Welcome to this September twenty twenty-six review from Dermatologic Surgery. Four pieces on the docket today — a reconstructive conundrum on the central forehead, a pointed counter-commentary on local anesthetic dosing calculators, a SEER-based look at how second cancers affect survival in melanoma patients, and a short case report on squamous cell carcinoma in situ turning up inside a preauricular sinus during Mohs. Let's get into it.

First up is a reconstructive conundrum — one of the case-based teaching pieces where the authors walk you through a defect and the differential of repair options before revealing what they actually did. The setup: an eighty-two-year-old man with melanoma in situ on the central forehead, leaving a defect a little over six by five centimeters after clearance. Central forehead, convex surface, large size — you know where this is going before they even ask the question.

The authors walk through the standard menu and why each option falls short. Direct closure is really only reliable up to about two and a half centimeters of width even with good laxity, and here they're dealing with more than double that. Second intention was dismissed outright for a convex, cosmetically prominent site like this — you'd expect a depressed, contracted scar and real risk of brow asymmetry. Skin grafts, full or split thickness, were framed as a functional fallback for patients who don't care about cosmesis, not a real option for someone who presumably does. Then the flap discussion gets more interesting for those of us who do this work: a single Burow's wedge advancement was dismissed as insufficient given how far medial and large this defect was — not enough laxity to recruit. A superior rotation flap was rejected for a reason worth remembering — it would drag hair-bearing scalp skin onto the forehead, which is an aesthetic non-starter. Bilateral rotation or advancement flaps with hairline incisions were considered but the forehead and scalp here were relatively immobile, and critically, even if the primary defect closed, the secondary defects at the hairline wouldn't have been closable. And a frontalis sling island pedicle flap was mentioned as a nice single-stage option — but only if the outer skull table had been exposed, which it wasn't here.

What they landed on was bilateral bipedicled bridge flaps, recruiting laxity from the temporal regions and preauricular cheeks bilaterally. This is worth pausing on conceptually, because bipedicled bridge flaps aren't a single entity — the authors reference a classification into four types based on blood supply. Type one is pure random-pattern flow through the pedicles. Type two, which is what they used here, preserves a named artery — in this case both the supratrochlear and supraorbital arteries — layered on top of the random-pattern subcutaneous plexus, giving a hybrid axial-plus-random supply. Types three and four apply more to the temple, adding perforator supply through fascial septae or preserved superficial temporal artery branches. Knowing which type you're raising tells you how aggressively you can undermine and how robust your vascular safety margin is.

Technically, they anesthetized with bilateral supraorbital and supratrochlear nerve blocks plus local infiltration, incised bilaterally from the lateral brow radiating out to the frontal hairline, dissected in the loose areolar plane above periosteum to preserve the neurovascular bundles, and undermined laterally over the deep temporal fascia to avoid the temporal branch of the facial nerve — a nice reminder that plane selection here is doing double duty, protecting both sensation and motor function simultaneously. They used an M-plasty inferiorly tucked into glabellar rhytids to shorten the closure line, handled the standing cones with a linear excision superiorly and another M-plasty inferiorly, and closed in layers. Postoperatively the patient did well and was described as highly satisfied at four-month follow-up, with a well-healed vertical primary scar and radial secondary scars — lines the authors note tend to heal favorably on the forehead.

The practical takeaway here is genuinely useful for anyone doing central forehead reconstruction: bipedicled bridge flaps are a single-stage option that let you borrow laxity from the temples and preauricular cheeks for defects too large for standard advancement or rotation approaches, and undermining in the supraperiosteal plane is what protects both your axial blood supply and the sensory nerves. This is a technique worth having in your back pocket specifically for that stubborn large central forehead defect where the usual local flaps run out of tissue.

Next is a counterpoint commentary — a rebuttal, not a study, so there's no methods or results to walk through, just an argument to follow. It's responding to a prior paper that proposed a calculator for maximum local anesthetic dosing when combining lidocaine and bupivacaine with epinephrine for infiltrative anesthesia. The commentary author, writing from a tumescent anesthesia background, argues the calculator rests on two flawed premises.

The first is that the seven milligram per kilogram threshold for lidocaine with epinephrine is evidence-based. The author states — based on his own Freedom of Information Act inquiry to the FDA — that this number traces back to a nineteen forty-eight approval letter for obstetric epidural use, with no actual toxicity data behind extending it to infiltrative subcutaneous dosing. His point is that the field has been anchoring safety practice on what he characterizes as an evidence-free number for decades, and that real-world toxicity events are driven by things a calculator can't fix anyway — interpatient variability, human error in concentration mix-ups, injection into unusually vascular tissue, or inadvertent intravascular placement.

His second objection is that the calculator treats lidocaine and bupivacaine as roughly interchangeable in terms of toxicity risk along its dosing diagonal, when bupivacaine, molecule for molecule, carries substantially higher cardiotoxicity risk. And he questions the entire premise that combining the two drugs offers a meaningful clinical benefit for infiltrative anesthesia in the first place, noting the evidence for bupivacaine's prolonged duration comes mostly from nerve blocks and neuraxial anesthesia with small injected volumes — a very different pharmacologic scenario than the larger-volume subcutaneous infiltration we do in dermatologic surgery.

There's no new data generated here — it's an opinion piece grounded in historical and pharmacologic argument. The practical relevance for your own practice is less about adopting or rejecting any specific calculator and more a reminder to think critically about where the seven milligram per kilogram number actually came from, to respect that bupivacaine toxicity carries a higher ceiling of risk than lidocaine toxicity, and to recognize that the marginal benefit of routinely combining the two agents for straightforward infiltrative anesthesia may be smaller than commonly assumed.

Third, a research letter using SEER data to look at second primary malignancies in cutaneous melanoma survivors — building on a body of literature showing melanoma survivors face elevated risk of second cancers, but asking a sharper question: does that risk actually translate into worse survival, or does it just reflect more scrutiny and incidental pickup of indolent disease that wouldn't have mattered anyway. A Swedish registry study had already suggested second primaries meaningfully blunt survival, but there was no comparable US population-level analysis — that's the gap this letter fills.

Methodologically, they pulled four hundred twenty-five thousand cutaneous melanoma patients from the SEER-17 database spanning 2000 to 2022, restricting to histologically confirmed cases. They excluded anyone who developed a second primary within two months of melanoma diagnosis — a sensible move to strip out surveillance-bias cases where the second cancer was likely already brewing and just got picked up incidentally during melanoma workup rather than being a truly independent later event. They also excluded patients with less than a year of follow-up, anyone with a cancer before their melanoma, and anyone who went on to develop a third or fourth malignancy, to keep the comparison clean between no-second-cancer and exactly-one-second-cancer groups. They deliberately restricted to non-melanoma second primaries since they'd already published on second melanomas and second non-cutaneous melanomas elsewhere.

The statistical workhorse here is the Weibull accelerated failure time model, which is worth unpacking briefly because it's an alternative to the more familiar Cox proportional hazards approach. Rather than modeling the instantaneous hazard ratio between groups the way a Cox model does, an accelerated failure time model directly models survival time itself, estimating how a covariate — say, developing a second cancer — stretches or compresses the expected timeline to death by some multiplicative factor. The Weibull version specifically assumes a particular shape for how risk changes over time, which lets the model produce those adjusted hazard ratios you'll see quoted. The reason this approach fits well here is the landmark analysis design: the authors evaluated survival at three fixed checkpoints — two, five, and eight years after melanoma diagnosis — deliberately defining second-primary status at each landmark rather than as a single time-varying flag. That landmark structure is specifically there to avoid immortal time bias, the trap where patients who happen to survive long enough to develop a second cancer look artificially like they're doing better simply because they had to survive to be counted in that group at all.

The numbers: about seven percent of melanoma patients developed a non-melanoma second primary. Those who did tended to be diagnosed with their original melanoma at an older age — mid-sixties versus late fifties — and were more likely male. The heart of the analysis is the hazard ratios by cancer type and landmark, and the pattern is genuinely striking. At the two-year mark, pancreatic second primaries carried the steepest survival penalty — over a four-fold increase in mortality risk, clinically about as dramatic as it sounds. By the five- and eight-year landmarks, thyroid cancer — usually thought of as an indolent, favorable-prognosis tumor — emerged as the biggest driver of excess mortality, more than doubling the hazard at both time points. And broadly, at the earlier landmarks, second primaries across a long list of sites — brain, breast, colorectal, kidney, leukemia, lung, lymphoma, ovary, prostate, thyroid, bladder, uterus — were all significantly associated with worse survival, and by eight years, nearly all of these remained significant except brain, ovary, pancreas, and uterus. Age over seventy was also an independent predictor of worse second-primary-specific mortality, with roughly a sixty percent higher risk.

The authors flag something clinically important here: brain second primaries were mostly glioblastoma, and glioblastoma plus pancreatic cancer is a recognized constellation alongside melanoma in CDKN2A-associated familial melanoma syndromes — worth keeping in the back of your mind when you're taking a family history on a melanoma patient.

The big-picture conclusion the authors draw is that this mortality penalty can't simply be explained away as overdiagnosis or surveillance detection bias — even second cancers with generally good prognoses, like prostate or bladder, were still associated with significantly worse survival in this population, which argues against the idea that we're just picking up harmless incidental disease through more intensive follow-up. The honest limitations here are real: this is registry data without granular information on comorbidity burden, immunosuppression status, or systemic therapy exposure, so there's meaningful room for residual confounding — a sicker patient in general might simply be both more prone to a second cancer and more likely to die regardless of that second cancer's direct contribution.

Practically, this isn't something that changes your surgical management of the primary melanoma, but it is a genuine reinforcement of the survivorship argument — melanoma patients need durable, longitudinal cancer surveillance beyond just melanoma recurrence, and this data gives you a more concrete answer when patients ask whether a second cancer diagnosis down the line actually matters prognostically. It clearly does, including for cancers they might assume are the "good kind" to get.

Last is a case report describing squamous cell carcinoma in situ discovered arising within a preauricular sinus during Mohs surgery — a nice example of an intraoperative pattern-recognition pitfall worth knowing even though it's not hugely common. Preauricular sinus is a congenital anomaly familiar to otolaryngology but rarely discussed in our literature, and the point of this report is exactly that gap.

The patient was a seventy-seven-year-old woman with a long-standing pigmented helical lesion that had become painful, biopsied elsewhere as a two-and-a-half centimeter squamous cell carcinoma in situ with ill-defined borders, then referred for Mohs. During the first two stages, the frozen sections showed a squamous-lined lumen with full-thickness atypia sitting within adipose tissue — histologically the kind of picture that could easily be mistaken for a tissue-processing artifact, the so-called "floater." Only on further questioning did the patient reveal she had a known preauricular sinus at that site, previously symptomatic with keratin debris, and the authors correlated that history with the frozen findings to confirm this was a genuine congenital sinus tract, not an artifact. Because the in-situ squamous carcinoma had extended into the sinus lumen, an additional stage was required, with a final defect of three-point-seven by three centimeters extending down to skeletal muscle, repaired with a transposition flap. Recovery was unremarkable.

The teaching point here is squarely about intraoperative histologic recognition. The authors lay out the differential clearly: a preauricular sinus shows up as a simple squamous-lined tract closely apposed to auricular cartilage, typically containing keratin debris — distinguishable from an adnexal neoplasm like microcystic adnexal carcinoma, which shows complex ductal and glandular differentiation and solid or cystic nests without that tight cartilage relationship, and also distinguishable from a simple tangentially-sectioned dilated pore or comedonal plaque. Misreading a sinus tract as a floater risks incomplete excision and leaving tumor behind if it happens to harbor malignancy, as it did here; conversely, overreading a sinus as invasive carcinoma risks inappropriate upstaging or unnecessary adjuvant treatment. The authors' management point is that when a keratinocytic neoplasm is found extending into the sinus lumen, complete excision of that involved tract is necessary for clear margins, and you should be prepared for the defect to extend deeper than expected — down to cartilage or muscle — given the tract's anatomy.

This is a single case report, so there's no cohort or statistics to critique — the value is purely pattern recognition. The practical takeaway is narrow but useful: if you encounter a squamous-lined tract intimately associated with cartilage on a periauricular frozen section, pause before calling it artifact, ask the patient directly about any history of drainage or a pit at that site, and if there is a coexisting keratinocytic tumor, anticipate that clearing it may require tracking the sinus deeper than the visible clinical lesion suggests.

That wraps up this September issue. To summarize the through-line across today's pieces: a technical reminder that bipedicled bridge flaps deserve a place in your central forehead reconstruction algorithm, a call to critically scrutinize the evidence base behind local anesthetic dosing dogma, population-level data reinforcing that second cancers meaningfully shorten survival in melanoma patients and warrant real long-term surveillance, and a pattern-recognition pearl for not mistaking a preauricular sinus for artifact on frozen section. Thanks for listening, and I'll see you next month.