at this point.



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With the sharp debridement now concluded, the next general step in treatment of diabetic foot infection is a pulsed lavaged irrigation utilizing a large volume of fluid generally 1-3 liters of volume. The fluid is generally a normal saline solution, although an antibiotic can be impregnated into the same solution.



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With the wound now decontaminated via the debridement and lavage, the next steps are appropriate hemostasis and wound dressing. For hemostasis, we most often utilize pressure and if necessary Bovie is applied and surgical ligatures or ties can be applied as necessary for vessels. Drain placement should certainly be considered, if the wound site is going to be primarily closed. However, the majority of diabetic foot infection debridement the wound is packed open for future planning of repeat debridement versus eventual secondary closure. The wound site can be dressed with a variety of topical agents. Some of these may include short term use of topical antimicrobial agents such as acetic acid or dilute Dakins solution.



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With a large soft tissue and bony defect often times created with the surgical debridement, one has to consider multiple options for eventual closure of these surgical wounds. Primary wound closure is rarely indicated in the face of diabetic foot infection and generally these patients are brought for future debridement and delayed primary closure versus healing via secondary intention. The secondary intention is considered, one should probably consider use of the negative pressure system or wound VAC therapy to augment this secondary closure. In addition, if the wound site is superficial, a split thickness skin grafting can be considered or combined for full thickness wounds with a rotational flap or free flap closure. An alternative to this is bioengineered tissues in combination often times with the VAC for granulating deep wounds and eventual superficial closure.



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As we have discussed earlier in this lecture the vascular status can play a very pivotal role in the success of treatment for diabetic foot infection. Once the debridement has been performed, one should constantly reassess the vascular status and particularly should reassess prior to any definitive amputation or wound closure. As you can see in these clinical photos each of these amputation levels at the midfoot, rearfoot, and forefoot were complicated by poor vascular status and one on to eventual failure.



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This is a case discussion involving a dorsal abscess in a patient who had a primary dorsal lesion. You can see the incisional planning and eventual deep incision and extensive nature of the debridement. This patient was brought to the operative room twice and there were significant soft tissue compromise and eventual skin loss from the level of the infection. You can note that the dorsal extensor retinaculum is exposed at the level of the ankle showing this subcutaneous dorsal infection.



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This patient with longstanding diabetes and a chronic ulcer underneath the fifth metatarsal head has gone on to significant abscess involving the entire plantar arch and as you can see from this lateral view there is also involvement laterally with several additional lesions that are formed secondarily to the abscess.



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This complicated diabetic foot infection obviously requires significant incision, debridement, and exploration. You can see here in these two views showing the extensile incision made through the plantar aspect of the patient’s foot involving the medial longitudinal arch and many of the deep compartments of the plantar central space.



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Continuing to follow the same patient you can see that further debridement was necessary to remove the skin flaps and the nonviable necrotic tissue, which was full thickness in nature. However, the underlying deep muscle bellies of the plantar longitudinal arch are viable and intact, as you can see in this illustration. Lateral view of the same foot is showing again further debridement of the skin and subcutaneous tissues, but viable deep soft tissues and muscle belly.



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Because of the viable deep muscle belly, this patient went on eventually to limb salvage. The decision was made to perform a split thickness skin graft involving this mostly nonweightbearing surface of the medial and longitudinal arch. Here you can see the plantar and oblique views showing complete coverage of this wound with resolution of the infection.



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This is a clinical presentation of a patient with a chronic ulceration who began to have some swelling and redness on the foot involving the dorsal aspect of the same extremity. Upon examination, it was noted that this ulcer did probe deeply into the dorsal space of the foot and indeed was the inciting event for this dorsal abscess, which required surgical debridement and exploration.



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This case involves a mid 30s male with history of type II diabetes poorly controlled who presents at the hospital emergency room with redness, swelling, and pain sudden onset to his left midfoot. He has no source for infection, no history of trauma, and no prior foot complications.



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This same patient had a small dorsal bedside I&D performed, which revealed no purulence and cultures were negative. An MRI was performed which showed no specific bone changes and one key clinical observation that should be made from this slide is the dilated veins noted at the level of the ankle and lower leg. This was a key clinical factor that let us to believe that this patient was in a hypervascular state and possibly a candidate for Charcot versus infection.



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After discharge long term, it was noted that indeed this patient did have a Charcot episode that required extensive offloading and careful management. Here you can see the radiographs at the time of the hospitalization, which were completely normal showing no significant bony changes versus these x-rays were obtained several weeks after discharge showing the significant midfoot disruption consistent with Charcot neuropathic osteoarthropathy.



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This next patient has a longstanding poorly controlled type II diabetes and has undergone a midfoot amputation secondary to infection. It is a concern after healing of this wound utilizing biogeneric tissues is that the patient remains in a fixed position of equinovarus, therefore predisposing to recurrent ulceration and infection underneath the residual fifth metatarsal stump at the lateral aspect of his foot.



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This patient was brought to the operating room for a prophylactic procedure to lengthen the Achilles tendon as well as transfer the tibialis anterior tendon to correct the equinovarus deformity. On the left, you can see the preoperative planning for the tendo-Achilles lengthening. On the right you can see harvesting of the tibialis anterior onto the dorsal aspect of the anterior leg and routing this tibialis anterior tendon through appropriate soft tissue tunneling onto the dorsolateral aspect of the midfoot.



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Given this patient’s history of longstanding ulceration underneath the residual fifth metatarsal stump, the choice was made to resect a portion of this fifth metatarsal stump and also to apply calcium sulfate antibiotic impregnated beads into the wound site. Here you can see the fashioning of those beads, which takes roughly 2 minutes to perform in the operating room with minimal attention. The beads are extracted from the template and a small number are placed into the wound site.



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This is our patient roughly 2 weeks postoperative. You can see the incision sites at the anterior, medial, and lateral aspects of the foot and leg. You can also see a few of the antibiotic pellets, which are exiting the wound plantarly. This is the wound roughly 6 weeks postoperative showing complete healing of the incision sites as well as the chronic ulceration underneath the fifth metatarsal stump and also you should note the correction of the equinovarus deformity on this view.



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This next patient presentation involves a 45-year-old Hispanic-American male with an infected ulcer on the plantar aspect of his right foot. The area under the fifth metatarsal head had previously been noted to be a callus, which had been treated with debridement. The patient did notice increased redness and swelling for one week and some drainage that was present from the ulcer site along with constitutional symptoms of fever for 3 days prior to admission.



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The patient’s past medical history included poorly controlled diabetes for 12 years including a fasting blood sugar of 175 or greater. The patient has a significant history of neuropathy, gastroparesis, and sexual dysfunction. The patient has a history of seizures and chronic headaches. In addition to medications include insulin, nitroglycerin, and Tegretol.



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The patient’s past surgical history includes incision and drainage of groin and back abscesses. He has an allergy to penicillin as well as aspirin. Socially, the patient admits to 15-pack a year history of smoking and his family history includes diabetes and endstage renal disease in his father with a complication of an above knee amputation.



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Physical examination, vascular exam shows a bounding DP and PT pulse bilaterally. There is a nonpitting edema to the dorsal aspect of the right foot and included increased warmth to the right foot. Neurologically, the protective sensation is absent in bilateral lower extremities. Dermatologically, there is 1.0 cm ulceration to the plantar aspect of the fifth metatarsal on the right foot with surrounding hyperkeratotic tissue undermining malodor and nonblanching erythema. Musculoskeletal examination shows an intrinsic minus foot type with significant soft tissue atrophy and bilateral hallux valgus deformity.



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In these clinical photos, you can see the ulceration evident at the plantar aspect of the fifth ray; however, you should note the significant amount of undermining poor tissue quality and a significant erythema extending plantarly and dorsally.



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Illustrated here are the CBC and chem.-7 for this patient.



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The patient was treated with bedside debridement of all undermined and nonviable tissue. IV antibiotics were begun. You can see here the stable nature of the erythema with no additional spread beyond the previously marked margin.



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These are the preoperative radiographs for the same patient. Here you can see some suspect changes to the fifth metatarsal head as well as the lateral base of the fifth digit.



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Lateral view preoperative x-ray of the same patient showing no soft tissue gas only a soft issue defect noted at the site of ulceration. No other significant changes seen.



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Continuing with the hospital course for this patient, he was brought to the operating room for partial fifth ray amputation, debridement, and exploration. Intraoperatively, it is noted that the patient had significant necrotic and hemorrhagic soft tissue throughout the fifth ray, which necessitated amputation of digit as well as the metatarsal head.



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At postoperative day 3, you can see the wound site with resolving infection, but increasing significant concern for ischemia particularly the dorsal flap with the black necrosis noted and surrounding gray tissue significant risk now for arterial compromise and peripheral vascular disease.



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Looking at the postoperative radiographs, you can see the evident partial ray amputation performed to the fifth ray and the tubing in place for the negative pressure wound VAC therapy.



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The hospital course continued for this patient. He was brought back to the operating room for a revisional fifth ray amputation. Intraoperatively, there was addition thrombosis of the dorsal skin and the soft tissue surrounding and the wound VAC was reapplied postoperatively for this patient. In addition, the patient began a course of daily hyperbaric oxygen therapy.



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Extensive arteriovascular workup was performed. However, this patient was deemed to have no appropriate interventions that could be performed and with a mostly viable wound at this point, the patient was prepared for hospital discharge and stringent local wound care continued hyperbaric oxygen therapy and wound VAC therapy were continued.

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Although, the patient was beginning to have a viable wound based at the time of hospital discharge. The significant vascular risk spectrum must be reconsidered and evaluated. From a microvascular perspective, this patient has uncontrolled diabetes with history of intermittent claudication. Microvascular, this patient has significant neuropathy and from a functional perspective, this patient has a history of gastroparesis and sexual dysfunction. The environmental factors influencing the vascular risk spectrum for this patient are also significant with a 15-pack year history of smoking and history of previous alcohol abuse. The family history also contributes to this patient’s vascular risk spectrum because of the history of diabetes and history of amputation and renal disease that his father sustained.



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With the continued challenge of peripheral arterial disease that was untreatable. The patient’s extensor tendons eventually became nonviable and were exercised at bedside. The patient did continue daily hyperbaric oxygen therapy Monday to Friday and moist dressing changes were performed twice daily. The patient did get readmitted to the hospital 1-month later with nonhealing problem ischemic wound, which eventually necessitated a transmetatarsal definitive amputation.



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Some examples of the complications that can result from diabetic foot infections and some of the information we have just reviewed in this lectured include those who perhaps have already sustained a partial foot or foot amputation and now are at risk for loosing further segments of their limb secondary to a recurrent infection or perhaps this patient who we saw earlier who has a first onset of a diabetic foot complication, which involves significant risk for limb loss and threatening infection and this individual who has a longstanding history of diabetes, no history of previous wound, but now a superficial infection secondary to an insect bite that requires advanced treatment and significant intervention to prevent this from going on to a limb threatening infection.



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Diabetic foot infection is a limb threatening and often times, life threatening disease. To best treat these, we must convert the infected wound to a clean wound aggressively and quickly and we must consistently manage these patients for a medical and surgical perspective. One key factor that can be left out is educating this patient appropriately to the step that they can take to prevent recurrence of yet another diabetic foot infection that would place them at further risk.



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I thank you very much for your attention and I certainly would welcome any questions or thoughts that you may have to e-mail at my address, which is steinberg@usa.net.



Thank you very much.



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