Welcome back to the journal review. This month we're working from the September twenty twenty-six issue of the Journal of the American Academy of Dermatology, and we've got three pieces on the docket — a quick surgical pearl on nail unit surgery, and then a two-part continuing medical education series on wound care that's genuinely worth your full attention even though wound care isn't always front and center in a Mohs and oncology practice. Let's get into it.

First up is a surgical pearl, so this is exactly what it sounds like — a short, practical technique tip rather than a data-driven study, and I'll treat it that way. The subject is subungual glomus tumor excision, and the authors are addressing a problem anyone who's dissected under a nail plate already knows in their hands: these tumors are small, vascular, and sit right up against the nail matrix, so your working space is essentially a keyhole. The traditional approach — grasping the tumor with forceps — tends to fragment it. And fragmentation isn't just cosmetically annoying on the pathology tray, it plausibly leaves residual tumor behind and, per the reference they cite, may raise recurrence risk.

Their fix is elegant and low-tech. After a window-type nail plate avulsion exposes the tumor, they pass a fine suture — 4-0 or 5-0 nylon or polypropylene, on a small curved needle — through the superficial portion of the tumor itself, under direct visualization, and tie it loosely to create a traction loop. Instead of pinching the tumor with forceps, you now have a handle to apply gentle upward traction while you dissect it free from the nail bed and matrix. The specimen can go to pathology with the suture still in place. The stated benefits are what you'd expect: less direct compression and crush artifact, better visualization and exposure during dissection, and a higher likelihood of an intact, complete excision with less collateral trauma to the matrix. They also flag that this isn't necessarily glomus-tumor-specific — anything with a similar soft, friable consistency and comparable morphology, like a subungual leiomyoma or a nerve sheath tumor, could plausibly benefit from the same maneuver. There's no outcomes data here, no case series, no complication rates — it's a pearl, presented as a technical solution with face-value rationale, and it reads as something you could adopt tomorrow with suture you already have on your tray. Practical, low-risk, and easy to fold into your next glomus tumor case.

Now to the meatier material — a two-part CME review on wound care, written by a group spanning Calgary, Toronto, Oregon Health and Science University, and Mayo Clinic. This is a review, not an original study, so there's no methods-and-results arc to walk through — instead I'll do what the paper does, which is synthesize the state of the evidence and translate it into a practical framework. Part One is the foundational piece: local wound care and dressing selection. The authors open with the honest observation that dermatology training often underprepares us for hands-on wound care, which is a fair point for a specialty that otherwise owns the ulcer differential.

They walk through the classic wound healing physiology — hemostasis, inflammation, proliferation, remodeling — but the clinically useful part is the emphasis on moisture balance. Air-exposed wounds form eschar, which physically increases the distance keratinocytes have to migrate and slows healing, whereas a moist wound environment preserves the growth factors and cytokines that drive autolytic debridement, angiogenesis, and re-epithelialization. That's the physiologic argument underlying essentially every occlusive and moisture-retentive dressing choice that follows.

The clinical assessment section gives you a framework worth internalizing even if you already know how to eyeball a wound: measure length, width, and depth at every visit, assess for undermining, and — critically — distinguish colonization from critical colonization from true infection. Low-level bacterial colonization can actually help healing through proteolytic activity, so the trigger for intervention isn't bacterial presence, it's the clinical shift — progressive tissue breakdown, purulent exudate, hypergranulation, and the systemic or local signs of infection: fever, escalating pain, swelling, erythema. They note the emerging role of infrared thermography for early infection detection but are candid that it isn't yet in mainstream clinical use. The endpoint of assessment is triage into one of three buckets: healable, nonhealable, or maintenance — a distinction that should shape expectations and dressing choice as much as the wound characteristics themselves. A pyoderma gangrenosum ulcer or a diabetic foot ulcer is healable; a palliative or unrevascularizable arterial ulcer is not; and a pressure ulcer in a patient who simply cannot offload is a maintenance wound, meaning the goal shifts from healing to symptom and exudate control.

On wound bed preparation, the debridement discussion is the practical core. Surgical debridement remains the workhorse — it reduces bacterial load, corrects undermined edges, allows tissue sampling, and has been shown to accelerate healing with serial treatments, though in complex ischemic wounds it needs to be paired with revascularization, not substituted for it. They cover mechanical debridement, including ultrasonic multimodal systems; autolytic debridement via occlusive moisture-retentive dressings; enzymatic debridement with collagenase ointment, which has actual biologic activity promoting keratinocyte and endothelial migration and angiogenesis, versus papain and bromelain, where the evidence is honestly called inconclusive; and biological debridement with medical maggots, which the authors note reduce antibiotic duration and stimulate healing in some studies, but where randomized trials have not shown a significant reduction in overall healing time compared to standard therapy — a nice example of a treatment with plausible mechanism and some positive signals that hasn't cleared the bar of a hard clinical endpoint in controlled trials.

Biofilm gets its own section, and the key practical point is that biofilm debridement plus lowering wound pH — for instance with hypochlorous acid irrigation — improves antimicrobial penetration and reduces bacterial regrowth more than saline alone, though the authors are upfront that larger trials are still needed despite promising small prospective studies.

Practical takeaway from Part One: this is squarely useful, workaday knowledge rather than practice-changing news — but the framework of healable-versus-nonhealable-versus-maintenance triage, and the colonization-versus-infection distinction, is worth explicitly building into how you document and manage any chronic wound that lands in your surgical practice, whether that's a slow-healing Mohs defect in a patient with venous insufficiency or a postoperative wound in someone with peripheral arterial disease.

Part Two picks up where Part One leaves off and moves into tissue-engineered skin substitutes and advanced therapies — again a review, so no methods or results section to dissect, just a structured synthesis of a genuinely fast-moving product landscape. The framing point up front is nomenclature: as of a twenty twenty-three international consensus document, what we used to call tissue-engineered skin substitutes or cell- and tissue-based products has been reclassified under the umbrella term CAMPs — cellular, acellular, and matrix-like products — specifically because the old terminology couldn't keep up with how heterogeneous this category has become.

The organizing logic is worth holding onto: CAMPs are sorted by cellularity, cellular versus acellular; by anatomic layer, epidermal, dermal, or composite; by material, natural versus synthetic; and by source, autograft, allograft, or xenograft. Cellular autografts, like Epicel, use the patient's own cultured keratinocytes and offer permanence and low rejection risk, but at a real cost — literally weeks of culture time, high expense, and a need for donor tissue that isn't always available, for instance in massive burn patients. Allografts and xenografts trade some of that biologic fidelity for off-the-shelf availability.

The clinically important framing point, and one I'd flag as directly relevant to anyone managing a stalled postsurgical wound, is the trigger for stepping up to a CAMP: the stated general recommendation is to consider these products when a wound stalls after about thirty days of standard care, though the authors note many wound care specialists now advocate moving to biologics earlier in wounds that look difficult to heal from the outset, rather than waiting out the full month. The mechanistic hook is the so-called edge effect — these grafts don't just physically cover the wound, they release cytokines from donor cells that stimulate epithelialization inward from the wound margin, functionally mimicking a split-thickness autograft without the pain and morbidity of a donor site.

On the evidence itself, the honest summary is this: pooled health technology assessments consistently show CAMPs outperform standard wound care alone for chronic wounds. But — and this is the limitation the authors are careful to state plainly — there is not enough head-to-head data to say any one product or product class is superior to another, whether you're comparing cellular to acellular allografts or comparing two products within the same category. For diabetic foot ulcers specifically, they note that Epifix, Apligraf, and Hyalograft 3D currently have the most robust comparative efficacy data relative to standard care, which is useful if you're trying to prioritize among the crowded field, but it's evidence of superiority over standard care, not proof of superiority over each other.

Practical takeaway for Part Two: this is background knowledge that matters for judgment and multidisciplinary conversations — knowing when to invoke a CAMP, understanding roughly how the categories differ, and being able to speak intelligently with wound care colleagues or when managing your own refractory postoperative defects. It is not practice-changing in the sense of altering your day-to-day surgical technique, but it is exactly the kind of framework that should shape how you counsel a patient with a slow-healing Mohs defect about why you're referring to wound care, or why you might reach for a biologic dressing yourself rather than waiting out a full month of dressing changes that clinically you already suspect won't work.

That wraps this episode — a nice suture trick for your next glomus tumor, and a two-part refresher that turns wound care from something we defer to other specialists into something we can speak, and practice, more fluently ourselves. Thanks for listening, and I'll see you next month.