Time Stamps

  • 02:15 Pearl 1: Pathophysiology
  • 08:20 Pearl 2: Diagnosis
  • 16:35 Pearl 3: Treatment
  • 20:35 Pearl 4: Antibiotics
  • 27:39 Pearl 5: Wound Care

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Show Notes

Pearl 1: Pathophysiology 

A Review of Foot Ulcers

  • Neuropathic (diabetic) ulcers
    • Usually plantar, weight-bearing, painless
    • Often have a vascular component
  • Arterial (ischemic) ulcers
    • Dry, punched-out, painful
    • Often around the ankle/foot
    • Require vascular evaluation
  • Venous ulcers
    • Typically ankle/shin
    • Edema, hyperpigmentation, drainage
    • Managed with compression + elevation
  • Pressure injuries
    • Over bony prominences (i.e. heels)
    • Require aggressive offloading

Evaluation and Management of Lower-Extremity Ulcers. N Engl J Med. October 18, 2017.

Why do diabetic foot ulcers develop?

  • The majority diabetic foot ulcers arise from a combination of:
    • Peripheral neuropathy
    • Foot deformity (bunion, hammer toe, Charcot changes)
    • Minor trauma (shoe irritation, blister, callus loss, stubbed toe)
  • Footwear matters 
    • Poorly fitting shoes are a major and under-recognized contributor.

Key clinical principle

  • Diabetic foot infections are “great masqueraders”:
    • Minimal pain
    • Patients may lack fever, leukocytosis, or erythema
    • May have hidden deep abscesses or osteomyelitis
  • Neuropathy masks symptoms → late presentation → deeper infection

Pearl takeaway: Always assume more disease than meets the eye.

Pearl 2: Diagnosis 

Start with a careful exam

  • Assess:
    • Temperature (hot vs cold)
    • Swelling
    • Odor
    • Discharge
    • Depth and location
    • Whether it tracks or has undermining

Probe-to-bone (PTB) test

  • One of the most powerful bedside tools
  • Technique:
    • Gently probe base and periphery of ulcer
    • Assess for bone, tendon, sinus tracts
  • Interpretation:
    • Positive PTB → strongly rules in osteomyelitis
    • Negative PTB → reassuring in low-pretest probability settings
  • Sensitivity/specificity approach those of MRI when used appropriately.

Initial workup

  • Clinical exam
  • Plain X-rays
    • Often underappreciated and very useful
  • Labs
    • ESR, CRP (± procalcitonin)

Advanced imaging

  • MRI
    • High sensitivity (>80–90%)
    • Lower specificity (~75–80%)
    • Bone marrow edema ≠ osteomyelitis
      • This can be seen with pressure injury or inflammation alone and doesn’t always mean osteomyelitis is present.
    • Useful to:
      • If the initial work-up is inconclusive or with cases of uncertainty
      • Guide surgical planning, if needed

Gold standard

  • Bone biopsy (histology ± culture)
  • Limitations:
    • Invasive
    • Logistically difficult
    • Might not be feasible depending on area of the leg/foot
  • Often not done solely to confirm diagnosis.

Pearl 3: Treatment 

  • Assess and optimize blood flow
    • Ulcers won’t heal — and antibiotics won’t penetrate — without adequate blood flow.
    • 2026 ADA guidelines 
      • All people with diabetes >50 years should undergo noninvasive arterial screening studies
    • Ankle-Brachial Indexes (ABIs):
      • Easy, low-cost, high-yield
        • ABI <0.9 
          •  ~98% specific and ~85% sensitive for peripheral artery disease
      • Consider broadly in patients with diabetes (even if pulses are palpable).
    • Vascular surgery may also ask for CTA with runoff
    • Ask:
      • Will this wound heal after debridement?
      • Does the patient need revascularization?
  • Source control
    • May include:
      • Abscess drainage
      • Surgical debridement
      • Partial or complete amputation
    • Surgical debridement is the primary therapy for osteomyelitis.
      • Purpose: turn a chronic ulcer into an acute, healing wound
        • Procedure can include:
          • Removal of all nonviable soft tissue and bone
          • Excision of callus tissue surrounding the ulcer
          • Removal of senescent fibroblasts in the wound bed
          • Removal of abnormal keratinocytes at wound edges
          • Reduction of bacterial burden
        • Only type proven efficacious in clinical trials for diabetic foot ulcer
    • Always check:
      • Did surgery achieve clean margins?
        • Residual infected bone affects antibiotic duration and strategy.
  • Debridement and/or Amputation in Diabetic Foot Infections (Expert opinion)
  • (Multifactorial, Goal = source control + limb preservation)
    • Extent of infection (primary driver):
      • Extensive infection + significant bone involvement → favors primary/open amputation for source control
      • Localized infection ± limited bone involvement → debridement ± limited amputation may be feasible
  • Bone involvement:
      • Widespread osteomyelitis → favors amputation
      • Focal bone involvement → consider bone debridement with limb preservation
    • Vascular status (key modifier):
      • Good perfusion → more likely to heal with debridement, can consider staged approach (debridement → reconstruction/closure)
      • Poor perfusion → favors more definitive procedure (amputation) due to poor healing potential
    • Clinical approach:
      • Balance infection control (prevent spread/progression) with preserving as much of the foot as possible
      • Often stepwise/staged, escalating if initial management fails
    • Reality:
      • Decisions are clinical, subjective, and individualized (no strict algorithm)

Pearl 4: Antibiotics

Should you hold antibiotics for cultures?

  • Unstable/septic patient → start antibiotics immediately.
  • Stable patient → consider holding if cultures will change management.
  • Key nuance:
    • In ischemic or necrotic tissue, antibiotics may not penetrate → cultures may remain positive or have decent yield even after antibiotics start.

IV vs oral therapy

  • Historical dogma: bone infections = IV only.
  • Modern evidence:
    • Route doesn’t determine bone penetration — blood supply does.
    • Large RCT (OVIVA trial) showed:
      • Oral therapy is non-inferior to IV for bone and joint infections, including DFI.
  • Practical approach:
    • Use IV in acute/septic phase.
    • Transition to oral once stable and on definitive therapy.

Duration of therapy

Blackshear L, Stead W, LaSalvia M. Antibiotic therapy in the diabetic foot. Clinics in Podiatric Medicine and Surgery. 2025;42(4):615–634.

Assessing for cure

  • Labs and imaging lag behind:
    • ESR/CRP may stay elevated.
    • MRI may look abnormal long after infection is controlled.
  • Best test of cure = clinical improvement over time.

Pearl 5: Wound Care

First question: Is the wound wet or dry?

  • Most diabetic foot wounds are:
    • Dry
    • Dirty
    • Neuropathic
  • Goals:
    • Clean the wound
    • Keep it moist (not dry!)

Wound cleansing agents

  • Common options:
    • Betadine
    • Hypochlorous acid
    • Acetic acid (antipseudomonal)
    • Diluted bleach (for very angry/infected wounds; short-term use only due to skin irritation)

Dressings

  • Dry wounds → Xeroform
    • Petrolatum-impregnated mesh
    • Adds moisture
  • Wet/weeping wounds → Aquacel
    • Super-absorbent fiber dressing

Practical bedside approach

  • Clean first → choose dressing based on wet vs dry:
  • When in doubt overnight or over the weekend:
    • Betadine + Xeroform is the best go to for dry diabetic foot infections.

Offloading = essential

  • Pressure impairs blood flow:
    • As little as 2 hours of continuous pressure can cause ischemia.
  • Interventions:
    • Elevation
    • Protective boots
    • Repositioning
    • Pressure-relieving surfaces

Transcript

Dr. John Giurini: I often describe diabetic foot ulcers as many times being the tip of the iceberg. You see this wound on the bottom of the foot, and it’s like, “Oh, that doesn’t look too bad”. One of the things to remember about diabetic foot infections and diabetic patients, as a rule, is they’ve been turned as the great masquerader.

Dr. Shreya Trivedi: Welcome to the Core IM 5 Pearls Podcast, bringing you high-yield evidence-based pearls. I’m Dr. Shreya Trivedi, and I’m joined by 

Dr. Colby Weil-Lonigan: Hi, everyone. I’m Colby Weil-Lonigan. I’m an internal medicine resident at BIDMC. Today, we’re tackling diabetic foot infections and foot osteomyelitis, a topic that feels routine, but is anything but simple.

Dr. Shreya Trivedi: Yeah. And I think one of the reasons why, at least for me, I feel like I haven’t clarified a lot of the pain points that come up with this topic is because I think there’s just a bunch of different specialties that kind of own it. So it’s kind of easy to defer to whatever podiatry or infectious disease or ortho or wound care is saying and not really solidify why did they recommend this for this one patient versus something else for another patient with maybe a slightly different presentation. So let’s do some simplification today. Test yourself by pausing after each of these five pearls.

Dr. Colby Weil-Lonigan: Pearl one, etiology of foot ulcers.

Dr. Shreya Trivedi: Why is thinking about the why of foot ulcers so important?

Dr. Colby Weil-Lonigan: Pearl two, workup and imaging.

Dr. Shreya Trivedi: Which diagnostics are most helpful and which ones can mislead you? Do you always need to get that foot MRI?

Dr. Colby Weil-Lonigan: Pearl three, surgical debridement and source control.

Dr. Shreya Trivedi: What actually does surgical debridement entail? Do we always need it? And when do we have to think about vascular flow?

Dr. Colby Weil-Lonigan: Pearl four, antibiotics.

Dr. Shreya Trivedi: Can we get away with PO antibiotics for osteomyelitis?

Dr. Colby Weil-Lonigan: Pearl five, wound care.

Dr. Shreya Trivedi: Why is the wound care nurse asking for xeroform and betadine for one patient versus aquacel and dakins for another?

Dr. Shreya Trivedi:  All right, Colby, we often see these patients with foot infection, and I think it’s so easy to jump into management, right? Do I hold antibiotics? Do I start? Which ones? Should I get the surgical team on board? But what I really appreciate is when we spoke to our discussions, they said, “Hold on. Wait a minute. Before you jump into management, it is so important to step back and ask why.“

Dr. Colby Weil-Lonigan: Yes, exactly. We talked to Dr. John Giurini, a podiatrist and nationally recognized expert in diabetic foot care.

Dr. John Giurini: Why did this ulcer develop in the first place? Is there an associated deformity that goes with that ulceration? Like a bunion, like a hammer toe. If it’s on the top of the foot, it could be related to shoe gear. So this is some of the investigative work that we do to understand the underlying cause of the ulceration. There was a paper, I think it was published in 1999 in diabetes care. They found that the combination of neuropathy, deformities plus minor trauma were the highest risk factors for development of ulcerations. That combination was responsible for 70 to 75% of ulcerations. So when you look at an ulcer, you can pretty much think about is there a foot deformity and has there been any microtrauma, including shoe irritation?

Dr. Shreya Trivedi: I get the neuropathy, I get the deformity, like bunion or hammer toe, being a nidus for diabetic foot infection. But I’ll admit, I used to think of minor trauma in diabetic foot infections as like blisters, a stubbed toe. But the last point he made surprised me, that just repeated shoe irritation without a clear injury can be enough to tip someone over into an ulcer.

Dr. Colby Weil-Lonigan: Yeah. All the more reason to ask our patients about their footwear. I mean, it’s always nice to get a new pair of shoes, but we really need to be aware of all the issues that they could potentially cause.

Dr. Shreya Trivedi: Yeah, definitely. And I guess if we dig deeper into the why of the foot ulcer, we classically learn about different types of ulcers, right? The classic diabetic neuropathic foot ulcer, the arterial or vascular ulcer, the venous ulcer, the pressure ulcer. In reality, of course, this is very multifactorial, but I think it’s still helpful to remember the classic presentations.

Dr. John Giurini: The diabetic ulcers usually can be a combination of vascular and neuropathic in nature. And the other thing about the diabetic ulcer, it’s usually in a weight-bearing area, so that’s pretty easy to differentiate. The arterial ulcer is usually a very ischemic, dry-looking ulcer. Usually, in and around the ankle joint, they tend to be very painful. So it’s important to know that because if it’s arterial ulcer, then you need to get vascular involved to address the vascular issue. If it’s a venous ulcer, again, you’re going to see these usually around the ankle area, the shin area. They’ll have a healthier look to it. There may be some serious drainage associated with it. The surrounding tissue is going to be abnormal. There may be edema, varicosities, and brawny hyperpigmentation of the shin. And it’s important to differentiate because with venous ulcers, the important thing to do there is elevation and compression.

So making those distinctions is important because the treatment plan and regimen will be slightly different for each one of those.

Dr. Colby Weil-Lonigan: Yeah. So I think what I’m taking away from this is that when we see these foot infections that have an ulcer, we really need to ask ourselves, one, is this a heel pressure injury? It needs more focus on offloading and wound care. Two, is this an arterial ulcer that needs vascular input to improve blood flow? Or three, is this ulcer more driven by like, say neuropathy, and we need to think about prevention? Lastly, for those venous ulcers around the shin or ankle, do we really need to be thinking about more compression and elevation?

Dr. Shreya Trivedi: Yeah. And we’ll link in the show notes a nice graphic for where each of these ulcers classically are and the differences in management. But as you’ll see when we talk about diabetic foot ulcers, knowing these will help in terms of the management and how a little bit of each might come into play.

Dr. Colby Weil-Lonigan: Yeah. So to recap, when we say diabetic foot ulcer, we’re usually talking about an ulcer that is neuropathic WITH a pressure-related wound at the bottom of the foot, and that’s plus or minus vascular blood flow issues.

Dr. Shreya Trivedi: Right. And the other things we need to be asking ourselves is to think, are there any foot deformities involved or any recent minor trauma like improper footwear?

Dr. John Giurini: Whenever you see a foot ulcer, to really examine it very closely, look at the ulcer itself. So I have that high index of suspicion.

Dr. Colby Weil-Lonigan: Yeah. So these patients may not have a fever, leukocytosis, erythema, or pain. This often leads to late presentations and potentially even deep infections.

Dr. Shreya Trivedi: Yes. I guess we have to always assume more meets the eye.

Dr. Colby Weil-Lonigan: Yeah. And I think this sets us up really nicely for Pearl two. And Pearl two will focus on how we actually assess and closely examine these ulcers with a special emphasis on how to make sure we’re not missing anything like osteomyelitis. 

Pearl 2: Work up and Imaging

Dr. Colby Weil-Lonigan: You really have to slow down when osteomyelitis is on the table because what looks like a small foot wound can often represent something much deeper.

Dr. Shreya Trivedi: Yeah. So when we are looking closer, this means don’t just upload a picture onto Epic, which I’ve definitely been guilty of doing before, but really assessing the temperature, is it hot, cold, is there any swelling, any discharge odor? And especially looking at the ulcer itself and particularly how deep is it and does it track?

Dr. John Giurini: I often describe diabetic foot ulcers as many times being the tip of the iceberg. You see this wound on the bottom of the foot, and it’s like, “Oh, that doesn’t look too bad.” But until you really probe it and manipulate it, you really don’t know how severe this might be.

Dr. Colby Weil-Lonigan: Which brings us to one of our most powerful bedside tools we have, probing the ulcer to evaluate for osteomyelitis.

Dr. John Giurini: Then I’ll take my probe and I’ll insert the probe into the ulcer. Gently, I don’t jam it in there, but I gently probe the base of the ulcer. I probe around the periphery of the ulcer to see if there’s any undermining, and then I’ll try to probe deep to see how deep it goes. That’ll tell me if there’s tendon involvement, if there is bone involvement. And to the point about the sinus tract, if I find that this ulcer now tracks proximally or distally, I know there’s a sinus tract, and there could be a collection of fluid and abscess in that area that may need to be opened and drained.

Dr. Shreya Trivedi: Interestingly, of all the things you can do in your workup, the probe to bone was emphasized the most across board, no matter who we talk to. We also sat down with Dr. Sandy Nelson, an infectious disease doctor at Mass General who walked us through her approach on the workup and where the probe to bone test sits within that.

Dr. Sandra Nelson: You should start with a combination of tests that include clinical evaluation, plain films, which are actually probably in some ways the best imaging studies that we have, and laboratory studies, including SED rate, C-reactive protein, and procalcitonin. And oftentimes, you can get to the diagnosis of osteomyelitis through those tests. Clinical evaluation, the element that is important for that is the probe to bone test. And the probe to bone test is actually an excellent test with very high sensitivity and specificity, really approaching what you get with MRI. And if you use it appropriately in the right clinical settings in a high pretest probability, a probe to bone test is going to definitively rule in osteomyelitis, and in a low clinical probability setting, that’s going to pretty satisfactorily rule out osteomyelitis. And so that’s the starting point.

Dr. Colby Weil-Lonigan: Okay. So a positive probe to bone test can basically rule in osteomyelitis.

Dr. Shreya Trivedi: Yes. And with that, let’s move from the exam to imaging. Of course, people often start with a plain x-ray, and if that shows signs of osteomyelitis, that might be all we need. But if things are unclear, then we might have to reach for an MRI.

Dr. Sandra Nelson: And then advanced imaging is really reserved for those tests in which the initial round of testing is not conclusive. And that’s the time that you might do an MRI. That’s probably your next best test in terms of both sensitivity and specificity for the diagnosis of osteomyelitis. I should also say that the other reason to do an MRI or to do advanced imaging is not only to confirm the diagnosis of osteomyelitis, but also to guide the need for and the extent of surgical management. And so sometimes you may have met the diagnostic criteria for osteomyelitis by other measures. You might have a very high set rate, a positive probe to bone test in a malodorous necrotic foot. That patient is going to have osteomyelitis, but it becomes important still to pursue the testing to then guide next steps.

Dr. Colby Weil-Lonigan: So surgical teams might want to get the MRI to further guide the interventions they might offer, but that all being said, MRI isn’t perfect, and this is a really important nuance to emphasize.

Dr. Sandra Nelson: When we look at studies around MRI, in terms of how to use MRI, I do have a big caution around this, which is that the specificity of MRI is not as high as we think it is. The sensitivity is pretty good. It’s over 80%, maybe approaching 90%, but the specificity is actually maybe 80%, maybe 75% depending on the clinical scenario. And the reason for that is that the earliest finding in osteomyelitis is one of bone marrow edema, and bone marrow edema is very nonspecific, and it’s seen in a whole variety of different entities, including pressure-related injury. And so if somebody has been walking on an open wound, they’re going to have some bone marrow edema underneath it. And so you’ll get a common read on an MRI, which is cannot exclude early osteomyelitis, which is very much not the same as there is osteomyelitis.

And so we just have to be careful about not overreading or overrelying on MRI because we then will overdiagnose and oftentimes the better thing to do in that setting is to say, okay, we’re going to treat for soft tissue infection, and then we’ll repeat other imaging modalities, perhaps a CT or a plain films, and then really make a decision about whether or not osteomyelitis is present before committing somebody to a full kind of treatment course for that.

Dr. Shreya Trivedi: I have definitely had smart ID colleagues stop me from ordering an MRI in cases where there was just concern that we’re going to get too much signal to noise ratio, right? Especially if these patients are already at such high risk for pressure being a part of their injury, and pressure itself can cause bone marrow edema, just as an example.

Dr. Colby Weil-Lonigan: And maybe the takeaway is that if we do get an MRI, we should read not just the impression, but go over the details of the report. Should I be asking my radiology colleagues how much of a slam dunk diagnosis those imaging findings are for osteomyelitis, or are they just calling it based on the amount of bone marrow edema?

Dr. Sandra Nelson: Really, the only way to confirm it is through bone biopsy, and that would be bone biopsy with the use of either histology and/or culture, and it’s debated as to which of those two is the better test. But I will also say that we don’t oftentimes go there strictly for the purposes of confirming osteomyelitis because there are risks associated with a bone biopsy, especially if there’s not another indication for surgery, and there’s oftentimes logistic hurdles to getting it done. This is especially true when you’re talking about a toe. It’s very hard to sample a toe without at least causing risk of injury. It’s a little bit different in the midfoot, but as a general rule, bone biopsy strictly to make the diagnosis is not commonly done. And commonly, we’re using these surrogate tests recognizing that they’re imperfect.

Dr. Shreya Trivedi: Oh, man. Where the ulcer is makes a difference. And I learned that the hard way. I still remember having a patient that was once admitted over the weekend. There was some concern of osteo of his third toe, and I for sure thought the game plan would be, “Okay, take to OR for bone biopsy or surgical debridement,” but now it makes sense why podiatry actually said no to the OR. It was just not a feasible area. 

Dr. Colby Weil-Lonigan: I know. I really thought the bone biopsy would be more of a priority, but I guess that might not always be the case. I think what I’m taking away from this is that a bone biopsy is the gold standard, but it might not always be practical and can do more harm than good.

Dr. Shreya Trivedi: So to recap, the next time I see a foot ulcer, I’m going to try to remember small wounds can be really hiding deeper disease, and I’m also going to challenge myself and next time I see one of these to go in with podiatry or the wound care nurse and have them kind of coach me through that probe to bone test.

Dr. Colby Weil-Lonigan: Yeah. I think I’m going to try to find those podiatry attendings and see what they can show me. And the key thing about MRI is that it’s sensitive, but not as specific, especially with bone marrow edema present, which can easily be seen in early osteo or with just a pressure-related injury, and are not alone in thinking about these things. Diabetic foot infections are often a team sport with at least ID, podiatry, and/or wound care to help think through things with you. 

Pearl 3: Treatment

Dr. Colby Weil-Lonigan: All right. Pearl three is all about treatment, which, as I found out, the mainstays of treatment for diabetic foot infections with or without osteo are source control and antibiotics.

Dr. Shreya Trivedi: Yes, but none of those things will work if we don’t have adequate blood flow. Ulcers won’t heal, and antibiotics won’t penetrate without adequate perfusion.

Dr. John Giurini: The majority are going to be neuropathic, but there can be a vascular component. So it’s important to identify that because if there’s a significant vascular component, it doesn’t matter what you do with the ulcer. If you don’t address the blood flow, it’s not going to heal. So that’s important.

Dr. Colby Weil-Lonigan: That’s exactly right. From what I learned, there are some vascular guidelines out there that say any diabetic patient older than 55 years old should get Ankle Brachial Index or an ABI. And this makes total sense to me because it’s an easy test. It’s just a ratio of the blood pressure between the ankles and that of the arms. They are quick, low cost, and really gives us a sense if peripheral artery disease is at play.

Dr. Shreya Trivedi: Yeah. And I’m sure there are different practice thresholds to get ABIs or not, but I think it’s not unreasonable. And especially I think from what I learned on the peripheral artery disease episode, where people can have bad PAD and still have palpable pulses, right? Whether it’s because they develop collateral blood flow or partial occlusions. For me, I feel like it’s not unreasonable to get it for all our patients with diabetes.

Dr. Colby Weil-Lonigan: Yeah, I agree. And I think the real key question for these diabetic foot wounds is, will this patient’s blood flow support healing after debridement or surgery? And to follow that, do we need to restore blood flow with an angioplasty or those other fancy things that vascular surgery might be able to offer? 

Dr. Shreya Trivedi: Great. Yeah. I feel like that’s like a do not pass go, must think about that. And then if there isn’t any blood flow issue, the next thing we want to also think about is source control, right? And that can be in many forms, ranging from draining an abscess if that’s present to doing a surgical debridement, and then, in some cases, an amputation.

Dr. Colby Weil-Lonigan: And surgical debridement is something I’ve heard thrown around a lot on words. I didn’t really fully appreciate what it entailed or how powerful a tool it was, but basically, what I learned is that the surgical team will debride the wound, remove anything around it, including bone, anything that really just looks grossly infected, and they can even do this at the bedside.

Dr. John Giurini: The treatment for osteomyelitis is surgical debridement, the primary treatment. IV antibiotics is an ancillary treatment. It’s a supportive treatment in those circumstances where maybe you can’t guarantee that you got all the infected bone out of there, or you want to suppress it further for a period of time.

Dr. Shreya Trivedi: One thing I’ve changed in my practice is to really look at that operative report and see if the surgical team got all the infected bone out or not, AKA was their good margins? And I know that’s something that the infectious disease team will ask about and it kind of helps determine their duration of antibiotics, which we’ll get to in Pearl four.

Dr. Colby Weil-Lonigan: And beyond surgery and antibiotics, we can’t forget the most basic part of treating these diabetic foot infections, which is optimizing their blood sugars and ensuring really good wound care. And Shreya, don’t worry, I learned all about wound care and I can’t wait to tell you about it in Pearl 5.

Dr. Shreya Trivedi: That’s going to be so good. So many knowledge gaps there. Okay. So to summarize mainstay treatment for diabetic foot infections with or without osteo of the foot, I think the first thing, do not pass go. We need to make sure we have good blood flow to that wound, right? That is so important because that’s going to give that wound the best shot for healing. And at the same token, adequate blood flow is going to make sure that our antibiotics are getting to the wound.

Dr. Colby Weil-Lonigan: And don’t forget about source control. This can be anything from draining an abscess to surgical debridement or even amputation.

Pearl 4: Antibiotics

Dr. Shreya Trivedi: Okay. Let’s talk about antibiotics. And here’s the thing that’s always made me pause, right? Patient comes in over the weekend, skeleton crew is on, no one’s definitively said yes or no to the OR for bone biopsy or surgical debridement. And the big question is, do we hold antibiotics to get cultures?

Dr. Colby Weil-Lonigan: And the answer is it’s nuanced. If your patient is unstable, like they’re septic, toxic, or crashing, definitely give antibiotics immediately. No debate there. But if they’re clinically stable and the cultures might meaningfully guide management, that might be your window.

Dr. Shreya Trivedi: Yeah. Imagine if they had MRSA in the past, Pseudomonas, or some resistant bug that required big gun antibiotics, then yeah, the culture would be helpful, or otherwise we’re just subjecting them blindly to weeks of broad spectrum antibiotics based on prior micro.

Dr. Colby Weil-Lonigan: Yeah, but here’s the twist. Even if you start antibiotics, cultures might still be useful.

Dr. Sandra Nelson: The other piece to consider is that these are often infections that are associated with some degree of vascular insufficiency, and vascular insufficiency leads to limited antibiotic distribution. And so oftentimes, if a patient has deep cultures collected 24, 48, 72 hours after starting antibiotics, those cultures are almost always still going to be positive and still positive in a way that we trust them. Once you’ve gotten beyond that, then it becomes a little bit less certain as to whether or not that the organisms that are recovered are fully representative of what’s in the deep tissues. When a patient goes to the OR, for example, they’re usually going to the OR because there’s some degree of tissue necrosis. So when there is tissue necrosis, the antibiotics aren’t getting there. It’s dead tissue. And so the cultures are very likely to still be active and reliable.

Dr. Shreya Trivedi: Oh, that is helpful to hear. Yeah. I didn’t appreciate that since antibiotics literally can’t get into necrotic or ischemic tissue, cultures might still grow the bug that was causing the issue. So I guess in a stable patient, we can try to hold the antibiotics if there’s a possibility of getting culture data. And at the same time, we might have some leeway knowing that we can start antibiotics, and it might not necessarily ruin the culture yield either.

Dr. Colby Weil-Lonigan: Yes, exactly right. Now let’s pivot to the next big question. IV versus PO. A lot of us reflexively go to IV for bad infections, especially osteomyelitis, but the data says we might be able to relax a bit.

Dr. Sandra Nelson: There have never been any clinical studies that suggest that antibiotics that are considered more bone penetrating actually perform better than others. And then on top of that data, we now have the very large AVIVA study, which was published, I want to say in 2019, which randomized patients with a bone and joint infection to either oral therapy or IV therapy culture-directed therapy for any type of bone and joint infection, including diabetic foot infections. And the take-home of this study, which is a very well-performed, powerful study over a thousand patients, was that there was no difference between the route of antibiotics and clinical outcomes. So we now have very good evidence that, as long as we’re using antibiotics well, that we can use oral therapy, and that includes for diabetic foot infection. This isn’t to say that when patients come into the hospital with sepsis, we should be using oral antibiotics.

This is really more in the definitive stage. You have to use your judgment. There are other reasons that we select IV therapy in the acute setting, but once we’re in a definitive management setting, many patients, if not most, can do well with oral therapy.

Dr. Shreya Trivedi: Wow. So patients can do just fine on oral antibiotics for bone and joint infections. Gosh, and then how long would we treat for?

Dr. Colby Weil-Lonigan: Yeah. So if it’s a diabetic foot infection without osteomyelitis, but they were say septic or had a lot of erythema around the wound, like maybe two centimeters out, or even if it was like a deep wound, then we typically would treat for about like two weeks or sometimes a little bit more than that. And in the absence of all of those things, diabetic foot infections are considered mild, and antibiotics can be given over one to two weeks.

Dr. Shreya Trivedi: Awesome. And then what about osteomyelitis, right? When there’s bone involvement, how does that change things?

Dr. Sandra Nelson: The most recent guidelines, actually, this has been a change, and I think this hasn’t made it pervasively. I think that people still don’t know about this, but the most recent guidelines indicate if a patient has had surgical debridement, even if their osteomyelitis is not completely resected, three weeks of treatment beyond surgical debridement is appropriate. And so I will say that not everyone agrees with that guidance, and it is based on literature on science that is not high-quality, large-scale, randomized controlled trials, but it is the best data that we have that suggests that anything beyond three weeks may not offer benefit. So I think for many people, if they’ve had a surgical procedure, three weeks is going to be sufficient, even when there is residual osteomyelitis.

Dr. Colby Weil-Lonigan: Wow. So three weeks, and that’s compared to the traditional guidelines of around four to six weeks. And sometimes I’ve even read that antibiotics can go all the way out to 12 weeks.

Dr. Shreya Trivedi: Yeah. And just to emphasize again, Dr. Nelson did say, not everyone agrees and the data isn’t perfect, but three weeks is the best evidence we have right now.

Dr. Colby Weil-Lonigan: Okay. And now our final teaching point. What do you tell your patients when they ask you, “How do I know if the osteo is gone? Should I get a repeat MRI?”

Dr. Sandra Nelson: None of those tests actually help. Separate takes a long time to come down. The problem with osteomyelitis is when it’s controlled, you can’t always tell the difference from blood work, whether it’s controlled or cured. I think the best test of cure is what I call the test of time. And if you stop antibiotics and their infection doesn’t come back, then they’re cured. Patients hate that because they don’t want their infection to come back, but we just don’t have anything else.

Dr. Colby Weil-Lonigan: Okay. So labs and imaging lag behind, ESR and CRP often stay elevated. MRI can still look bad long after the infection is under control, but the big picture is if they’re improving, you’re winning. Even if the MRI hasn’t gotten the memo yet.

Dr. Shreya Trivedi: Exactly. And then to summarize antibiotics of diabetic foot infections and osteomyelitis? If the patient’s unstable, yes, start antibiotics, but if they are stable and cultures might change management, you can consider holding, but starting antibiotics doesn’t necessarily ruin your yield, especially if there’s necrotic tissue.

Dr. Colby Weil-Lonigan: And I think that next time I have a patient who is clinically improving, I’ll talk to ID about transitioning to oral options early since oral options work too.

Dr. Shreya Trivedi: Yes. In terms of duration of antibiotics, it really depends on severity. For soft tissue infections with an ulcer can range anywhere from one to two weeks or so.

Dr. Colby Weil-Lonigan: And for osteomyelitis after debridement, newer guidelines suggest three weeks might be enough.

Pearl 5: Wound Care

Dr. Shreya Trivedi: Okay. Pearl five, all about wound care. Again, Colby, I am so excited to learn why am I ordering this versus that?

Dr. Colby Weil-Lonigan: Yeah, me too. I really had a fun time learning about all of this and teaching myself, but let me start us off with the first basic branch of wound care. Is the wound wet or dry?

Dr. Shreya Trivedi: Yeah. And I think from what I’ve seen, most diabetic foot wounds are usually on the drier, dirtier side.

Dr. Colby Weil-Lonigan: Yeah. We sat down with one of our wound care nurses that we have the pleasure of working with at BIDMC. Her name’s Brittany Nation. And she said, unless there’s massive edema or weeping, the main goals are simple. Clean the wound and keep it moist.

Nurse Specialist Brittany Nation: When you’re looking at a wound, the basics really come down to clean your wounds. If your wounds are clean and you put good moist topical therapy on a wound, that’s step number one. So putting the old wives tail of just keep it dry, keep it the air to it, that is no longer. There’s so much evidence out there that a moist topical therapy is needed. Our bodies know how to heal. They know what they need to do. We just have to help them out.

Dr. Shreya Trivedi: What a beautiful mantra. We are just supporting our body’s healing. And to do that, we need to keep these wounds clean and keep them moist.

Dr. Colby Weil-Lonigan: Yes. These wounds are not a rotisserie chicken.

Dr. Shreya Trivedi: Oh man, thinking about Costco. All right. So Colby, tell us, what do we have that in our toolkit to keep these dry wounds more moist?

Dr. Colby Weil-Lonigan: Xeroform. Most of us have heard of it, but I really didn’t know exactly what it was, but it’s that thin yellow mesh that goes directly onto the wound. It contains petrolatum to keep the wound moist, and this will be your go- to dressing for those really dried wounds.

Dr. Shreya Trivedi: Yeah, man. I’ve ordered that so many times and I had no idea what it did, but okay. So use Xeroform to moisten that wound. Okay, but what if Colby on the off chance there was edema and weeping, like say this person had really bad heart failure, and that was complicating wound healing?

Dr. Colby Weil-Lonigan: Yeah, that would be the circumstance where we would start reaching for something like Aquacel, which is basically just a super absorbent fiber. Aquacel, it’s used for those wet wounds that have really heavy drainage.

Dr. Shreya Trivedi: Okay, that makes sense. So Aquacel to absorb the wet wound, maybe AAA for absorbing, but for most of the time, these wounds are dry and we want to give it moisture and that’s going to be with Xeroform. All right, Colby, where do we go from here?

Dr. Colby Weil-Lonigan: Then we have to think about how are we going to clean the wound? AKA, what antimicrobial cleanser will we use? This honestly depends on what your hospital or unit carries, but the foremost common antimicrobials out there are Betadine, hypochlorous acid, acetic acid, and diluted bleach.

Dr. Shreya Trivedi: Diluted bleach?

Dr. Colby Weil-Lonigan: Yes. Crazy. I know diluted bleach is otherwise known as Dakin’s on your floor, is used for those wounds that have very active are angry infections, but we don’t typically use it for very long or very often, just because it’s super irritating to the skin. And then on the other hand, I just wanted to mention the other cleanser that I thought was very interesting, which is acetic acid. And it’s a special wound cleanser to note because it has antipseudomonal properties.

Dr. Shreya Trivedi: Okay. So it sounds like most of the time we’re going to be reaching for betadine or hypochlorous acid. These are just first-line wound cleansers. And then there’s the two other ones to know, which is diluted bleach or dakins for the angry-looking infections. And then if we’re worried about Pseudomonas, we might be reaching for acetic acid. Colby, I feel like I’m getting the hang of wound care.

Dr. Colby Weil-Lonigan: I know it’s not that bad, but putting this all together, practically what this looks like is clean first with either betadine, hypochlorous acid, diluted bleach, or acetic acid. Then choose a dressing based on if the wound is wet with something like Aquacel or if it’s dry with Xeroform.

Nurse Specialist Brittany Nation: If you’re questioning something and you just need to get through the night, put on Betadine, put on a Xeroform dressing. You can’t go wrong with that. And then throw a wound consultant, throw a podiatry consult in, and then they can be more formally evaluated.

Dr. Shreya Trivedi: Okay. Betadine in Xeroform, it is. My takeaway is Betadine and Xeroform is basically the peanut butter jelly of wound care.

Dr. Colby Weil-Lonigan: I love our food analogies, but yes. I would emphasize that wound care isn’t just what you put on the wound, but it’s also what you take off of it, i.e. Pressure. Offloading as much pressure off the wound as possible is super important for wound healing.

Dr. John Giurini: Studies have shown that as little as two hours of constant pressure is enough to occlude the local blood flow and lead to ischemic changes. So it’s important in those patients to elevate, keep the pressure off the mattress, put them in protective boots, things like that.

Dr. Shreya Trivedi: Two hours of pressure, that’s like a Netflix season finale. Gosh, so much good teaching here, Colby. Let’s summarize wound care. And what I’m taking away is first, we need to clean the wound, and that could be either with hypochlorous  acid, betadine, and if it’s a very active infection, diluted bleach or acidic acid, if we’re concerned about Pseudomonas. And then, since most wounds are on the dry side, we want to keep it moist with something like Xeroform.

Dr. Colby Weil-Lonigan: Yes, clean first, then choose a dressing based on wet versus dry.

Dr. Shreya Trivedi: And then when in doubt, most dry diabetic foot wounds, we can get away with Betadine and Xeroform, and that’ll get us through the weekend or the night. 

And that is all for today. Thank you so much for listening. If you got some value from this episode, our ask is to please share it with at least just one other colleague who might also get a good aha from this episode. I know I did.

Dr. Colby Weil-Lonigan: Thank you to our reviewers, Dr. Noah Rosenberg and Dr. Barry Rosenbaum. And thank you to Dr. Cathy Cichon for the accompanying graphics. This episode was made as part of the digital education track at BIDMC.

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