This document discusses the management of various skin lesions and defects. It provides information on diagnosing and treating common benign and malignant skin lesions such as basal cell carcinoma, squamous cell carcinoma, and melanoma. It also reviews options for reconstructing skin defects created by wide excision of malignant lesions, including the use of skin grafts versus flaps. Flaps are preferred when there is poor vascularity or reconstruction of facial structures is needed. The document concludes by discussing a case of excising a squamous cell carcinoma of the lower lip and reconstructing the defect using a free anterolateral thigh-tensor fasciae latae flap.

1. RICHARD BODOR, MD
UCSD DEPT OF PLASTIC SURGERY
VA Medical Center, San Diego
Kevin Broder, MD
VA Plastic Surgery
KARIN ESCHAGH, MS3, UCSD
Wound Basics, Lumps, Bumps and Rashes, for GWEP 2018

2. 79-year-old woman referred to you for many large nodular skin lesions on upper torso……..
As you palpate, it starts to bleed. So you pull out your dermascope…..

3. Dermoscope reveals blotches of blue and black
with a brown pigmentation at the border of the lesion
What is the next step in management ….

4. A-B-D-D-E
• Assymetry
• Border Irregularity
• Color variability
• Diameter > 8mm
• Elevation, Evolution, Excitement

5. Pathology results: nodular melanoma
•What is the next best step in
management…
• Initial biopsy
• Path Report
• Margins Excision
• Reconstruction
• Tumor Board
• Adjuvant Therapies
• Follow up

6. Learning Objectives
• Recognition of Several Common Benign versus
Malignant skin lesions
• Management of common congenital skin lesions and
rashes
• Management of common malignant skin neoplasms
• Use of flaps/grafts for skin defect closure

7. Common Rashes

8. Fungal Skin Rashes

9. Fungal Skin Rashes

10. Bacterial Skin Infection Rash

12. Common Benign
Skin Lesions

14. Common Acquired Nevi
• 3 types: Junctional, Dermal, or Compound
--Compound: pigmented, papular with smooth or warty surface.
Aggregate of melanocytes from deep dermis to epidermis.
-- Intradermal: tan to skin-colored papules with soft, rubbery texture.
Nevus cells only in dermis.
-- Junctional : brown/black macules. Cells in dermoepidermal junction.

16. Seborrheic Keratosis
• Common benign epidermal tumors
• Often seen with older age. Common around Head
and Neck areas
• “Stuck On” appearance
• Pigmented brown to yellow with greasy surface

18. Cysts
• Cystic changes of hair follicle epithelium, leading to dermal
cyst filled with keratin and lipid debris. Often with the
orifice (central pore) on the skin surface.
• Epidermal inclusion cyst (implantation of epidermal elements into the dermis).
Originate from the epidermis. Contain keratin.
• Sebaceous cyst (pilo-sebaceous units). Originate from the sebaceous glands.
Contain sebum. Also known as steatocystomas and less common than
commonly described.
• Other variants

19. Pilar Cyst
• Similar to epidermal inclusion cyst, but in different
anatomic areas typically. Contain keratin also like
epidermal inclusion cysts
• Firm, often on scalp, sometimes multiple. Most
often in Hair bearing areas
• Also termed Trichelemmal cysts
• Originate from the hair follicles.

21. Precancerous
Skin Lesions

23. Actinic Keratosis
• Associated with sun exposure
• Palpable, erythematous, scaly.
• Often on face or bald scalp, dorsum of hand.
• May become squamous cell carcinoma (SCC).

24. Dysplastic Nevi
• Presentation:
-- “Atypical moles”
-- often mistaken for melanoma
• Histology:
-- cluster of melanocytes
• Origin:
-- Sporadic or familial
• Concerns:
-- 3 to 20-fold
higher risk of melanoma (Halpern et al. 1993)
which increases with an increase in the number of atypical moles
-- approximately half of melanomas that arise in these patients develop de novo, and do not evolve from a precursor
atypical nevus. However, it can still occur (Tucker et al. 2002)
• Management:
--Close- follow up with total body baseline photography
-- “Ugly Duckling Sign:” lesion that looks clinically & dermoscopically different from the other predominant pattern of
nevi.
-- Warning signs: (1) shades of blue, red, white (2) new lesion in pt over 40 years old

25. Congenital
Skin Lesions

27. Congenital Melanocytic Nevi
• Begin in Utero, disruption in normal growth of
melanoblasts
• Small or Large (entire trunk)
• Dark with irregular borders
• Covered with hair
• Malignant potential 5-10%, increased with size

28. Management of Giant Congenital Nevi
• If less than 20 cm: perform excision with skin grafting
• Giant Nevi are > 20cm (> 2% BSA): multiple staged approach with
expansion of donor tissue with serial excisions or using skin flaps.
---Tissue Expansion
• A silicone balloon attached
to tubing is placed under the
skin (above muscle layer)
while deflated and then
gradually filled with saline
over time to allow skin to stretch.
Then expander is removed, nevus
excised, and skin flap is created
from expanded tissue.

29. Tissue expansion stages

30. Newborn with a verrucous, oily lesion….

31. Sebaceous nevi
• present at birth appear
• Appear as waxy, hairless, yellow-orange plaques usually on the scalp, head, or
neck.
• After puberty, they can become more nodular and wart-like high risk (15 – 20%)
of transforming into bcc.
• Treatment: serial removal with tissue expansion may be recommended to avoid
excessive tension in the area which would impair wound healing.

32. Malignant Diseases
of the skin

33. Malignant Diseases of the Skin
• Over 1 million new cases of skin cancer annually, accounting for 35-40%
of all new cancers (2): Melanoma versus non-melanoma
• Ultraviolet (UV) radiation is primary risk factor
-- UVB has more energy and causes more damage
• Of the Non-melanoma skin cancers:
-- BCC (70%), SCC (25%).
• Skin cancers can arise from areas of chronic inflammation: burns, scars,
ulcers, and sinus tracts.
• Squamous Cell Cancer: Marjolin’s Ulcer. Chronic Wounds.
Aggressive with poor prognosis

34. High Risk Individuals
• Xeroderma Pigmentosum:
--inherited disease of faulty DNA repair of UV damage
• Albinism:
-- little or no production of melanin
• Familial basal cell nevus (Gorlin’s syndrome)
-- rare autosomal dominant disorder with germ-line mutation in human patched gene (PTCH)
which results in developmental abnormalities & early BCCs.
• Epidermodysplasia verruciformis:
-- hereditary skin disorder with abnormal susceptibility to HPV
• Chronically immunosuppressed/long term steroid users

36. Basal Cell Carcinoma
Presentation:
1. Nodular:
Most common. Smooth, dome-shaped,
round, waxy, or pearly papule
with telangiectasias.
2. Superficial: -
-30%. Frequently on trunk. Shiny,
scaly papule, or erythematous
patch.
3. Morhpeaform: 5-
10% smooth, indurated, yellow
plaque with ill-defined borders.
Skin looks taut due to fibroblastic response.

37. Treatment of BCC
• Excision is preferred management
--1.0 cm margin of normal tissue
Wider margins of resection are suggested for morphea-like fibrosing tumors (since tumor
cells invade normal tissue well beyond visible margins).
• If BCC < 0.5 cm
Cryotherapy (freezing), electrodessication and curettage (spoon-like instrument with
electrocautery).
• Moh’s surgery:
Preferred for BCC’s in cosmetically sensitive areas (face) in order to preserve normal
tissue. When margins are determined to be clear, wound is closed primarily, skin-grafted,
or covered with tissue flap.
• 5-fluorouracil (topical chemotherapy):
Used when too many superficial BCC’s to excise or patients with extensive skin damage.
• Radiation therapy:
Recommended for elderly who are not good surgical candidates.

39. Squamous Cell Carcinoma
• Arises from keratinocytes of epidermis de novo or from
ulcers/burns/osteomyelitis
• Potential for metastasis
(correlates with size/grade)
More often those from ulcers
• Most commonly as an ulcerated,
erythematous nodule or erosion with necrotic base
• Bowen’s disease (SCC in situ):
red patch/crusting plaque.
• Microscopically: irregular nests of
epidermal cells that infiltrate the
dermis.

40. Squamous Cell Treatment
• Surgical Excision with 1 cm recommended margin
• Potential to spread to regional lymphatics: Recommend sentinel node
biopsy for those with lesions larger than 2.0 cm in diameter.
• Patients with 4 or more nodal metastases may also require radiation
therapy.
• For SCC in situ: Surgical Excision, or in certain cases
--Photodynamic therapy [porphyrins produce tumor cell cytotoxicity
after stimulation by light]
--Topical immune response modifier [Imiquimod uses anti-tumor
property of immune cells and local cytokines].

42. Melanoma
• UV radiation is a primary cause (including intense
episodic exposure). “Bad burns in childhood”
• In African American population, 70% are found on
the palmar surface of the hands and the feet (Acral
Lentiginous melanoma). Can be under nails. Famous
case: Bob Marley singer.
• Melanomas typically have: 2 distinct growth phases:
1) Horizontal 2) Vertical phase (when there becomes
an increased likelihood of invasion)

43. A.) Superficial Spreading (70%):
--legs in women, back in men
B). Nodular (10-15%):
--**most malignant due to dominant vertical growth
--more commen in men
C.) Lentigo maligna (5-10%):
--slow growth
--often on face, neck, and head
-- more common in elderly
--borders are usually very ill-defined
D.) Acral lentiginous
--palmar surface
of hands/feet, subungal

44. Treatment
• Excisional Biopsy is preferred
• Treatment is wide excision
--1 mm deep 1 cm width margin
--2 mm deep 2 cm width
--3 mm deep formerly: 3 cm width
(now: 2cm max for all)
• Closure may need skin flap
• Or grafts, reconstructions, etc.
• Sentinel Lymph node biopsy is often also performed (intermediate
depth melanomas obtain this most typically).
--If Sentinel nodes are positive, complete node dissection is then
performed.
• If high risk of relapse: Interferon-alpha (pro-inflammatory cytokine) or
other adjuvant therapy. Most: small overall benefit and high toxicity

45. So back to our patient…..what do we do with defects from wide
excisions….

46. Algorithm for Surgical resection of Skin lesions
Kruse-Losler et al. 2006

47. Flaps versus grafts
• Graft:
--consists of epidermis and some/all of dermis
--removed from body, completely devascularized, and replaced in another
location
--survival relies on a well-vascularized bed
--graft adheres by fibrin deposition within 72 hours

48. •Flap:
-- has its own blood supply
--useful for covering areas with poor vascularity
--used to reconstruct full thickness of facial structures

49. Excision of squamous cell carcinoma of the lower lip. Defect closure with
anterolateral thigh-tensor fasciae latae free fasciocutaneous flap (4).

50. (A) Malignant melanoma on the forehead
(B) Postop result 6 weeks after resection and defect closure with free radial forearm flap(3).
The radial vein and artery were
anastomosed with the
superficial temporal artery and
vein close to the defect.

51. References
• (1). Halpern AC, Guerry D 4th, Elder DE, et al. A cohort study of melanoma in patients with dysplastic
nevi. J Invest Dermatol 1993; 100:346S.
• (2). Tucker MA, Fraser MC, Goldstein AM, et al. A natural history of melanomas and dysplastic nevi: an
atlas of lesions in melanoma-prone families. Cancer 2002; 94:3192.
• (3). Kruse-Losler, B; Presser, D,etc. Reconstruction of large defects on the scalp and forehead as an
interdisciplinary challenge: Experience in the management of 39 cases. Univ of Muenster, Germany. European
Journal of Surgical Oncology. Volume 32, Issue 9, November 2006, Pages 1006–1014.
• (4). Kae-Bang Tzeng, Wen-Hsiang Chien, et al. One-stage reconstruction of large lower lip defect and oral
competence with free composite anterolateral thigh-tensor fasciae latae flap. Formosan Journal of Surgery,
Volume 45, Issue 2, April 2012, Pages 63–68
• (5) Ciresi KF, Mathes SJ. The classification of flaps. Orthop Clin North Am 1993; 24:383.
• (6). Lawrence, Peter F. Essentials of General Surgery, 5th edition. LWW: 2013. Chapter 24: Surgical Oncology:
Malignant Diseases of the Skin and Soft Tissue.
• (7): Lawrence, Peter F. Essentials of General Surgery, 5th edition. LWW: 2013. Chapter 7: Wounds and Wound
Healing.