Welcome back to the journal review. This is our walkthrough of Dermatologic Surgery for October 2026, and we've got four pieces worth your time this month — a cautionary case report, a practice-focused review on perioperative blood pressure, a quirky but genuinely useful occupational health study on surgical lighting, and a systematic review on systemic therapy in transplant patients with advanced skin cancer. Let's get into it.

First up is a communication — essentially a case report with a teaching point — titled "Amelanotic Spindle Cell Melanoma Misdiagnosed as Atypical Fibroxanthoma: A Practical Reminder for Mohs Surgeons." You know the setup already: atypical fibroxanthoma sits on a clinicopathologic spectrum with pleomorphic dermal sarcoma, and the standard teaching is that Mohs surgeons should stay alert for PDS or undifferentiated pleomorphic sarcoma hiding under an AFX label, especially with deep invasion. What this case adds is a sharper warning about a different impostor — spindle cell melanoma — and specifically about over-trusting a negative S-100 stain to exclude it.

The patient was an 88-year-old man with a five-centimeter ulcerated nodule on the posterior scalp. A shave biopsy came back negative for S-100, Melan-A, and pankeratin, with only focal CD68 positivity, landing the diagnosis squarely on AFX. He was referred for Mohs. But at the time of surgical evaluation, there was clinical concern for substantial subclinical spread and deep extension, so a frozen section was taken specifically to rule out PDS or UPS. That frozen section showed a deeply invasive spindle cell proliferation — not the picture you'd expect from garden-variety AFX. That discrepancy prompted a conversation with the dermatopathologist and additional staining on the original biopsy block, which this time turned up positive SOX10 and S-100. The revised diagnosis: amelanotic spindle cell melanoma, with a mitotic rate over one per square millimeter, putting it at T3b. The patient was redirected to a melanoma center for staging and multidisciplinary management rather than proceeding with Mohs for a sarcoma.

The teaching point here is squarely about the limits of immunostaining, not about surgical technique. S-100 is often treated as if it effectively rules out melanoma, but its sensitivity for spindle cell melanoma specifically is only around ninety percent, and that number drops further when you're working from a superficial biopsy, which is exactly the scenario that generates most AFX diagnoses in the first place. The authors cite data suggesting that something close to one in ten spindle cell melanomas could be misclassified as AFX purely because of a falsely negative S-100. SOX10, by contrast, is reported as essentially one-hundred-percent sensitive for this entity, which is exactly what flipped the diagnosis here. They also flag that MART-1, which Mohs surgeons reach for reflexively in melanoma frozen sections, has poor sensitivity for the spindle cell variant specifically, so it would not have bailed anyone out in this scenario even if it had been used intraoperatively.

The practical takeaway, and I'd call this genuinely practice-changing at the margins: when you're handed an "AFX" diagnosis and you see perineural invasion, vascular invasion, or extension into the subcutis on your own evaluation — features that don't fit the superficial, indolent behavior of true AFX — don't stop at a negative S-100 from the outside biopsy. Have a low threshold to request SOX10, and if your lab can run SOX10 on frozen section intraoperatively, that's a reasonable option to build into your workflow for these ambiguous spindle cell cases. The stakes are real: this is the difference between treating locally with Mohs and routing a patient to immunotherapy and systemic staging for a melanoma with metastatic potential.

Next is a review article: "Perioperative Blood Pressure Management in Dermatologic Surgery: An Overview of Current Practices and Gaps." This is a narrative synthesis, not a meta-analysis — the authors searched PubMed, Embase, and Cochrane for anything addressing blood pressure management, surgical decision-making, or outcomes tied to hypertension in cutaneous surgery, plus analogous office-based procedures and the general perioperative literature, and built a practical framework from it. There's no new patient data and no inferential statistics here, so think of this as a curated expert synthesis rather than a study to critique methodologically.

The core message is that rigid blood pressure cutoffs are not well supported, and the field should move toward a risk-stratified approach instead. Some grounding numbers: Mohs surgery overall carries a strikingly low complication profile — bleeding complications around seven-tenths of a percent, and serious adverse events around two-hundredths of a percent — and even patients with known hypertension or cardiovascular disease don't show a meaningfully elevated risk of postoperative MI or stroke after Mohs. That said, a large cohort of roughly fifty-nine thousand Mohs patients did find that essential hypertension was associated with higher rates across a dozen categories of postoperative complications, including infection, hematoma, hemorrhage, and dehiscence, with hematoma rates reported somewhere between one-tenth of a percent and just over two percent depending on the series. Blood pressure readings at or above one-forty over ninety have been linked to increased intraoperative bleeding risk, but — and this is the key nuance — higher preoperative blood pressure mainly seems to prolong operative time rather than drive worse outcomes like infection or hematoma.

Where does the line actually get drawn? The synthesized recommendation is that surgery can generally proceed, with appropriate caution, up to two-hundred over one-ten in an asymptomatic patient. Above that threshold, or in the presence of symptoms suggesting acute end-organ damage, the move is to attempt first-line de-escalation — rest, anxiolytics, basic calming measures — and if blood pressure remains elevated, defer and refer to the primary care provider. The authors are explicit that general noncardiac surgery guidelines, including tools like the NSQIP calculator or the Revised Cardiac Risk Index, were built for general anesthesia cases and likely overestimate risk when applied to local-anesthesia dermatologic procedures — worth keeping in mind next time someone tries to import an inpatient surgical threshold wholesale into your clinic.

A few other practical pearls worth flagging. A simple thirty-minute rest period before remeasuring resolves an elevated reading to an acceptable level in over three in ten patients without any other intervention — so don't be too quick to cancel a case off a single anxious-moment reading. Bladder distension alone can raise blood pressure by up to fifteen points, so having patients void before the procedure is a free intervention. Caffeine avoidance on the day of surgery is another low-cost suggestion. Intraoperative monitoring, interestingly, doesn't appear to add much value in healthy patients under local anesthesia — small studies of patients undergoing Mohs showed blood pressure staying stable or even trending down during the case, which tracks with surveys showing only a minority of dermatologists routinely monitor blood pressure intraoperatively anyway. Postoperatively, the approach is to treat reversible drivers like pain and anxiety first, reserve emergency department referral for those with symptoms of end-organ damage above one-eighty over one-ten, and counsel patients to avoid heavy lifting or Valsalva maneuvers that could precipitate bleeding.

One more nuance that's clinically important: asymptomatic severe hypertension, so-called hypertensive urgency, defined as systolic at or above one-eighty or diastolic at or above one-ten, is actually common in outpatient settings — around one in twenty readings. Current evidence argues against aggressive acute lowering or reflexive ED referral for these patients, since aggressive correction can itself cause harm, and since nearly six in ten of these patients are still poorly controlled six months later regardless of what's done acutely. That raises a fair question the authors pose explicitly: does rescheduling a cutaneous procedure for an asymptomatic hypertensive patient actually buy any long-term cardiovascular benefit? The evidence doesn't clearly say yes.

Practically, I'd call several of these points practice-changing in the sense that they formalize what many experienced Mohs surgeons already do intuitively but haven't had literature to point to: continue home antihypertensives through the perioperative period, use something like five milligrams of diazepam for anxiety-driven elevations rather than reflexively canceling, measure blood pressure at the initial consult rather than only day-of, and reserve deferral for genuinely severe, symptomatic elevations rather than moderate ones.

Third, an original study, and a fun one: "Reflected Surgical Lighting Exposure at the Mohs Surgeon's Eye Level: Quantifying Effects of Working Distance, Drape Color, and Lamp Positioning." This is a device-based experimental pilot study, not a clinical trial — no patients, no IRB needed, because it's entirely a simulated surgical setup. They built a standardized facial model on a reclined Mohs chair, hung a ceiling LED surgical light forty inches above the field, and used a calibrated lux meter positioned at a simulated surgeon's eye level to measure how much light bounces back up at the operator.

The design rationale is straightforward once you see it: this is a physics-and-ergonomics characterization question, not a population-inference question, so the authors stuck with descriptive statistics — means, standard deviations, ranges across fixed experimental conditions — and didn't run significance testing. That's the right call here; when you're measuring a deterministic physical phenomenon under controlled, repeatable conditions rather than sampling variable biological subjects, there isn't the kind of sampling uncertainty that p-values are built to handle. They varied working distance across fourteen, twenty, and twenty-six inches, tested two lamp orientations — perpendicular to the field versus positioned behind and over the surgeon's shoulder — two drape colors, white and blue, three simulated Fitzpatrick skin-tone categories, and four lamp intensity settings, taking triplicate measurements at each combination.

The results are intuitive but the magnitudes are worth knowing. Baseline ambient light alone, with the surgical lamp off, produced about one-twenty lux at eye level — everything above that is attributable to the surgical lamp's reflection. Across all tested configurations, reflected illuminance ranged from around one hundred up to about twelve hundred lux. Working distance was the single strongest driver: fourteen inches produced roughly one-and-a-half to two times more reflected light than twenty inches, and two to three times more than twenty-six inches. Drape color came in a close second — at a twenty-inch working distance, white drapes averaged around five-twenty lux compared to roughly two-fifty lux with blue drapes, which is about a two-fold difference, or a fifty-two percent reduction in ocular exposure simply by switching drape color. Lamp intensity showed a clear dose-response relationship from the lowest to highest settings, but the effect size was smaller than distance or drape color. Lamp positioning behind the shoulder rather than perpendicular to the field also reduced exposure, again with a smaller magnitude than distance or drape. And simulated skin tone made essentially no meaningful difference.

The honest limitation here is that this is a benchtop simulation with a mannequin, not real intraoperative conditions with actual human tissue, actual case durations, or real surgeon head movement, and there's no established biologic exposure threshold to say what level of cumulative lux-minutes actually causes ocular strain or long-term harm — the authors are careful to say their exposure metric is illustrative, not a validated clinical threshold. So this is best read as hypothesis-generating and practically suggestive rather than definitively linking light exposure to a clinical ocular outcome.

Where does that leave you practically? This falls into the "interesting and plausibly actionable, not yet proven to change outcomes" category, but the actions it suggests cost essentially nothing: operating from a slightly greater working distance when precision allows, defaulting to blue rather than white drapes, and orienting your overhead lamp behind your shoulder rather than perpendicular to the field, are all free modifications that meaningfully cut reflected light reaching your eyes without compromising visualization of the field. Given how commonly Mohs surgeons report eye strain and fatigue, these are reasonable low-burden habits to adopt now, even while we wait for someone to connect this exposure data to actual longitudinal ocular outcomes.

Last piece, a systematic review: "Systemic Therapies for the Treatment of Cutaneous Malignancies in Solid Organ Transplant Recipients." The background here is one you already live with — transplant recipients carry dramatically elevated skin cancer risk from their immunosuppression, with roughly a sixty-five-fold increase in cutaneous squamous cell carcinoma, tenfold for basal cell carcinoma, threefold for melanoma, and something like a twenty-four-fold increase for Merkel cell carcinoma compared to the general population, and these tumors tend to behave more aggressively with worse survival. The problem the paper addresses is that transplant recipients are essentially always excluded from the clinical trials that established our systemic therapy options — checkpoint inhibitors, talimogene laherparepvec, and hedgehog pathway inhibitors — so everything we know about using these drugs in this population comes from scattered case reports.

Methodologically, this is a PRISMA-structured systematic review, preregistered on PROSPERO, pulling from PubMed, Embase, and Scopus, and the authors pooled case-level data across one hundred one included sources plus one novel institutional case, extracting demographics, immunosuppressive regimens, and three outcomes — tumor response, graft rejection, and graft failure. Because they had multiple candidate predictors they wanted to evaluate simultaneously against binary outcomes — did the graft reject, yes or no; did the tumor respond, yes or no — they used logistic regression, run first as univariate associations and then adjusted in a multivariate model. This is the right tool here because the outcomes are categorical rather than continuous, so ordinary linear regression doesn't apply; logistic regression instead models the log-odds of the outcome as a function of each predictor, and the output — the odds ratio — tells you how much a given factor multiplies the odds of that outcome occurring. The real value of moving to the multivariate step is confounding control: a factor that looks protective or harmful on its own might just be riding along with something else, like sicker patients receiving more aggressive immunosuppression and also having worse tumor biology, and the multivariate model tries to isolate each variable's independent contribution once the others are held constant.

Onto the numbers. Among one hundred ninety-six transplant recipients treated with checkpoint inhibitors — a mix of squamous cell carcinoma, melanoma, and Merkel cell carcinoma — the overall response rate was about thirty-nine percent, and if you count stable disease as a win too, roughly fifty-eight percent avoided progression. But the cost was real: graft rejection occurred in about thirty-seven percent of patients, and outright graft failure in about twenty-two percent. On regression analysis, having more baseline immunosuppressive agents going into treatment was protective against both rejection and failure, cutting the odds roughly in half for rejection and to around a third for failure — which makes intuitive sense, since a deeper baseline immunosuppressive cushion presumably buffers against immune-mediated graft attack when you add a checkpoint inhibitor on top. Tacrolimus-based regimens, on the other hand, were associated with a meaningfully reduced tumor response, roughly a sixty percent reduction in the odds of response, suggesting tacrolimus may blunt the antitumor immune activation checkpoint inhibitors are trying to achieve. mTOR-based regimens and cemiplimab specifically were both associated with fewer rejection events. Notably, after full multivariate adjustment, no single factor remained independently significant for graft rejection — a nice real-world illustration of how a univariate signal can wash out once you control for the company it was keeping — whereas for graft failure, both the number of immunosuppressive agents and sirolimus use remained independently protective even after adjustment.

The smaller arms of the review are the more encouraging part, though they come with an obvious caveat: in just ten transplant patients treated with talimogene laherparepvec, the objective response rate was ninety percent, with zero graft rejections or failures reported. In six transplant patients with basal cell carcinoma treated with hedgehog pathway inhibitors, the objective response rate was eighty-three percent, again with no graft loss. The authors' own illustrative case fits this encouraging checkpoint-inhibitor story too — a kidney transplant recipient with treatment-refractory locally advanced facial squamous cell carcinoma who achieved a complete response on cemiplimab without any rejection, showing that good outcomes are achievable even with the higher-risk drug class when things go well.

The obvious limitation, which the authors acknowledge implicitly through their methodology, is that this entire evidence base is built from pooled case reports and small case series rather than prospective trials, which means real publication bias risk — dramatic successes and dramatic failures are more likely to get written up than unremarkable outcomes — and the T-VEC and hedgehog inhibitor numbers in particular come from such small samples, ten and six patients respectively, that those response rates should be read as hypothesis-generating rather than reliable effect estimates. There's also substantial heterogeneity in how rejection and response were documented across the included reports.

For your practice, I'd frame the takeaway this way: this is not practice-changing in the sense of a new algorithm you should implement tomorrow, but it is genuinely practice-informing for how you counsel and coordinate with transplant teams. If a transplant patient needs systemic therapy for advanced skin cancer, this data supports an active conversation about immunosuppressive regimen optimization before or alongside starting a checkpoint inhibitor — favoring mTOR-based regimens like sirolimus over tacrolimus-heavy regimens where feasible, done in direct coordination with the transplant team, not unilaterally. And for appropriate candidates, particularly basal cell carcinoma or injectable, accessible melanoma lesions, hedgehog pathway inhibitors and T-VEC look like they may carry a meaningfully lower graft-risk profile than checkpoint inhibitors, worth raising early in multidisciplinary discussions even though the supporting numbers are still thin.

That wraps our four articles this month — a sharp reminder to not let a negative S-100 lull you into complacency on an atypical spindle cell lesion, a practical risk-stratified framework for blood pressure that should make you more comfortable proceeding through moderate elevations, some genuinely free ergonomic tweaks to protect your eyes in the Mohs suite, and a sobering but useful look at the real tradeoffs of systemic therapy in your transplant patients. Thanks for listening, and we'll see you next month.