Part 2
Surgical and Cosmetic Dermatology

SURGICAL DERMATOLOGY

Skin cancer

Surgical margin guidelines

Tumor Type	Tumor characteristics	Excision Margin
Melanoma (see melanoma guide pg.)	In‐situ	0.5–1 cm or Slow Mohs
consider SLN Bx for > 0.8 mm or ulceration	≤1 mm 1.01–2 mm >2 mm	1 cm 1–2 cm 2 cm
Basal Cell Carcinoma (BCC)	Low risk BCC Well‐defined borders Small size Area L < 20 mm Area M < 10 mm Area H < 6 mm Nodular or superficial subtype Primary tumor	3–4 mm
Basal Cell Carcinoma (BCC)	High Risk BCC Poorly defined margins Larger Size Area L > 20 mm Area M > 10 mm Area H > 6 mm High risk tumor or patient features (see indication for mohs below)	Mohs or 5–10 mm
Squamous Cell Carcinoma (SCC)	Low risk SCC Well‐defined borders Small size Area L < 20 mm Area M < 10 mm Area H < 6 mm Well differentiated histology Primary tumor	4–6 mm
Squamous Cell Carcinoma (SCC)	High Risk SCC Poorly defined margins Larger Size Area L > 20 mm Area M > 10 mm Area H > 6 mm High risk tumor location (ear, lip) High risk tumor or patient features (see indication for mohs below)	Mohs or 6–10 mm
Dermatofibrosarcoma protuberans (DFSP)	NCCN favors Mohs over WLE	2–4 cm to level of deep fascia
Merkel Cell Carcinoma	NCCN favors WLE. Can do Mohs if it does not interfere with SNLBx	1–2 cm to investing fascia layer Advised SLNBx.

Source: Adapted from Nahhas AF et al. J Clin Aesthet Dermatol. 2017 Apr; 10(4):37–46. Huang C and Boyce SM. Surgical margins of excision for basal cell carcinoma and squamous cell carcinoma. Semin Cutan Med Surg. 2004; 23:167–173.

Indication for Mohs micrographic surgery

Adapted from Ad Hoc Task Force, et al. AAD/ACMS/ASDSA/ASMS 2012 appropriate use criteria for Mohs micrographic surgery. J Am Acad Dermatol 2012; 67:531.

Location

High risk/area “H”: “mask” areas of face (central aspect of face, eyelids [including inner/outer canthi], eyebrows, nose, lips [cutaneous/mucosal/vermillion], chin, ear and periauricular skin/sulci, temple), genitalia (including perineal and perianal), hands, feet, nail units, ankles, and nipples/areola.

Moderate risk/area “M”: cheeks, forehead, scalp, neck, jawline, and pretibial surface.
Low risk/area “L”: trunk and extremities (excluding pretibial surface, hands, feet, nail units, and ankles).

High‐risk tumor features

Recurrence/incomplete prior excision
Aggressive features (high risk of recurrence):
- BCC: with morpheaform, fibrosing, sclerosing, infiltrating, micronodular, or metatypical/keratotic type.
  - Size: Area L > 20 mm; Area M > 10 mm; Area H > 6 mm
- SCC with sclerosing, basosquamous, small cell, poorly/undifferentiated, spindle cell, pageotid, infiltrating, keratoacanthoma on the face, single cell, clear cell, lymphoepithelial, sarcomatoid, Breslow depth 2 mm or greater, and Clark’s level IV or greater
- Perivascular/perineural invasion
- Other tumors: adenocystic carcinoma, adnexal carcinoma, apocrine/eccrine carcinoma, atypical fibroxanthoma, DFSP, extramammary paget disease, leiomyosarcoma, merkel cell carcinoma, and malignant fibrous histiocytoma

High‐risk patient features

Immunocompromised (IC): transplant recipient, HIV, hematologic malignancy, or immunosuppressive medications
Genetic syndromes: basal cell nevus, XP, and bazex syndromes
Prior radiated skin: tumor arising in site of prior radiation treatment
Patient with history of aggressive skin cancer with no known risk factors

Melanoma ‐ AJCC TNM classification

Major changes in AJCC eighth edition

Round to 0.1 mm decimal for tumor depth
Changes to T1a and T1b to 0.8 mm threshold
Removal of mitotic rate for T category (recorded but not impacting T category)
N category – “microscopic” vs. “macroscopic” redefined as “clinically occult” and “clinically apparent”.
Pregnostic stage III subgroup changed (increased to IIIA–IIID)
N subcategories revised based on number of tumor involved lymph nodes
M1 categories changed – LDH no longer upstage to M1c, additional of CNS metastases to M1d.

Tips:

0.8–1.0 mm = T1b or Stage IB
Nodal involvement → at least stage III
Distant mets → stage IV

T classification

Tx	1° tumor cannot be assessed
T0	No evidence of 1° tumor
Tis	Melanoma in situ
T1	≤1.0 mm	a: <0.8 mm with no ulceration b: 0.8–1.0 mm with no ulceration or <1.0 mm with ulceration
T2	1.0–2.0 mm	a: no ulceration b: + ulceration
T3	2.0–4.0 mm	a: no ulceration b: + ulceration
T4	>4.0 mm	a: no ulceration b: + ulceration

N classification

			Survival %
			5 yr	10 yr
Nx	Nodes cannot be assessed/not performed
N0	No regional lymphadenopathy/metastases detected
N1	1 node	a: no MSI, node clinically occult b: no MSI, node clinically detected	84 76	75 71
N1	0 node	c: MSI present	81	75
N2	2–3 nodes	a: no MSI, node clinically occult b: no MSI, node clinically detected	79 71	71 71
N2	1 node	c: MSI present, node detectable or occult	69	59
N3	4+ nodes	a: no MSI, node all clinically occult b: no MSI, >1 node clinically detected or matted	60 64	46 57
N3	2+ more nodes	c: MSI present, node clinically detectable or occult	52	43
Microsatellite instability (MSI) = any in‐transit, satellite, locally recurrent, or microsatellite metastases

M classification

M	Site	Serum LDH
Mx	Distant mets cannot be assessed	N/A
M0	No distant mets	N/A
M1a	Distant skin, soft tissue including muscle, and/or nonregional lymph node	(0) Normal (1) Elevated
M1b	Lung mets	(0) Normal (1) Elevated
M1c	Non‐CNS visceral mets	(0) Normal (1) Elevated
M1d	CNS mets	(0) Normal (1) Elevated

Adapted from AJCC Cancer Staging manual, Eighth Edition (2017). Balch CM et al. Final version of 2009 AJCC melanoma staging and classification. J Clin Oncol 2009; 27:6199–6206. Gershenwald JE et al. Melanoma staging: evidence‐based changes in the American Joint Committee on cancer eighth edition cancer staging manual. CA Cancer J Clin 2017;67:472–492.

Clark level

Level I	Confined to the epidermis (MIS)
Level II	Invasion past basement membrane into the papillary dermis
Level III	Tumor filling papillary dermis to the junction of the superficial reticular dermis
Level IV	Invasion into the reticular dermis
Level V	Invasion into the subcutaneous tissue

Clark level is no longer recommended as a staging criterion and is used for staging tumors ≤1 mm² only if mitotic rate cannot be determined.

Breslow depth

Breslow tumor thickness is measured in mm from the top of the granular layer of the epidermis (or the base of an ulcer) to the deepest point of tumor invasion using an ocular micrometer.

Melanoma ‐ AJCC TNM staging and survival

	Clinical staging			Pathologic staging			Survival (%)
	T	N	M	T	N	M	5 yr	10 yr
IA	T1a	0	0	T1a	0	0	99	98
IB	T1b T2a	0	0	T1b T2a	0	0	99 96	96 92
IIA	T2b T3a	0	0	T2b T3a	0	0	93 94	88 88
IIB	T3b T4a	0	0	T3b T4a	0	0	86 90	81 83
IIC	T4b	0	0	T4b	0	0	82	75
IIIA	Any T^*	N1–3	0	T1–2a T1–2a	N1a N2a	0	93	88
IIIB				T0 T1–2a T1–2a T2b–3a	N1b–c N1b–c N2b N1a–2b	0	83	77
IIIC				T0 T0 T1a–3a T3b–4a T4b	N2b–c N3b–c N2c–3c Any N N1a–2c	0	69	60
IIID				T4b	N3a–c	0	32	24
IV	Any T	Any N	M1	AnyT	Any N	M1a M1b M1c M1d	9–27	16 3 6

Gershenwald JE et al. Melanoma staging: evidence‐based changes in the American Joint Committee on Cancer Eighth Edition cancer staging manual. CA Cancer J Clin 2017;67:472–492.

^*There are no Stage III subgroups in clinical staging.

Melanoma: treatment guidelines

Breslow depth (mm)	Margin (cm)	SNL^*	Physical exam^**	Workup^***	Adjuvant treatment
In situ	0.5–1	No	q6 mo x 1 yr then yearly	Symptom specific (CT, PET, MRI)	—
<1	1	No^*	q6–12 mo × 5 yr then yearly	Symptom specific (CT, PET, MRI)	—
1.01–2.00	1–2	Yes	q6–12 mo × 5 yr then yearly	Symptom specific (CT, PET, MRI)	—
2.01–4.00	2	Yes	q3–6 mo × 2 yr, q3–12 mo × 3 yr, then yearly		Clinical trial Observe
>4	2	Yes			Clinical trial Observe IFN α
Stage III SLN +, micromet	WLE (as above)	LND or clinical trial	q3–6 mo × 2 yr, q3–12 mo × 3 yr, then yearly	CXR, CT, brain MRI, and/or PET/CT scans q3–12 mo (optional) Baseline imaging for staging and symptom‐specific evaluation (CT, PET, MRI)	Clinical trial Observe IFN α High‐dose ipilimumab
Stage III Clinical + nodes, macromet	WLE	FNA or bx of + LN, then LND	q3–6 mo × 2 yr, q3–12 mo × 3 yr, then yearly		Clinical trial Observe IFN α High‐dose ipilimumab Biochemotherapy^┼ ±RT to nodal basin if Stage IIIC
Stage III in‐transit	WLE + FNA or Bx of in‐transit lesions	Yes	q3–6 mo × 2 yr, q3–12 mo × 3 yr, then yearly	CXR, CT, brain MRI, and/or PET/CT scans q3–12 mo (optional) Baseline imaging for staging and symptom‐specific evaluation (CT, PET, MRI)	Intralesional BCG, IL‐2, IFN, talimogene laherparepvec (T‐VEC) IFN α Limb perfusion with melphalan Clinical trial (preferred) Radiation tx Systemic tx
Stage IV	FNA or bx	Yes	q3–6 mo × 3 yr, q4–12 mo × 2 yr, then yearly	Chest/abd/pelvic CT, MRI brain and/or PET CT for baseline staging and symptom‐specific evaluation, LDH BRAF testing (metastatic disease)	Systemic therapy preferred See NCCN Guidelines Clinical trial Anti‐PD1 monotherapy BRAF mutated: Targeted therapy (combination therapy with dabrafenib/trametinib or vemurafenib/cobimetinib) Second line: Dacarbazine Temozolomide High‐dose IL2

Source: Adapted from NCCN Practice Guideline in Oncology‐ v.2.2016 Melanoma.

^*Sentinal lymph node should be performed at the time of Wide Local Excision. Consider in tumor <1 mm if initial bx with mitotic rate ≥1 mm², ulceration, positive deep margin, angiolymphatic invasion, or young age. The yield and clinical significance of SLNBx in Stage IA is unknown and is generally not recommended.

^**Followup: At least annual skin exam for life, educate patient in monthly self‐skin and lymph node exam. (Bichakjian et al. Guidelines of care for the management of primary cutaneous melanoma. JAAD 2011; 65:1032–1047)

^***Evaluation: Routine imaging/lab tests not recommended in Stage 0/IA disease. In Stage IB, may consider nodal basin ultrasound prior to SLNB for patients with equivocal regional lymph node physical exam (NCCN guidelines 2.2016). CT, PET, and MRI may be performed to evaluate specific sxs.

^┼Regimens include dacarbazine, temozolomide, paclitaxel, vinblastine, IL‐2, IFNα‐2b, and combinations thereof (see NCCN guidelines).

Squamous cell carcinoma (SCC)

NCCN stratification of low versus high risk cutaneous SCC

Parameters	Low risk	High risk
Clinical H&P
Location/size (including peripheral rim of erythema)	Area L < 20 mm Area M < 10 mm	Area L ≥ 20 mm Area M ≥ 10 mm Area H
Borders	Well defined	Poorly defined
Primary vs. recurrent	Primary	Recurrent
Immunosuppression	−	+
Site of prior radiation or chronic inflammatory process	−	+
Rapidly growing tumor	−	+
Neurological symptoms	−	+
Pathology
Degree of differentiation	Well or moderately differentiated	Poorly differentiated
High‐risk histological subtype	−	+
Depth (thickness or Clark’s level)	<2 mm or I, II, III	≥2 mm or IV, V
Perineural, lymphatic, or vascular involvement	−	+
Recommended TX	EDC in nonterminal hair‐bearing area Standard excision with 4–6 mm margin to subq RT for nonsurgical cases	Mohs surgery Standard excision may be considered with 6 mm margins RT for nonsurgical cases

Source: Adapted from National Comprehensive Cancer Network stratification of low versus high‐risk cSCC.

National Comprehensive Cancer Center. NCCN Clinical Practice Guidelines in Oncology; Squamous Cell Carcinoma (V2.2018). 2018; www.nccn.org, 1 February 2018.

Area H = “mask areas” of face (central face, eyelids, eyebrows, periorbital, nose, lips [cutaneous and vermilion], chin, mandible, preauricular and postauricular skin/sulci, temple, and ear), genitalia, hands, and feet.

Area M = cheeks, forehead, scalp, neck, and pretibia.

Area L = trunk and extremities (excluding pretibia, hands, feet, nail units, and ankles).

High‐risk histologic subtype: Acantholytic (adenoid), adenosquamous (showing mucin production), desmoplastic, or metaplastic (carcinosarcomatous) subtypes.

SCC TNM classification: tumor classification AJCC vs BWH

BWH classification provides better prognostication in patients with localized disease (stratifies T2 into a and b)

	AJCC eighth ed	Brigham and Women’s Hospital
Tx	1° tumor cannot be assessed	1° tumor cannot be assessed
Tis/T0	SCC in situ	SCC in situ
T1	<2 cm in greatest diameter with fewer than two “high‐risk” features	0 risk factors
T2	2–4 cm, or with two or more “high‐risk” features	T2a: 1 risk factor T2b: 2–3 risk factors
T3	>4 cm minor bone erosion perineural invasion (tumor cells within nerve sheath > 0.1 mm or clinical/radiographic involvement of names nerves) or deep invasion (beyond subq fat or >6 mm to the base of tumor)	4 risk factors or bone invasion
T4a	Tumor with gross cortical bone/marrow invasion
T4b	Tumor with skull base invasion and/or skull base foramen involvement
	AJCC high‐risk factors: >2 mm thickness Clark level ≤IV perineural invasion primary site ear, non‐hair‐bearing lip Poorly differentiated histology	BWH risk factors: tumor diameter ≥2 cm poorly differentiated histology perineural invasion tumor invasion beyond the subcutaneous fat

SCC AJCC TNM staging

	T	N	M
0	Tis	0	0
I	T1	0	0
II	T2	0	0
III	T3 T1–3	0 1	0 0
VI	T1–3 Any T T4 Any T	2 3 Any N Any N	0 1
		N1 = 1 LN+ ≤3 cm ENE− N2 = 1 LN+ ≤3 cm ipsilateral ENE+ 1 LN+, >3 and ≤6 cm ipsilateral ENE− or 1 LN+ ≤3 cm ipsilateral ENE+ ≥2 LN+ all ≤6 cm ipsilateral ENE− N3 = ≥1 LN+ >6 cm ENE+ 1 LN+ ≤3 cm ENE+ contralateral or ≥1 LN+ >3 cm ipsilateral ENE+ or ≥2 LN+, any ENE+ ENE+, with extranodal extension; ENE−, without extranodal extension	M0 = no distant mets M1 = distant mets

SCC ‐ Treatment of advanced disease

Regional disease (in‐transit and regional LN mets) – LN dissection, adjuvant radiation ± concurrent systemic therapy
Distal mets – Multidisciplinary approach (NCCN)
- First line: Cisplatin ± 5‐Fluorouracil
- Second line: Epidermal Growth Factor Receptor (EGFR) inhibitors
  - Monoclonal antibodies: Cetuximab, Panitumumab
  - Tyrosine kinase inhibitors: Erlotinib, Gefitinib
- Emerging: Checkpoint inhibitors – Anti‐PD‐1 inhibitors: Nivolumab, Pembrolizumab

Prophylactic antibiotics and antivirals

Guideline for Prophylactic antibiotics

Use of antibiotic prophylaxis for endocarditis indicated for surgical procedure on infected tissue in patients with high‐risk cardiac lesion or as detailed below

Antibiotic (trade size)	Adults	Children
*All sites except oral and groin/lower extremity:*
Cephalexin (500 mg, 250 mg/5 ml)	2 g	50 mg/kg
Dicloxacillin (500 mg, 250 mg/5 ml)	2 g	50 mg/kg
If penicillin allergic
Azithromycin (250, 500 mg)	500 mg	15 mg/kg
Clarithromycin (500 mg, 250 mg/5 ml)	500 mg	15 mg/kg
Clindamycin (300 mg)	600 mg	20 mg/kg
Oral site:
Amoxicillin (500 mg, 250 mg/5 ml)	2 g	50 mg/kg
If penicillin allergic
Azithromycin (250, 500 mg)	500 mg	15 mg/kg
Clarithromycin (500 mg, 250 mg/5 ml)	500 mg	15 mg/kg
Clindamycin (300 mg)	600 mg	20 mg/kg
Groin and lower extremity site
Cephalexin (500 mg, 250 mg/5 ml)	2 g	50 mg/kg
If penicillin allergic
Trimethoprim‐Sulfamethoxazole, double strength	1 tab
Levofloxacin	500 mg

One hour prior to surgery: (all p.o. doses).

Algorithm for antibiotic prophylaxis

Algorithm from a box with lists of high-risk cardiac conditions and high risk for prosthetic joint infection to a box with list of the nature of the surgery, and then to boxes labeled no antibiotic and antibiotic prophylaxis.

Guideline for prophylactic antivirals

History of HSV infection of the orofacial area is an indication for prophylaxis for facial resurfacing, chemical peels, dermabrasion, PDT, and orofacial surgery. Treat for 7–14 days with acyclovir, valacyclovir, or famciclovir to suppress viral reactivation during reepithelialization.

Acyclovir (Zovirax)	400 mg tid × 7–14 d
Valacyclovir (Valtrex)	500 mg bid × 7–14 d
Famciclovir (Famvir)	250 mg bid × 7–14 d

Antiseptic scrubs

Agent	Mechanism of action	Gram +	Gram −	Mycobacteria	Viruses	Fungi	Spores	Speed of action	Residual activity	Other
Alcohol 60–95%	Denature proteins (bacterial cell wall)	+++	+++	+++	+++	+++	−	Fast	None	Flammable with laser/cautery Allow to dry on surface
Chlorhexidine 2–4% (Hibiclens)	Impairs cell membrane	+++	++	+	+++	+	−	Intermed	Excellent	Ototoxicity, keratitis, skin irritant
Iodine 3% (Lugol)	Oxidation	+++	+++	+++	+++	++	+	Intermed	Minimal	Skin irritant Inactivated by blood/sputum
Iodophors– (Betadine) Povidone–iodine 7.5–10%	Oxidation/ substitution by free iodine: disrupts S─H and N─H bonds, C═C bonds in fatty acids	+++	+++	+	++	++	−	Intermed (needs to dry)	Minimal	Skin irritant (less than iodine) Inactivated by blood/sputum May cross‐react with radiopaque iodine Surfactant + iodine = iodophor
TechniCare PCMX Chloroxylenol	Disrupts cell membrane	+++	+	+	+	+	Unknown	Slow	Good	Addition of EDTA increases its activity against pseudomonas
Triclosan 0.2–2%	Disrupts cell wall, inhibits fatty acid synthesis, binds bacterial enoyl–acyl carrier protein reductase (ENR, fabI)	+++	++	+	+++	−	Unknown	Intermed	Good	Forms chloroform and dioxins when combined with chlorine in tap water
Benzalkonium (Quaternary ammonium)	Dissociation of cell membranes; disrupts intermolecular interactions	++	+	+/−	+ Lipophilic	+/−	Unknown	Slow	Good	Use only in combination with alcohols Eyedrop preservative Easily inactivated by cotton gauze/ organic materials

Source: Adapted from CDC. MMWR Recomm Rep. 2002 Oct 25;51(RR‐16):1–48.

Anesthetics

Mechanism of action

Reversibly inhibit nerve conduction by blocking sodium ion influx into peripheral nerve cells = prevent depolarization of nerves.

Practical tips to decrease pain with injections:

The patient

Distract, pinch the skin
Consider topical anesthesia (i.e. LMX) prior to infiltration

The anesthetic agent

Warming to 37–42 ºC
Buffered lidocaine with bicarb (increase the pH 3.3 → 7.4)

Add 1 cc 8.4% NaHCO₃ to 10 cc Lidocaine 1% with epi

The injection technique

Fine needle (27, 30, or 32 gauge)
Inject slowly
If possible, through a dilated pore or wound edge
Deeper injections into SQ area hurts less (go from deep subdermal to tight dermal)
Minimize needle punctures by moving in a fan shape
Consider nerve blocks or ring blocks

Standard formula for buffered Lidocaine

1% Lidocaine with epinephrine 1:100 000

Ingredient	Quantity
Lidocaine 1%	50 ml
Sodium bicarbonate 8.4%	5 ml
Epinephrine 1:1000	0.5 ml

Tumescent anesthesia

Lidocaine 0.05–0.1% + Epinephrine 1:1 000 000

Max Tumescent is 35–50 mg/kg

Peak Lidocaine level at 12–14 hours

Ingredient	Quantity
Normal saline 0.9%	1000 ml
Lidocaine 1%	50–100 ml
Sodium bicarbonate 8.4%	10 ml
Epinephrine 1:1000	1 ml

Topical anesthetic (see drug section pg 197)

EMLA cream^*	lidocaine 2.5% and prilocaine 2.5%
LMX	lidocaine 4 and 5% in liposomal delivery cream
Lida‐Mantle	lidocaine 3% cream
Topicaine	lidocaine 4% and 5% gel
Pliaglis	lidocaine 7% and tetracaine 7% cream

Source: Cavef et al. Arch Derm 2007;143:1074–1076.

^*Risk of methemoglobinemia. Also, may create artefactual vacuolization/swelling of the upper epidermis and basal layer damage/clefting.

Pharmaceutically compounded topical anesthetic

BLT	20% benzocaine, 6% lidocaine, 4% tetracaine
TAC	0.5% tetracaine, 1:2000 epineprine, 11.8% cocaine
LET	4% lidocaine, 1:2000 epineprine, 0.5% tetracaine
Lasergel	10% lidocaine, 10% tetracaine
23/7	23% lidocaine, 7% tetracaine

Adverse reaction to local anesthetics

Condition	Pulse	BP	Signs and symptoms	Management
Vasovagal Rxn	▼	▼	Diaphoresis, hyperventilation, nausea	Trendelenburg, cool compress
Epinephrine Rxn	▲	▲	Sweating, tachypnea, HA, palpitation	Reassurance, beta‐blocker
Anaphylaxis	▲	▼	Tachycardia, bronchospasm	Epinephrine 1:1000 × 0.3 ml SQ. Antihistamine, airway maintenance
Lidocaine toxicity
1–6 μg/ml	Nl	Nl	Tongue and circumoral paresthesia, metallic taste, tinnitus, lightheadedness	Observe
6–9 μg/ml	Nl	Nl	Tremors, nausea, vomiting, hallucination, muscle fasciculations	Diazepam, airway maintenance
9–12 μg/ml	▼	▼	Seizures, cardiopulmonary depression	Respiratory support
>12 μg/ml	—	—	Coma, cardiopulmonary arrest	CPR/ACLS

Source: Adapted from Snow SN and Mikhail GR. Mohs Micrographic Surgery Second Edition. Chapter 14. Table 14–3.

Local anesthetic

Generic name	Trade name	Pregnancy category^†	Potency	Onset (min)	Without epinephrine		With epinephrine^†
Generic name	Trade name	Pregnancy category^†	Potency	Onset (min)	Duration (min)	Max dose (mg/kg) for adults	Duration (min)	Max dose (mg/kg) for adults
Amide (“i” before – caine = amide)
Lidocaine	Xylocaine	B	Intermed	<2	30–120	4.5 (30 cc for 70 kg)	60–400	7 (50 cc for 70 kg)
Bupivacaine	Marcaine, Sensorcaine	C*	High	2–10	120–240	2.5	240–480	3
Mepivacaine	Carbocaine	C*	Intermed	3–20	30–120	6	60–400	8
Prilocaine	Citanest	B	Intermed	5–6	30–120	7	60–400	10
Etidocaine	Duranest	B	High	3–5	200	4.5	240–360	6.5
Ester
Procaine	Novocain	C	Low	5	15–30	10	30–90	14
Chloroprocaine	Nesacaine	C	Low	5–6	30–60	10	—	—
Tetracaine	Pontocaine	C	High	7	120–240	2	240–480	2
Other – in patients who might be allergic to above
Diphenhydramine hydrochloride1% solution		B	—	5	15–180	Sedation with >25 mg (2.5 cc of 1%)	—	—
Normal saline with benzoyl alcohol preservative		—	—	—	—	—	—	—

^†Epinephrine is pregnancy category C. Low doses (diluted 1:300,000 can be used during pregnancy)

^*Bupivacaine and mepivacaine: pregnancy category C due to potential for fetal bradycardia

	Metabolized by	Excretion	Allergic reaction
Amide	Liver p450 enzyme (caution in patients with liver disease)	Kidney	Rare, due to preservative methylparaben (if allergic: switch to preservative‐free lidocaine)
Ester	Tissue pseudocholinesterase	Kidney	More common Due to metabolite to PABA (p‐aminobenzoic acid) (if allergic: switch to amides)

Nerve blocks*

See Plates 1–4.

Surgical Anatomy

Anatomy of the face

Cosmetic unit of the central face

Diagram of the a human face with lines indicating the Lateral ridge, nasofacial sulcus, alar crease, columella, philtral crest, melolabial fold, vermilion-cutaneous junction, mentolabial crease, etc.

From Robinson JK (ed.). Atlas of Cutaneous Surgery, first edition. WB Saunders: 1996, p. 2, figure 1.2, with permission.

Cosmetic units of the cheek

Diagram of the anterolateral view of the face with lines indicating preauricular, malar, lower cheek, alar base nasolabial, and supramedial.

From Robinson JK (ed.). Atlas of Cutaneous Surgery, first edition. WB Saunders: 1996, p. 2, figure 1.4, with permission.

Cosmetic units of the forehead

Diagram of the anterolateral view of the face with lines indicating superior eyebrow, glabellar, general forehead, and temporal.

From Robinson JK (ed.). Atlas of Cutaneous Surgery, first edition. WB Saunders: 1996, p. 2, figure 1.3, with permission.

Cosmetic units of the nose

Courtesy of Dr. Quan Vu

Anatomy of the nasal cartilage

Diagram displaying the front and lateral views of the nasal cartilage with lines marking the nasal bone, septal cartilage, lateral cartilage, lateral crus, medial crus, and alar cartilage.

Courtesy of Dr. Quan Vu

Anatomy of the ear

From Robinson JK (ed.). Atlas of Cutaneous Surgery, first edition. WB Saunders: 1996, p. 186, figure 3.1, with permission.

Cosmetic units of the eye

From Robinson JK (ed.). Atlas of Cutaneous Surgery, first edition. WB Saunders: 1996, p. 3, figure 1.5, with permission.

Anatomy of the eye

Diagram displaying a lateral cross section of the eye with lines marking the frontalis muscle, orbital fat, orbital septum, retroorbicularis fat, orbicularis oculi muscle, levator aponeurosis, tarsus, etc.

From Robinson JK (ed.). Atlas of Cutaneous Surgery, first edition. WB Saunders: 1996, p. 3, figure 1.5, with permission.

Danger zones in surgery

Diagram displaying the lateral view of a human head with parts of temporal, zygomatic, buccal, and marginal mandibular branches enclosed by a box. At the right are magnified views (detailed) of the enclosed parts.

From G Bernstein. J Dermatol Surg Oncol, 1986; 12(7):725, figure 6, with permission.

Temporal branch of CN VII:
- Most vulnerable location: mid‐zygomatic arch.
- Nerve course: Nerve exits the superior–anterior portion of the parotid gland, then courses 0.5 cm below the tragus to 1.5 cm above the lateral eyebrow. Nerve lies just beneath the skin, subcutaneous fat, and SMAS.
- Motor innervation: frontalis, upper portion of the orbicularis oculi and corrugator supercilii
- Damage: inability to raise eyebrow and wrinkle forehead. Results in a flat forehead and droopy eyebrow.
Marginal mandibular branch of CN VII:
- Most vulnerable location: mid‐mandible 2 cm lateral to the oral commissure.
- Nerve course: Nerve exits the inferior–anterior portion of the parotid gland, then courses along the angle of the mandible across the facial artery and vein. May be 2 cm or more below the inferior edge of the mandible if the head is rotated or hyperextended. Lies beneath the skin, subcutaneous fat, and SMAS.
- Motor innervation: orbicularis oris, risorius, mentalis, and depressor muscles of the mouth.
- Damage: drooping of the mouth, inability to pull the lip laterally and inferiorly with smiling.
Great auricular nerve (C₂ and C₃):
- Most vulnerable location: 6.5 cm below the external auditory canal along the posterior border of the sternocleidomastoid muscle.
- Nerve course: Nerve courses toward the lobule posterior to the external jugular vein.
- Damage: Sensory innervation, results in numbness of the inferior 2/3 of the ear and adjacent cheek and neck
Spinal accessory nerve (CN XI):
- Most vulnerable location: Erb’s point.
- Nerve course: Nerve exits from behind the SCM at Erb’s point and courses diagonally and inferiorly across the posterior triangle. Draw a line from the angle of the jaw to the mastoid process – Erb’s point is located 6 cm vertically below the midpoint of this line at the posterior border of the sternocleidomastoid (within a 2 cm area). Also may define area by drawing a line horizontally across the neck from the thyroid notch to the posterior border of the sternocleidomastoid (1 cm above and 1 cm below).
- Innervation: location of the great auricular, less occipital, and spinal accessory nerve. The spinal accessory nerve innerves the trapezius muscle.Damage: winged scapula – inability to shrug the shoulder and abduct the arm.

Danger zone of the neck: Erb’s point

Diagram displaying anatomy of the neck with lines marking the lesser occipital nerve, great auricular nerve, external jugular vein, transverse cervical nerve, supraclavicular nerve, trapezius muscle, etc.

From RG Wheeland RG (ed.). Cutaneous Surgery, first edition. WB Saunders: 1994, p. 61, figure 5.13, with permission.

Dermatomal distribution of sensory nerves

From Leventha: Fractures, dislocations, and fracture‐dislocations of the spine. In Canale et al (eds.) Campbell’s Operative Orthopaedics, tenth edition. Mosby: 2003, Figure 35.1, with permission.

Anatomy of the lower extremity venous system

Modified from Min RJ, et al. Duplex ultrasound evaluation of lower extremity venous insufficiency. J Vasc Interv Radiol 2003 14: 1233–1241, with permission.

Anatomy of the great saphenous vein

Diagram displaying the anatomy of the lower extremity venous system, with lines marking the superficial circumflex iliac vein, femoral vein, anterior lateral tributary, anterior tributary vein, etc.

Left: Anatomy of the perforator veins with lines marking the proximal thigh PV, distal thigh PV, etc. Right: Anatomy of the short saphenous vein with lines marking the small saphenous vein, popliteal vein, etc.

Anatomy of the nail

From RK Scher and CR Daniel. Nails: Therapy, Diagnosis, Surgery, second edition. WB Saunders: 1997, p. 13–14, figures 2.1, 2.2a, 2.2b, with permission.

Top: Diagram of a fingernail with plate, bed, solehorn, distal nail fold hyponychiyum, matrix, etc. being marked. Bottom: Diagram of a toe nail with eponychium, plate, bed horny layer, volar skin, etc. being marked.

Cutaneous reconstruction

Diagram displaying a human head with circle markers on the head, forehead, eyelids, nose, philtrum, ears, chin, and cheek. Each part has a corresponding magnified view (detailed).

From Wheeland RG (ed.). Cutaneous Surgery, first edition. WB Saunders: 1994, p. 51, figure 5.6, with permission.

Undermining depths in reconstruction

Scalp	Subgaleal (relatively avascular)
Forehead	Subgaleal (for large defects) or subcutaneous fat above frontalis fascia
Temple/zygomatic arch	Superficial subcutaneous fat above temporal branch of facial nerve
Mandible	Superficial subcutaneous fat above marginal mandibular branch of facial nerve
Ear	Above perichondrium
Lip	Above orbicularis oris
Nose	Above perichondrium/periosteum
Rest of face	Superficial subcutaneous fat, above the parotid duct
Terminal hair‐bearing area	Deep to hair papillae
Lateral neck	Superficial subcutaneous fat above spinal accessory nerve
Trunk/extremities	Above muscular fascia
Hands and feet	Subdermal

Reconstruction algorithm: STAIRS

Second intention

Cosmetic result of wound healing by second intention according to anatomical site

Diagram displaying a human head with discrete shades for satisfactory, variable, and excellent cosmetic result (light–dark).

Ideal for
1. Concave areas: Periorbital (medial canthus), temple, conchal bowl, and alar crease
2. Shallow defects: i.e. shins
3. Fair‐skinned patient (wound tends to heal with whiten scar)
4. Poor operative candidates
May take weeks/months to heal, so patient must be able to perform wound care
May heal with atrophic, hypertrophic, white scar
Can perform delayed repair/graft at 2–4 weeks

Cosmetic result of wound healing by secondary intention according to anatomical site.From Zitelli JA. Wound healing by secondary intention. JAAD 1983;9(3) 407–415; with permission

Simple linear closure

3–4:1 Length:width ratio
Orient along relaxed skin tension lines (RSTLs) at junction of cosmetic subunits

RSTL on the face showing orientation of simple linear closure.

Schematic of an eye with length of 3–4 x (depicted by a horizontal two-headed arrow) and diameter of x (depicted by a vertical two-headed arrow). At the right is a horizontal line with short vertical lines.

From S Burge, R Rayment. Simple Skin Surgery. Blackwell Scientific Publications: 1986; with permission.

M‐plasty

Modification of the linear closure
GOAL: Shortens the length of a scar

Schematic of an eye with 30° angle at the left and right (with V-shaped cut) sides, with a right arrow pointing to a horizontal line with a V-shaped line at the right.

Transposition flap

GOAL: Redistribute tension vectors
Flap rotates about a pivotal point at the base of the pedicle and is transposed over an island of normal skin
Pivotal restraints may limit its movement
Wide undermining necessary to prevent pincushioning
Common flaps: rhombic, bilobe, z‐plasty, banner, and nasolabial (melolabial)

Rhombic

Used for small defects where adjacent tissue is available to rotate onto defect.
Changes the tension vector along the secondary defect (perpendicular to tension across primary defect).
Classic rhombic (Limberg) consists of parallelogram with 60º and 120º.
Common locations: medial canthus, upper 2/3 of nose, lower eyelid, temple, and peripheral cheek.

Schematic displaying a rhombus containing an oval, with an angle of 60° from a horizontal line (linked to the rhombus) and an oblique line (top) and a rhombus with horizontal lines connected to 2 V-shaped lines (bottom).

Modifications of rhombic flaps

Webster 30º

Narrower flap, easier to close secondary defect

Less reorientation of tension vectors

Schematic of the modifications of rhombic flaps, with a diamond shape containing a circle. The diamond is linked to a 30° angle. At the right is representation of the diamond with its bottom right side being flapped upward.

Dufourmentel

Compromise between Limberg and Webster flap

Extend dotted lines then bisect them

Second incision parallel to defect midline

Schematic of a Dufourmental flap depicted by a diamond shape with an ellipse. The diamond is linked to a 60° angle. At the right is the representation of the diamond at the left with its bottom right side being flapped upward.

Bi‐rhombic flap

Bilobe

Used for small defects 1–1.5 cm in size. Common location: lower 1/3 of nose
Tension is shared between the secondary and tertiary defects

Zitelli modified bilobe flap

Determine the location of standing cone, then draw ~90º (Zitelli modification) line
First lobe is at 45º – equal or slightly smaller than defect
Second lobe is at 90º to the standing cone
Wide undermining in the submuscular plane to prevent trapdoor effect

Z‐plasty

GOAL: changing the direction of a scar or to elongate a scar.
Limbs of the Z should be equal lengths.

The degree of the limbs determines both the direction and length of final scar.

3 Schematics of Z-plasty depicting 75% length gain with direction of final scar at 90°, 50% length gain with direction of final scar at ~65°, and 25% length gain with direction of final scar at ~40° (top–bottom).

Advancement flap

GOAL: modification of the linear closure, with standing cones (burow triangle) displaced to a more desirable position (i.e. away from free margin).
Tension vector remains parallel to the motion of the flap.
Types of advancement flaps: U‐plasty, H‐plasty, burow advancement, modified crescentic advancement, O → T, and island pedicle.

U‐plasty/O → U: unilateral advancement

Burow triangles created away from defect in one direction.
Useful along eyebrow and helical rim.

Schematic depicting U-plasty/0 to U: unilateral advancement, with arrows linking a diamond containing an ellipse, an irregular shape with an ellipse, and a rectangular shape with hatched lines, opened on the right side.

H‐plasty/O → H: bilateral advancement

Burow triangles created away from defect bilaterally.
Useful if tissue reservoir is available bilaterally.

Schematic depicting H-plasty/0 to H: bilateral advancement, with arrows linking a diamond containing an ellipse, a box with an ellipse, and an I-shape with hatched lines.

Burow’s advancement flap: unilateral advancement

Displaces one of the standing cone to a more desirable location.
Useful if defect is along lateral upper cutaneous lip → may displace one of the standing cone to the nasolabial folds.

Modified crescentic advancement flap: unilateral advancement

Modification of the burow triangle.
Crescentic standing cone removed along the flap to lengthen it.
Eliminates the need for excision of a standing cone.

O→ T/T‐plasty/A → T: bilateral advancement

Displaces one of the standing cone bilaterally.
Useful adjacent to a free margin or along the junction between two cosmetic units (brow, eyelid, forehead, and lip).

Schematic depicting Q→T/T-plasty/A→T: bilateral advancement, with a diamond shape with an ellipse linked by arrows to an irregular shape with an ellipse, then to 2 perpendicular lines with hatched lines.

V→Y advancement/Island pedicle/Kite flap

Island of tissue detached from periphery but with underlying subcutaneous and muscular pedicle.
Caution: no undermining to base of island – must keep flap attached to underlying pedicle to ensure good blood supply.

Schematic illustrating the V→Y advancement, island pedicle, and kite flap.

Interpolation flap

GOAL: coverage of large defects requiring flap with robust blood supply.
Commonly axial pattern flap – based on named direct cutaneous artery.
Robust blood supply allow greater length:width ratio.
Two‐staged procedure.
Base is usually located at some distance from defect. Pedicle must pass over or under an intervening bridge of intact skin.

Types of flaps: paramedian, nasolabial, and abbe.

Flap	Arterial supply	Defect location	Pedicle division
Paramedian forehead	Supratrochear artery	Large distal nasal defect	2–3 wk
Retroauricular helical	Random flap: rich vascular supply from posterior auricular, superficial temporal, and occipital branches	Large helical rim defect	3 wk
Nasolabial	Angular artery	Large ala defects	2–3 wk
Abbe	Superior or inferior labial artery	Large lip defect	3 wk

Rotation flap

GOAL: covering a defect when there is an abundant surrounding tissue reservoir.
Pivotal flap with a curvilinear incision – the flap and defect form a semicircle.
Rotates in an arc about a pivotal point near the defect.
Distributes the tension vector along the curvilinear line.
Common locations: scalp, lateral cheek, infraorbital, and temple.
Types of rotation flaps: unilateral rotation, bilateral rotation (O → Z), pinwheel, dorsal nasal flap, and Tenzel/ Mustarde flaps.

Unilateral rotation flap

Usually flap is inferiorly/laterally based to improve lymphatic drainage and decrease flap edema.
Consider backcut to improve mobility.

O–Z plasty/bilateral rotation flap

Useful when there is insufficient tissue reservoir for unilateral flap.
Common location: scalp.

Dorsal nasal rotation/Reiger/Hatchet flap

Useful for nasal defect <2.5 cm on the lower 2/3 of the nose, best if midline.
Flap along the entire nasal dorsal.
Undermine at the level of the perichondrium/periosteum
Backcut in the glabella.

Mustarde/Tenzel rotation flap

Laterally based cheek rotation flap.
Useful for defect along supramedial cheek/lower eyelid.
Mustarde flap mobilizes entire cheek for defect >½ of eyelid.
Tenzel flaps mobilizes partial cheek for defect <½ eyelid.

Skin graft

GOAL: surgical defect which cannot be closed with adjacent local skin or allowed to heal by second intention; useful for larger wounds, especially in areas that require tumor surveillance.

Stages of skin graft

Stage	Events	Graft	Timeline
Imbibition	“Ischemic period” – nutrient through osmosis (bolster improves osmosis)	Dark color, edematous	24–48 h
Inosculation	Anastomosis of existing blood vessels	Pink	48–72 h (up to 10 d)
Neovascularization	New capillary ingrowth to graft from wound bed	Hypopigment, less edema	6–7 d

Three major types:
1. Full thickness skin graft (FTSG) = epidermis + full dermis
2. Split thickness skin graft (STSG) = epidermis + partial dermis
3. Composite graft = skin (epidermis and dermis) + additional component (cartilage or fat)

FTSG

Minimal contraction ~15%.
Better cosmesis than STSG – good color, texture, and thickness match.
Must have intact perichondrium/periosteum for survival – higher metabolic demand than STSG = higher rates of graft failure.
Most useful for defects less than 3 cm.
Common sites: eyelids, medial canthus, helical rim, conchal bowl, nasal tip, and digits.
Good donor sites: preauricular/postauricular area, supraclavicular, standing cones (burow graft), conchal bowl, upper eyelid, and forehead.

STSG

Higher risk for contraction, poor cosmesis.
Useful for very large defects: can use fenestration/meshing to enlarge size.
Donor site heal by second intention can be painful.
Large grafts need to be harvested with special equipment.
Better survival than FTSG due to low nutritional requirements
- Thin: 0.005–0.012 in.
- Medium: 0.012–0.018 in.
- Thick: 0.018–0.028 in.

Composite graft

Less likely to contract, better cosmesis.
Highest risks for necrosis due to avascular tissue (cartilage) and thicker graft.
Useful when bulk and structural support is needed – i.e. nasal alar defects.

Type of graft	Nutritional needs	Risk of graft failure	Cosmesis and tissue match	Contraction risk	Durability/strength	Sensation
FTSG	High	Higher	Good	Low	Good	Good
STSG	Low	Lower	Poor	High	Poor	Fair
Composite	High	Highest	Good	Low	Excellent	Fair

Causes of graft failure

Poor blood and nutritional supply: nicotine use, nutritional deficiency, and collagen vascular disease.
Poor graft bed contact: graft movement (activity, trauma, and poor immobilization), hematoma, seroma.
Infection: immunosuppression, diabetes, systemic disease, and poor wound care.
Physician technique: incomplete defatting, high tension due to inadequate size, rough tissue handling, and excessive cautery.

Sutures

Absorbable

Material	Origin	Filament	Tensile strength 50%	Absorption	Reactivity	Degradation
Plain gut	Animal collagen^*	Twisted	1 wk	14–80 d	High	Proteolysis
Fast absorbing gut	Animal collagen^*	Twisted	3–7 d	21–42 d	High	Proteolysis
Vicryl rapide	Polyglactin	Braided	5 d	42 d	Moderate	Hydrolysis
Monocryl	Poliglecaprone	Monofil	1 wk	90–120 d	Low	Hydrolysis
Chromic gut	Plain gut tanned with chromium salts	Twisted	2–3 wk	30–80 d	High, less than plain gut	Proteolysis
Dexon	Polyglycolic acid	Braided	2–3 wk	90 d	Low	Hydrolysis
Vicryl	Polyglactin	Braided	3 wk	80–90 d	Moderate	Hydrolysis
PDS	Polydioxanone	Monofil	4 wk	180 d	Low	Hydrolysis
Maxon	Polyglyconate	Monofil	4 wk	180 d	Very low	Hydrolysis

^*Gut made from mucosa/submucosa of sheep or beef intestine.

Nonabsorbable

Material	Origin	Filament	Tensile strength	Reactivity	Elasticity	Handling
Silk	Silk	Braided or twisted	Low, 3–6 mo	High	Inelastic Soft suture	Best
Prolene/Surgilene	Polypropylene	Monofil	High, 2 yr	Least	Very elastic Stiff suture	Fair–good
Ethilon/Monosol/Dermalon	Nylon	Monofil	High, losing 10–20%/yr	Low	Mild elasticity Stiff suture	Fair
Surgilon/Nurolon/Mersilene	Nylon	Braided	High, Losing 10–20%/yr	Moderate	Mild elasticity	Good
Ethibond/Dacron/Novafil	Polyester	Monofil or braided	High, Permanent	Low	Mild elasticity	Very good
	Polybutester	Monofil	High	Low	Very elastic	Very good

Suture removal time

Area	Removal time (days)
Face	4–5
Neck	5–7
Scalp	7
Trunk	7–12
Extremities	10–14

Electrosurgery^*

Modality	Terminals	Gap output	Voltage	Amperage	Capability
Electrodessication	1	Markedly damped	High	Low	Superficial destruction
Electrofulguration	1	Markedly damped	High	Low	Superficial destruction (Spark gap)
Electrocoagulation	2	Moderately damped	Mod	Mod	Deep penetration and destruction, Good hemostasis
Electrosection	2	Undamped	Low	High	Cutting

^*Electrocautery = not electrosurgery, no electric current, uses heat conduction.

Wound healing

Time	Tensile strength vs. baseline
1 wk	5%
1 mo	40%
1 yr	80%

Three phases of wound healing: Inflammatory (days) → Proliferation (weeks) → Remodeling (months)
Platelets are the ﬁrst cells to appear
Collagen: Early in wound healing, Collagen III predominates, then later replaced by Collagen I.

Wound dressing

Type	Brand name	Composition	Absorptive	Others	Indications
Adhesive dressing
Hydrocolloids	Duoderm Hydrocol	Hydrophilic base and adhesive with polyurethane	Good, absorbs water and forms gel with exudates	May leave in place 1–7 d depending on exudate	Pressure ulcers, second intention wounds Wound with low‐to‐moderate exudates
Film dressing	Tegederm Op‐site Bioocclusive	Polyurethane file	None (may cause fluid collection) Gas permeable	Impermeable to bacteria	Best used in conjunction with alginate/hydrogen. Good for monitoring wounds. Lacerations/abrasions/STSG donor site
Nonadhesive dressing
Alginates	Sorbsan Algiderm	Cellulose like polysaccharide Alginic acid	Highly	Hemostatic agent: releases Ca++	Highly exudative wounds Contraindicated for dry wounds
Hydrogels	Tegagel Flexigel Curagel	Cross‐linked polymers with up to 80–90% water Semitransparent gel	Limited, not suitable for exudative wounds	Cooling/pain relief Useful for dry wounds by rehydrating the area	Abrasion wounds (post laser, peels)
Foam dressing	Flexzan Allevyn Aquacel Kendall	Hydrophilic foam, polyurethane, silicone	Highly, gas and water permeable	Compresses chronic leg wounds, conforms to body contours	Pressure ulcer, exudative wound
Gauze dressing	Telfa pad Vaseline gauze, Xeroform		Excellent	Cheap, readily available	Use to cover nonocclusive, nonadherent dressing

Cosmetic Dermatology

Laser

Laser fundamentals: type, wavelength, depth, target and usage

Laser	Wavelength (nm)	Type	Depth (μm)	Target	Usage
CO₂	10 600	IR	20	Water	Resurface, destruction, coagulation, cut
Erbium: YAG	2 940	IR	1	Water	Superficial resurface, destruction
Thulium	1 927	IR	400	Water	Nonablative fractional resurfacing
Erbium:glass	1 550	IR	400–1500	Water	Nonablative fractional resurfacing
Nd:YAG	1 440, 1 450	IR	400–2000	Water	Nonablative resurfacing, nonablative fractional resurfacing
Long pulsed Nd:YAG	1 320	IR	400–2000	Water	Nonablative resurfacing
Nd:YAG	1 064	IR	1600–3000	Mel, Hb	Deep dermal pigment, black/ blue tattoo, hair removal, non‐ablative resurface, leg veins, telangiectasia
Diode	800, 810, 930	R	1400	Mel	Dermal pigment, hair removal, leg veins, vascular
Q‐Switched Alexandrite	755	R	1300	Mel	Tattoo (black, blue, and green), epilation, pigmentation
Q‐Switched Ruby	694	R	1200	Mel	Epidermal/dermal pigment, tattoo (black, blue, and green), hair removal
Argon‐pumped dye	630, 514, 488	O, G, B	600	Hb, mel	Vascular, epidermal pigment
Pulsed dye laser (PDL)	585–595	Y	600	Hb, mel	Vascular, hypertrophic scar
Copper (Bromide) vapor	578, 511	Y, G	400, 300	Hb, mel	Vascular, epidermal pigment
Krypton	568 531	Y G	400	Hb, mel	Vascular, epidermal pigment
Frequency‐doubled Q‐switched Nd:YAG/ KTP	532	G	400	Mel, Hb	Vascular, epidermal pigment, red tattoo
Flash lamp pumped PDL	510	G	300	Mel, Hb	Vascular, hypertrophic scar
Argon	488, 514	B	200, 300	Mel, Hb	Vascular, epidermal pigment
Excimer	351, 308, 193	UV	0.5	Protein	Psoriasis, vitiligo, LASIK
Intense pulsed light (IPL)	515–1,200		Up to 3000	Hb, mel	Epidermal/dermal pigment, vascular, hair removal

IR: infrared; R: red; O: orange; Y: yellow; G: green; B: blue; UV: ultraviolet; Mel: melanin; Hb: hemoglobin; KTP: Potassium‐titanyl‐phosphate.

Laser definitions

	Unit	Definition
Wavelength	nm	—
Energy	J	—
Power	W	Rate of energy delivery, laser output
Fluence	J/cm²	Amount of energy delivered per area
Pulse width	sec	Duration of laser exposure
Spot size	mm	Diameter of laser beam
Thermal relaxation time	sec	Time needed for the heated target to cool by 50% of its peak temperature through diffusion
Chromophore		Target of laser

Laser principles (LASER = Light Amplification by Stimulated Emission of Radiation)

monochromatic (single wavelength)
coherent (in phase with time and space)
collimated (parallel waves)

Selective photothermolysis: selective heating of a target chromophore occurs:

selected wavelength is preferentially absorbed by the target chromophore
energy is high enough to damage the chromophore
pulse duration of the laser is shorter than the thermal relaxation of the target

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Tags: Handbook of Dermatology A Practical Manual

Mar 13, 2021 | Posted by admin in Dermatology | Comments Off