Skin and Soft Tissue

Skin and soft tissue disorders span benign and premalignant lesions, cutaneous malignancies (melanoma, BCC, SCC, Merkel cell carcinoma), soft tissue sarcomas (extremity, retroperitoneal, and superficial), and a broad spectrum of infections and inflammatory conditions (cellulitis, necrotizing fasciitis, hidradenitis suppurativa, pilonidal disease). Surgery’s role ranges from diagnostic biopsy and wide local excision to lymph node dissection, complex reconstruction, and multimodal therapy coordination. This review covers the essential decision trees: when to excise, how much margin, when to stage with imaging, when systemic therapy is indicated, and how to recognize life-threatening infections.

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Benign and Premalignant Lesions

Dysplastic Nevi

Atypical moles with risk of progression to invasive melanoma. Graded by degree of atypia: mild, moderate, or severe.

• Management: Excise with 2–5 mm margins.
• Moderate/severe atypia: Re-excise to clear margins.
• Dysplastic Nevus Syndrome (FAMM): Autosomal dominant; 50% develop melanoma by age 60. Require full-body skin surveillance every 6–12 months.

Congenital Melanocytic Nevi (CNM)

Present at birth or within first 6 months.

• Small (<1.5 cm): Most common; low malignant potential.
• Medium (1.5–19.9 cm): Intermediate risk.
• Large (>20 cm): 5–20% risk of melanoma; complete excision or close surveillance if excision is morbid.

Spitz Nevi

Rapidly growing benign lesions, common in children.

• Benign lesions: Typically monitor unless atypical (>1 cm, asymmetry, ulceration); excise with 5 mm margin if needed.
• Spitzoid lesions in adults: Usually represent melanoma with Spitzoid features → excise with 2–5 mm margins.
• Challenge: Histologically difficult to distinguish benign Spitzoid nevi from Spitzoid melanoma.

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Melanoma

Etiology and Pathology

• Risk factors: Intermittent severe sunburns (most important, especially early in life), fair skin, blue/green eyes, red hair, immunosuppression.
• Mutations: CDKN2A (40% of pedigrees; codes for p16 and ARF), BRAF (40–50% of sporadic cases; activating), RAS (15–20%), KIT (non-sun-exposed), PTEN (non-sun-exposed), TERT promoter (70% of all melanomas; most commonly mutated gene).
• Melanoma-associated syndromes:
  • FAMMM (CDKN2A mutation): 50% melanoma by 60, 90% by 80; also pancreatic and breast cancer risk.
  • Xeroderma pigmentosa: Nucleoside repair defect; early-onset melanoma; strict photoavoidance.
  • Giant congenital nevus: 5–20% malignant potential.
  • Familial BK mole syndrome: Atypical nevi >5 mm as precursors.
  • BRCA2, CDK4 mutations.

Diagnosis and Biopsy

• Clinical presentation: ABCDE (Asymmetry, Border irregularity, Color variation, Diameter >6 mm, Evolving).
• Biopsy technique: Full-thickness biopsy (punch or excisional) through dermis to subcutaneous fat for accurate Breslow thickness assessment.
• Avoid shave biopsy — risk of incomplete thickness assessment and sampling error.
• Excisional biopsy orientation: Along long axis of extremity for better margin control.

Histologic Classification and Depth Assessment

• Breslow thickness: Depth in mm from top of granular layer to base of tumor; most accurate prognostic indicator.
• Clark level: Invasion through histologic layers (original classification, now less commonly used).

Melanoma types:

• Lentigo maligna melanoma: Older patients, chronic sun-exposed skin (face), darkens over time; worst at head/neck.
• Superficial spreading: Most common type; variable presentation.
• Acral lentiginous: Very aggressive; nail bed, palmar, or plantar surfaces; often dark brown/black.
• Nodular: Second most aggressive; deepest at presentation; often with metastatic disease.
• Desmoplastic melanoma: <4% of melanomas; >60 years old; head/neck region; rarely harbors BRAF mutations; pure vs. mixed (>90% vs. 10–90% stromal fibrosis); low positive SLNB rate; very sensitive to anti-PD1 therapy.

Staging and Workup

• T staging: Based on thickness (T1 ≤0.8 mm, T2 0.8–1.0 mm, T3 1.0–4.0 mm, T4 >4.0 mm) and ulceration (add “b” if ulcerated).
• N staging: Nodal involvement per AJCC 8th edition.
• M staging: Distant metastases (now includes N-positive disease as stage IV).
• Stage grouping:
  • Stage I: T1–2, N0, M0.
  • Stage II: T3–4, N0, M0.
  • Stage III: Regional node involvement or in-transit mets.
  • Stage IV: Distant metastases.
• Imaging: CT chest/abdomen/pelvis; add CT neck for head/neck primaries; PET/CT for extremity location; brain MRI as indicated.

Surgical Margins

• Melanoma in situ / thin (≤1 mm): 0.5–1.0 cm margin.
• Intermediate (1–4 mm): 1–2 cm margin (NCCN/AJCC consensus).
• Thick (>4 mm): 2 cm margin.
• Excision depth: Down to (but not including) muscular fascia.

Reconstruction

• Primary closure for small defects.
• Skin grafts for moderate defects (healing of palms/soles may be difficult; allow granulation before grafting weight-bearing areas).
• Rotational, advancement, or free flaps for large or sensitive areas.
• Mohs micrographic surgery for facial lesions (best cosmesis and margin control).

Lymph Node Management

Sentinel Lymph Node Biopsy (SLNB):

• Current guidelines:
  • T1b melanoma (0.8–1.0 mm or <0.8 mm with ulceration).
  • T2–T3 (1.0–4.0 mm).
  • Consider if risk >5% via nomogram.
  • Young age (<42 yo), head/neck location, lymphovascular invasion, mitotic index >2, ulceration.
• Technique:
  • Preop lymphoscintigraphy with technetium-99 sulfur colloid (identifies nodal basin); includes SPECT scan for head/neck.
  • Intraoperative lymphatic mapping with isosulfan blue or methylene blue.
  • Remove: highest gamma-count node, “rule of 10” (nodes ≥10% of highest count), blue nodes, grossly positive or firm nodes.
  • Stain: S-100, HMB-45, Melan-A, SOX10.
  • Caution: Methylene blue injected too superficially → skin necrosis. Only technetium-99 sulfur colloid safe in pregnancy.

Lymphadenectomy:

• MSLT-1: Showed survival benefit for SLNB + completion lymph node dissection (CLND) vs. observation if positive SLN (62% vs. 41.5% 10-year survival).
• MSLT-2 and DeCOG-SLT: Failed to show survival improvement for CLND vs. active surveillance (ultrasound of nodal basin q4 months for 2 years, then q6 months for 5 years).
• Current approach: Clinically evident nodal disease → complete therapeutic lymph node dissection.

Regional lymph node dissection regions:

• Axilla (levels I–III): Long thoracic nerve (winged scapula if injured), thoracodorsal nerve (latissimus weakness), intercostal brachial nerve (upper arm numbness; most common injury), axillary vein (bleeding/thrombosis).
• Groin: Superficial dissection (femoral triangle + 5–7 cm above inguinal ligament) for staging; deep dissection only for PET-positive nodes or clinical involvement. Watch for saphenous vein; femoral triangle bordered by inguinal ligament (superior), sartorius (lateral), adductor (medial).
• Head/neck: Modified radical neck dissection (spares SCM, IJV, spinal accessory nerve) vs. radical dissection (removes all three); assess for drainage via lymphoscintigraphy + SPECT; if drains to parotid → parotidectomy vs. selective resection.

Locoregional Recurrence

• Local recurrence: Regrowth within 2 cm of excision scar → WLE to negative margins.
• Satellite metastasis: Lesion within 2 cm of primary; typically seen on pathology → WLE.
• In-transit metastasis: Lesion >2 cm from primary and proximal to draining nodal basin → WLE; if numerous, consider immunotherapy.
• Management of multiple lesions: Systemic immunotherapy (pembrolizumab, ipilimumab, nivolumab), intralesional therapy (Talimogene laherparepvec [T-VEC]), or isolated limb perfusion/infusion (tourniquet + melphalan, TNFα, dactinomycin).

Adjuvant Therapy (Stage II/IIIA)

• Indication: Thick primary (>4 mm) or nodal metastasis with disease burden >1 mm.
• Options:
  • Anti-PD-1 (pembrolizumab): Infusion-based; reduces recurrence by ~50%.
  • BRAF/MEK inhibitors (dabrafenib + trametinib if BRAF mutation present): Oral therapy; also reduces recurrence by ~50%.
• Both improve recurrence-free survival; choice based on mutation status, comorbidities, and patient preference.

Systemic Therapy (Stage III/IV)

High-risk node-positive (IIIB–D, resectable):

• Neoadjuvant ipilimumab + nivolumab or pembrolizumab.

Unresectable or metastatic:

• BRAF V600 mutant: BRAFi (vemurafenib, dabrafenib) + MEKi (cobimetinib, trametinib); high initial response but resistance develops.
• BRAF wild-type: Anti-PD-1 (nivolumab, pembrolizumab) or anti-PD-L1 (atezolizumab); or combo anti-PD-1 + anti-CTLA-4 (ipilimumab; high toxicity but durable responses).
• Emerging: Tumor-infiltrating lymphocyte (TIL) therapy, T-Vec, PV-10.
• Regional therapies (hyperthermic isolated limb perfusion, isolated limb infusion) do not improve overall survival.

Surveillance

• Stage IA–IIA: PE q4–6 months for 2 years, then annual; no imaging.
• Stage IIB+: PE q3 months for 2–3 years, then q6 months for up to 5 years; CT CAP q3–12 months for 2 years, then q6–12 months for 3 years.
• Positive SLNB (no CLND): Regional nodal US q4 months for 2 years, then q6 months for 5 years.

Special Presentations

• Lentigo maligna (head/neck): Margins ≥0.5–1.0 cm (larger if subclinical spread); lymphoscintigraphy + SPECT for all head/neck melanomas; if drains to parotid → parotidectomy vs. selective resection; non-surgical options: radiation, topical imiquimod.
• Acral melanoma (hand/foot): Excision + SLNB; digits → amputation at proximal joint; difficult wound coverage (skin grafts often needed).
• Anal melanoma: Rare (<1% of melanomas), aggressive, high distant recurrence (5-year survival ~20%); historically APR, now sphincter-sparing excision + adjuvant radiation; consider neoadjuvant radiation for large lesions; inguinal lymphadenectomy only if clinically positive.
• Melanoma of unknown primary: Presents as enlarged node or soft tissue mass; complete staging (PET/CT, brain MRI); if no additional disease → complete lymphadenectomy or surgical resection of solitary lesion; prognosis as good as or better than known primary.
• Desmoplastic melanoma: Pathologic re-review recommended; case-by-case SLNB decision (low positive rate); adjuvant radiation individualized; very sensitive to anti-PD1 (consider neoadjuvant pembrolizumab if locally advanced).
• Melanoma in pregnancy: Perform WLE early (won’t impact SLNB accuracy later); defer SLNB until postpartum if possible; histologic evaluation of placenta at delivery for metastatic disease (rare but reported).

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Non-Melanoma Skin Cancers

Basal Cell Carcinoma (BCC)

Epidemiology & pathogenesis:

• Most common cancer worldwide; 80% of nonmelanoma skin cancer.
• Risk factors: Sun exposure, fair complexion, immunosuppression, radiation, Fhx.
• Genetic syndromes: Xeroderma pigmentosum, albinism, Muir-Torre, Fanconi anemia, Li-Fraumeni, nevoid basal cell syndrome.
• Pathogenesis: Hedgehog signaling pathway; nearly all sporadic BCC harbors pathway defects.
• Locally destructive; low metastatic potential.

Types:

• Nodular (80%): Translucent/pearly with raised telangiectatic edges; head/neck 80%, extremities 20%.
• Superficial: Slow-growing scaly pink plaque; trunk/extremities.
• Sclerosing/morpheaform: Poorly defined indurated sclerotic plaque.
• Basosquamous: Features of BCC + SCC; aggressive with metastatic risk per SCC component.

Diagnosis: Biopsy (punch or excisional); histology shows epidermal tumor islands with palisading near stroma.

High-risk features: >2 cm, poorly defined margins, recurrence, immunosuppression, perineural involvement.

Treatment:

• Standard: WLE with 4–5 mm margin.
• Adjuvant radiation: For perineural invasion or positive margins where re-excision unacceptable.
• Advanced/metastatic: Neoadjuvant Hedgehog inhibitors (Vismodegib, Sonidegib); anti-PD-1 (Cemiplimab) as second-line.

Squamous Cell Carcinoma (SCC)

Epidemiology & pathogenesis:

• Second most common skin cancer (20% of nonmelanoma); originates from keratinocytes.
• Risk factors: UV exposure (proportional to cumulative), smoking, immunosuppression, chronic viral (HPV), industrial carcinogens (tars, oils), chronic ulcers/scars, genetic syndromes (xeroderma pigmentosum, oculocutaneous albinism, dystrophic epidermolysis bullosa).
• Pathogenesis: TP53 mutations (most common), CDKN2A, RAS, NOTCH1/2.
• Precursor lesions: Actinic keratosis, cutaneous horn → may progress; treat with 5-fluorouracil, imiquimod, cryotherapy, photodynamic therapy, electrotherapy.

Presentation: Red, poorly defined plaques or nodules; ulceration, induration, adherent crust.

Diagnosis: H&P, biopsy, US/FNA for suspicious nodes (if FNA+, get PET or CT).

Prognostic factors:

• Diameter >2 cm: Doubles recurrence risk, triples metastasis risk, 19× risk of death.
• Depth >6 mm: Highest association with recurrence/metastasis.
• Perineural involvement of large-caliber nerves (≥0.1 mm): 47% local recurrence, 35% metastasis.
• High-risk sites: Central face or diameter >6 mm; forehead/neck or diameter >10 mm.
• Poor differentiation: Aggressive.

Treatment:

• Neoadjuvant immunotherapy: For locally advanced (invasive, clinically positive nodes).
• Surgery:
  • Low-risk (<2 cm): WLE with 4–6 mm margin.
  • High-risk/recurrent: 6–10 mm margins.
  • Mohs surgery: For difficult cosmetic areas.
  • Marjolin ulcer (aggressive SCC in chronic wound/scar): 2 cm margins.
• Adjuvant radiation: If unable to obtain clear margins, extracapsular extension, extensive perineural/lymphovascular invasion.
• Regional lymph node metastasis: Lymphadenectomy.
• Systemic therapy: Cemiplimab (anti-PD-L1), pembrolizumab (anti-PD-1).

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Merkel Cell Carcinoma (MCC)

Epidemiology & biology:

• Rare, aggressive neuroendocrine skin cancer; high distant recurrence.
• Risk factors: Sun exposure, fair skin, immunosuppression, Merkel cell polyomavirus (MCPyV).
• Two distinct biologic subsets: MCPyV-associated (better prognosis) and non-viral.
• Historic 5-year survival ~15%; improving with radiation and immunotherapy.
• Presents as shiny, skin-colored or reddish-purple rapid-growing soft tissue mass (sometimes painless).
• Histology: Small round blue cells; stain positive for common neuroendocrine markers.

Workup: PET/CT, MCPyV antibody titer testing; high rate of upstaging to unresectable disease.

Treatment:

• Neoadjuvant immunotherapy (avelumab, pembrolizumab, retifanlimab, nivolumab) for locally advanced or clinically palpable nodes.
• Localized disease: WLE with SLNB; 2 cm margin down to fascia/pericranium.
• Positive SLNB: Complete therapeutic lymph node dissection (TLND) or nodal radiation if TLND not tolerated.
• Adjuvant radiation: Improves overall survival; consider for tumor >1 cm, recurrent disease, inability to re-excise with margins; apply to nodal basin if +SLNB but cannot do TLND, extracapsular spread, or bulky nodal disease (≥4 axillary, ≥10 inguinal nodes).
• Metastatic: Anti-PD-L1 or anti-PD-1 first-line; response rates up to 56%, 5-year OS ~26%.

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Soft Tissue Sarcomas (STS)

Extremity Sarcomas (50–60% of STS)

Epidemiology:

• Most common locations: Proximal thigh > lower leg > upper arm > shoulder/axilla.
• Most common histologic subtypes: Undifferentiated pleomorphic (UPS), liposarcoma, synovial, myxofibrosarcoma.
• Origin: Connective tissue, bone, muscle, peripheral nerve sheaths.
• Environmental factors: Lymphedema, radiation, trauma, chemicals, viruses (HHV-8, EBV, SV40).
• Presentation: Painless mass; >70 histologic types; difficult diagnosis even for high-volume centers.
• Genetic associations: Neurofibromatosis type 1, Li-Fraumeni, FAP.

Diagnosis:

• Imaging: MRI with contrast FIRST (best soft tissue definition).
• Biopsy: Core needle preferred; if incisional, must include incision line in future WLE.
• Staging: Image entire involved compartment; CT chest (lung most common met site); TMN per AJCC 8th edition.
• T staging: Divided by size: T1 (0–5 cm), T2 (>5–10 cm), T3 (>10–15 cm), T4 (>15 cm).
• N/M: All nonmetastatic grade 1 = stage I; nonmetastatic grade 2–3 = stage II–III; N-positive or M-positive = stage IV.
• No role for PET.

Surgical margins: 1–2 cm; place clips for radiation targeting; limb-salvage approach preferred.

Radiation:

• Indication: High-grade tumors >5 cm; decreases local recurrence, does not improve overall survival.
• Neoadjuvant: Double wound complication rate but avoids irreversible late effects (fibrosis, immobility).
• Adjuvant: Serious late morbidity; many centers prefer neoadjuvant in younger patients.
• Tailor approach to patient age/tolerance.

Chemotherapy:

• Indication: High risk of metastatic disease (high-grade, leiomyosarcoma, dedifferentiated liposarcoma >5 cm).
• Regimens: Doxorubicin + ifosfamide ± dacarbazine.
• Most chemosensitive: Myxoid liposarcoma, synovial sarcoma.

Special category — “CARES” (may have nodal involvement):

• Clear cell, Angiomyosarcoma, Rhabdomyosarcoma, Epithelioid, Synovial.
• Discuss at MDT; consider SLNB if will change management.

Surveillance: Clinical assessment q3–6 months for 2 years, then q6 months, then annually; CT per protocol.

Prognostication: Sarculator nomogram for survival prediction.

Retroperitoneal Sarcomas (RPS)

Epidemiology:

• Only 15% of STS; diagnosis often delayed (deep location).
• Most common: Adults—liposarcoma, leiomyosarcoma, UPS; Children—rhabdomyosarcoma, Ewing.
• Presentation: Abdominal fullness, early satiety, abdominal/flank pain.
• Outcomes best at high-volume centers: ≥11–20 RPS annually.

Treatment:

• Surgical resection with negative margins; en bloc resection of contiguous involved organs.
• Adjuvant radiation: Consider for pelvic or fixed retroperitoneal STS.
• Similar multimodal approach (surgery + radiation ± chemotherapy) as extremity STS.

Dermatofibrosarcoma Protuberans (DFSP)

Biology:

• Second most common cutaneous SarcOMA (after Kaposi).
• Arises from fibroblasts in dermis; fascicular whorls of spindle cells.
• Overexpression of PDGFB (tyrosine kinase activation).
• High local recurrence; low metastatic potential unless fibrosarcomatous transformation (5–15%).

Diagnosis & planning: MRI with contrast; if fibrosarcomatous transformation, add CT chest.

Treatment:

• Neoadjuvant imatinib (Gleevec) if locally advanced or metastatic.
• Surgery: WLE with 2 cm margin or Mohs.
• Adjuvant radiation: DFSP highly radiosensitive; use for close/positive margins.
• Recurrent/unresectable disease: Gleevec.

Surveillance:

• DFSP: H&P q6–12 months; no imaging.
• Fibrosarcomatous transformation: H&P + CXR q3–6 months for 3 years, then annually for 10 years total.

Desmoid Tumor

Pathology:

• Low-grade fibrosarcoma; spindle-shaped fibroblasts.
• Ki67 stain shows variable mitotic index.
• B-catenin stain (+) distinguishes from scar tissue.
• 40% recurrence rate.

Epidemiology: Most common—women, sporadic; often anterior abdominal wall; intraabdominal associated with Gardner syndrome/FAP.

Treatment:

• WLE with function-sparing clear margins.
• Radiation: For unresectable, positive margins.
• Systemic: NSAIDs (sulindac), antiestrogens (tamoxifen), Gleevec, doxorubicin (growth stabilization).
• Observation acceptable in some cases.

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Soft Tissue Infections

Superficial Infections

Cellulitis:

• Usually monobacterial; most common: MSSA/MRSA, beta-hemolytic streptococcus.
• Treatment: Augmentin, cephalexin, dicloxacillin, doxycycline, linezolid, TMP-SMX.
• Bite wounds: Augmentin or flagyl/clindamycin + gram-positive coverage.
• Risk factors: Lymphedema, immunosuppression, diabetes.

Erysipelas:

• Form of cellulitis; young and elderly; involves epidermis; sharply demarcated raised edges.
• Caused by Group A streptococcus.

Impetigo:

• Usually in children; superficial, highly contagious.
• Caused by staphylococci.

Abscess:

• Fluctuance, erythema, warmth; US shows hypo-echoic collection.
• Treatment: Incision and drainage, pack wound.

Deep Tissue Infections (Necrotizing Soft Tissue Infections; NSTI)

Clinical presentation:

• Red flags: Pain out of proportion, SIRS, mental status changes.
• Lab findings: Leukocytosis, hyponatremia, hypocalcemia.
• Physical findings: Edema, bullae, skin necrosis, crepitus.

Classification:

• Type I: Polymicrobial (gram-positive cocci, gram-negative rods, anaerobes); often elderly with comorbidities.
• Type II: Monomicrobial—group A streptococci, other beta-hemolytic strep, staphylococci; any age, without comorbidities; classic presentation is streptococcal toxic shock (STSS) with superantigen M protein → massive ineffective immune response → shock.
• Type III: Saltwater/freshwater NSTIs (Vibrio, Aeromonas species).
• Type IV: Gas gangrene (Clostridium perfringens from soil, farming, drug injection); thin malodorous fluid, gram-positive rods on stain; requires clindamycin to block toxin production.

LRINEC score: Stratifies risk of NSTI vs. deep soft tissue infection.

• Score <5: Low risk.
• Score 6–7: Intermediate risk.
• Score 8+: High risk for NSTI.

Antibiotic coverage:

• Type I/II: Broad-spectrum (e.g., ampicillin/sulbactam, piperacillin/tazobactam) + clindamycin (blocks toxin production).
• Vibrio/Aeromonas: Ceftazidime + quinolone (cipro) or tetracycline (doxy).

Surgical management: Aggressive debridement; often multiple returns to OR; may require amputation.

Finger Infections

Paronychia:

• Infection of soft tissue fold on fingernail side; follows disruption between nail bed and fold.
• If infection travels proximally → must remove that portion of nail.
• Treatment: Elevate lateral ¼ of nail plate; incision along lateral fold if needed.
• Chronic paronychia: Topical steroids.

Felon:

• Fingertip pulp infection; follows trauma, diabetes (fingerstick).
• Treatment: Longitudinal incision along midline volar surface; release all septa.

Herpetic whitlow:

• Clear, coalesced vesicles; self-limited (2–4 weeks).
• No surgical treatment; acyclovir in first 48 hours shortens course.

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Hidradenitis Suppurativa (HS)

Pathophysiology:

• Disease of the hair follicle (not apocrine glands despite location in apocrine-bearing areas).
• Follicular occlusion → rupture → inflammatory response.
• Altered skin microbiome, innate immune dysfunction, diet, comorbidities.
• NOT an infection: Abscesses are sterile or colonized.

Epidemiology:

• Most common in women, African Americans, smokers, Down syndrome.
• Family prevalence (gamma secretase gene mutations).
• Affects intertriginous areas: Perianal, inframammary fold, vulva, groin, gluteal folds, axilla.
• Usually symmetric; recurrent “boils” that progress to chronic induration, discharging tunnels (sinus tracts), scarring.

Hurley Classification:

• Grade I: Localized abscesses without sinus tracts or scarring.
• Grade II: Recurrent abscesses with sinus tracts and scarring separated by normal skin.
• Grade III: Diffuse disease with multiple interconnected sinus tracts, abscesses, scarring involving entire anatomic unit.

Management:

• Nonoperative: Daily topical clindamycin gel + antiseptic wash (benzoyl peroxide); oral tetracyclines, antiandrogens (spironolactone); laser hair removal.
• Moderate/severe: Immune modulators (adalimumab, infliximab); do NOT stop for surgery.
• Operative: De-roofing (excise roof/epidermis and gelatinous lining; heal by secondary intention) or excision (down to subcutaneous tissue; regional vs. WLE per extent).
• Closure: Usually heal by secondary intention; skin grafts high recurrence risk; do NOT primarily close (highest recurrence).

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Pilonidal Disease

Pathophysiology:

• Hair shed and lodged in intergluteal cleft at areas of localized trauma; sitting causes follicle rupture.
• Plugged with keratin → granulomatous foreign body reaction → sinus tract develops and drains.

Epidemiology: Young, hirsute men with deep natal clefts.

Prevention: Weekly shaving, laser hair removal, hygiene.

Presentation: Abscess, pain, tenderness; exam shows dermal pits/sinus tracts.

Acute abscess: Incision and drainage 1–2 cm off midline; 60% healing rate.

Chronic sinus tracts:

• Unroofing: Place fistula probe through openings, cauterize between, destroy granulation tissue.
• Excision: Inject methylene blue, excise all affected tissue to sacrococcygeal fascia.

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Pressure Wounds (Pressure Ulcers)

Staging:

• Stage 1: Skin intact, reddened >1 hour after pressure relief; nonblanching; potentially reversible.
• Stage 2: Blister or break in dermis; partial-thickness dermis loss; potentially reversible.
• Stage 3: Full-thickness tissue loss with visible subcutaneous fat; no exposed bone/tendon/muscle; temporary stage (muscle rapidly undergoes ischemic necrosis).
• Stage 4: Exposed bone, joint, muscle, or tendon.
• Unstageable: Base covered by slough or eschar; true depth unknown without debridement.

Management:

• Repositioning, offloading, hydrocolloids, debridement of necrotic/infected tissue.
• Medical optimization: Nutrition, glycemic control, smoking cessation.
• Flaps for stage 4 defects.

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Lymphedema

Classification:

• Primary: Hereditary.
• Secondary: Damage to lymphatic system (surgery, radiation, trauma, infection); affects cancer survivors.
• Risk factors: SLNB (low risk), lymphadenectomy (high risk), radiation, obesity, sedentary lifestyle.
• Common basins: Inguinal > axillary > cervical.

Staging:

• Stage 0: Subclinical; unable to see; heavy limbs, tight jewelry.
• Stage 1: Spontaneously reversible; pitting edema improves with elevation.
• Stage 2: Irreversible; fibrosis in interstitial space; does not resolve with elevation alone; progresses to fat hypertrophy.
  • 2a: Pitting edema visible.
  • 2b: No visible pitting (fibrosis/fat hypertrophy predominate).
• Stage 3: Elephantitis; massive limb swelling, scar tissue, skin hardening.

Treatment: Compression, lymphatic massage, exercise, hygiene; lymphovenous bypass (anastomoses between lymphatics and veins distal to obstruction); vascularized lymph node transfer (risk of donor-site lymphedema).

Surgical prevention:

• Reverse mapping: Inject blue dye/ICG into upper extremity and radiotracer into breast; remove radioactive hot nodes while identifying/protecting lymphatics (mainly for axillary surgery).
• Lymphangitis: Infection of lymph vessels; tender red streaks up extremity; treat with antibiotics.

Stewart-Treves Syndrome

• Lymphangiosarcoma secondary to chronic lymphedema; aggressive; presents as skin ulceration.
• Biopsy: CD31+, CD34+; negative for cytokeratin AE1-3, S100.
• Most common metastasis: Lung.
• Treatment: Radical resection (sometimes amputation), adjuvant radiation, chemotherapy (paclitaxel), anti-angiogenic agents.

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Rapid-Fire Questions

• Q: A 35-year-old presents with a 1.2 cm dark lesion with irregular borders on the back. What biopsy technique should you use?
  A: Full-thickness punch or excisional biopsy down to subcutaneous fat to accurately assess Breslow thickness; never shave biopsy.

• Q: What is the most commonly mutated gene in melanoma?
  A: TERT (telomerase reverse transcriptase) promoter; mutated in 70% of melanomas.

• Q: A 50-year-old with a 2 mm melanoma on the leg—do they need SLNB?
  A: Yes if high-risk features (T1b criteria: 0.8–1.0 mm or <0.8 mm with ulceration, young age <42, head/neck location, lymphovascular invasion, high mitotic index, ulceration); use nomogram to assess if risk >5%.

• Q: How are recurrent SCC of the skin treated differently?
  A: 6–10 mm margins (vs. 4–6 mm for low-risk) and consider Mohs for cosmetically sensitive areas; adjuvant radiation if unable to obtain clear margins or high-risk features present.

• Q: A patient with GSW to the thigh with muscle necrosis, pain out of proportion, and mental status changes. What is the most likely diagnosis?
  A: Necrotizing soft tissue infection (NSTI); requires emergent broad-spectrum antibiotics (including clindamycin) and aggressive surgical debridement.

• Q: What are the three pillars of extremity sarcoma treatment?
  A: Surgery (limb-salvage 1–2 cm margins), radiation (for grade 2–3 >5 cm; neoadjuvant to avoid late effects), chemotherapy (for high metastatic risk).

• Q: How do you differentiate a melanoma from a Spitz nevus in an adult?
  A: Spitzoid lesions in adults usually represent melanoma with Spitzoid features and should be excised with 2–5 mm margins; the distinction is often difficult histologically.

• Q: What are the LRINEC score categories for necrotizing soft tissue infection?
  A: <5 (low risk), 6–7 (intermediate), 8+ (high risk for NSTI).

• Q: After axillary lymph node dissection for melanoma, patient develops winged scapula. What nerve was injured?
  A: Long thoracic nerve (innervates serratus anterior).

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Quick Reference Table — Melanoma Margins

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Quick Reference Table — SCC High-Risk Features

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Quick-Reference Cards

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Related Case Preps

• Lumpectomy and Sentinel Lymph Node Biopsy — technique for cancer sentinel mapping.
• Splenectomy — for comparison of lymph node dissection techniques.

Related Topic Reviews

• Breast — cancer staging and systemic therapy parallels.
• Hernias — wound closure principles.

Suggested Reading

• VUMC Global Surgical Atlas: Negative Pressure Dressing Application
• VUMC Global Surgical Atlas: Split Thickness Skin Grafting
• VUMC Global Surgical Atlas: Full Thickness Skin Grafting

References

• Chassin’s Operative Strategy in General Surgery — Skin and soft tissue chapter.
• Clinical Scenarios in Surgery — Melanoma and SCC chapters.
• NCCN Clinical Practice Guidelines: Melanoma, Merkel Cell Carcinoma, Non-Melanoma Skin Cancer.
• AJCC Cancer Staging Manual, 8th Edition — Melanoma and STS staging.
• EAST Guidelines — Soft tissue infection and necrotizing fasciitis.
• Balch CM et al., J Clin Oncol 2009 (PMID 19204204) — Melanoma staging.
• Cormier JN, Pollock RE, CA Cancer J Clin 2004 (PMID 15313192) — Soft tissue sarcoma overview.