FIGURE 20.2 Scabies of the axillary fold.
(Courtesy of Henry K. Wong, MD, PhD.)
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Cutaneous Viral Infections and Exanthems
Viral infections are well studied for the effect they can have on the skin by both direct infection of the skin
and mucus membranes and the cutaneous manifestations of a viral illness through exanthemas. Human
papillomaviruses (HPVs) are DNA viruses that often induce benign papillomas or warts but have the
potential to cause cancerous lesions in the skin. The virus is passed by person-to-person contact or by
contact with a contaminated surface. The virus affects basal keratinocytes. Anogenital HPV infections
represent the most common sexually transmitted infection in the United States and include high-risk
types such as HPV 16 and 18, which have been implicated in cervical and anal cancers. 11 These high-risk
strains are the target of prophylactic HPV vaccines and have been shown to protect from the target-
specific HPV types when given prophylactically. 12
Herpes virus represents a large family of DNA viruses that are known to have a clinical history of
infection, latency period, and reactivation. Common examples include herpes simplex, which presents
with vesicular eruptions usually in the orolabial and genital regions (Figure 20.3), varicella-zoster virus
(chicken pox/shingles; Figure 20.4), Epstein-Barr virus (EBV), and cytomegalovirus. Topical and systemic
antiviral therapies have been helpful in modifying the disease presentation.
FIGURE 20.3 Herpes simplex virus infection of the gluteal area.
(Courtesy of Henry K. Wong, MD, PhD.)
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FIGURE 20.4 Varicella-zoster virus infection of the hip in a dermatomal distribution.
(Courtesy of Henry K. Wong, MD, PhD.)
Viruses can also present with clinical manifestations, especially in the juvenile population. Some of these
exanthemas (a skin eruption occurring as a sign of a general disease) can be pathognomonic for a virus,
whereas others are more generalized. Diagnosis is aided by identification of other symptoms, including
low-grade fever, malaise, GI complaints, and rhinorrhea to help suggest it is the manifestation of viral
illnesses. Some common examples include hand, foot, and mouth (Coxsackie virus), measles (rubeola),
German measles (rubella), Fifth disease (parvovirus B19). Generally, treatment is supportive; however,
some of these can pose a significant health risk if left untreated.
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Fungal Infections
Fungal skin infections are also common and classified based on depth and extent of involvement.
Superficial infections include dermatophytoses and tinea versicolor along with cutaneous candidiasis.
Deeper infections include sporotrichosis and result from the organism being deposited in the dermis or
subcutaneous tissue. They can have a prolonged course and are often treated with topical agents to avoid
the side effects of systemic antifungals. Diagnosis is usually clinical but can be made with scrapings.
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Dermatologic Manifestations of Sexually Transmitted Diseases
The most common sexually transmitted diseases (STDs) with skin changes include syphilis, gonorrhea,
chancroid, and lymphogranuloma venereum. Syphilis has mucocutaneous manifestations that range from
a chancre typically in the genital (sometimes oral) area in the primary stage of the disease to widespread
papulosquamous eruptions (Figure 20.5) in the secondary stage and in the last stage may present with
granulomatous nodules called gummas. The lesions of the primary and secondary stage are highly
contagious, and care must be taken when examining patients suspected of having the disease.
FIGURE 20.5 Syphilis of the palm and ring finger.
(Courtesy of Henry K. Wong, MD, PhD.)
Gonorrhea is an STD that can manifest with cutaneous pustules along with arthritis and fever.
Disseminated gonococcal infections should be treated with IV ceftriaxone. Chancroids are another STD,
causing genital ulcers and inguinal lymphadenopathy. Treatment is with antimicrobials.
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Benign Skin Lesions
Contact Dermatitis
Contact dermatitis is a common condition that is caused by a delayed hypersensitivity reaction (type IV)
within the skin that clinically presents with pruritus and a well-demarcated, erythematous, sometimes
vesicular patch (Figure 20.6). It is typically localized to the area of contact by the allergen. Common
allergens include poison ivy and nickel. Patch testing remains the standard for identification where
allergens are placed on the skin and the patient is monitored for a response to identify causative agents
after 48 hours. Treatment starts by avoiding the offending allergen. If there is a reaction, corticosteroids
are the treatment of choice and have many formulations that can be administered depending on severity
of reaction, with topical being the most common form for milder presentations. 13,14
FIGURE 20.6 Contact dermatitis due to nickel (A) and necklace (B).
(Courtesy of Henry K. Wong, MD, PhD.)
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Eczema (Atopic Dermatitis)
Eczema (atopic dermatitis) is a benign condition that often develops in infancy and childhood with
relapsing curse of pruritus that may become chronic. It may be accompanied by other disorders such as
allergic rhinitis, asthma, food allergies, and more rarely eosinophilic esophagitis. There is usually an age-
specific distribution pattern affecting extensor surfaces, face, and neck in infants and then flexor surfaces
later. Management typically involves patient education, daily use of moisturizers, and use of anti-
inflammatory medications (topical corticosteroids) during a flare up. Severe disease may require the use
of systemic medications. 15
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Nevi (Benign Melanocyte Proliferation)
Congenital nevi are present at birth or appear in infancy and are classified based on their size (small,
medium, large, and giant). Common acquired melanocytic nevi include:
Junctional nevi: where there is proliferation of the melanocytes at the dermal-epidermal junction
Intradermal nevi: with the melanocytes being located in the dermis
Compound nevi: with both intraepidermal and intradermal complexes of melanocytes
Differentiating these from melanoma can be difficult, and often the ABCDE pneumonic—asymmetry,
border irregularity, color variation, diameter >6 mm, enlarging or evolving—is used as a guide for when
to intervene with biopsy and further workup (Figure 20.7, Table 20.1). 16
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FIGURE 20.7 ABCDE mnemonic as a guide for assessing pigmented lesions.
(From )
TABLE 20.1
Indication for Mohs Excision in Primary Lesions
Areas with high rate of treatment failure (periorbital, periauricular, Nose, paranasal)
Tumor with poorly delineated clinical borders or arising from scar tissue
Tumors with aggressive malignant features
SCC: Breslow depth >2 mm, poorly differentiated or undifferentiated, spindle cell, acantholytic, sclerosing, small cell, clear cell,
lymphoepithelioma-like, sarcomatoid
BCC: Morpheaform (sclerosing), micronodular, basosquamous(metatypical), infiltrating
Location in critical structures such as the eyelid or where desirable to preserve as much uninvolved tissue as possible
Perineural invasion
Dermatofibrosarcoma protuberans
Microcystic adnexal carcinoma
Reprinted from Connolly, SM, Baker, DR, Coldiron, BM, et al. AAD/ACMS/ASDSA/ASMS 2012 appropriate use criteria for Mohs
micrographic surgery: a report of the American Academy of Dermatology, American College of Mohs Surgery, American Society for
Dermatologic Surgery Association, and the American Society for Mohs Surgery. J Am Acad Dermatol. 2012;67(4):531-550. Copyright © 2012
American Academy of Dermatology, Inc. and the American Society for Dermatologic Surgery, Inc. With permission.
BCC, basal cell carcinoma; SCC, squamous cell carcinoma.
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Rosacea
Rosacea is a common chronic inflammatory facial dermatosis usually affecting lighter-skinned
individuals and typically appearing in middle age. Clinically, it has variable presentation from facial
flushing and telangiectasias to papules and pustules. There are four subtypes, and treatment includes
patient education on skin care and need for maintenance therapy along with the use of topical and oral
antibiotics such as doxycycline and topical ivermectin. 17
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Seborrheic Dermatitis
Seborrheic dermatitis is characterized by sharply demarcated patches or plaques that can range from
pink-yellow to red-brown and may have flaky greasy scales. It typically affects areas high in sebaceous
glands including the face, scalp, ears, parasternal region, and sometimes intertriginous areas. It may
present in infancy cradle cap where it tends to have a more limited course or in adults typically presents as
a chronic relapsing course and often affects the scalp. Treatment in infants is often satisfactory with
emollients, with more extensive cases requiring ketoconazole and low-potency steroids to suppress
inflammation. In adults, the condition usually responds well to topical azoles (e.g., ketoconazole along
with emollients).
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Psoriasis
Psoriasis is a common inflammatory disease affecting the skin that causes characteristic silver scaly,
erythematous plaques that are often well demarcated (Figure 20.8). It typically affects the scalp, extensor
surface of elbow and knees, and intergluteal folds. It can also affect the nails, hands, and trunk. The
disease is thought to be caused by T-cells interacting with dendritic cells and other innate cells of
immunity. The pathognomonic pathologic finding is accumulation of neutrophils as spongiform pustules
in the epidermis. Other associated manifestations include arthritis but also some cardiovascular diseases
and depression. Treatment of the condition depends on disease severity with mild forms being treated
with topical steroids and other topical agents such as vitamin D analogues. Patients with more advanced
disease can be treated with phototherapy and immunomodulators, which have shown to be effective in
more severe disease forms. Treatment of the disease should focus on managing acute flares as well as
maintenance when not having flares because it is a chronic disease process. 18
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FIGURE 20.8 Psoriasis of the back.
(Courtesy of Henry K. Wong, MD, PhD.)
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Urticaria (and Drug Eruptions)
Urticaria, commonly referred to as hives, welts, or wheals, is typically a well-circumscribed intensely
raised pruritic plaque. It is usually caused by a trigger, such as food, insect bites, or drugs. Urticaria may
also present with angioedema, representing deeper swelling in the skin and typically affecting the face
and lips, extremities, and genitals. It is mediated by mast cells and basophils releasing mediators that
include histamine. A majority of new acute urticaria lesions are self-limiting, but in severe cases, chronic
cases, and cases that include angioedema, H1 blockers and glucocorticoids can be considered for
treatment. 19
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Acne
Acne represents a common dermatologic condition affecting the pilosebaceous units and typically
presents in adolescence. Commonly affected areas include the face and upper trunk. Clinical
manifestations can vary but are generally broken down into inflammatory (papules, pustules, and
nodules) and noninflammatory (open and closed comedones). Clinical presentation varies in severity,
and many factors are known to play a role in disease manifestation including genetics, hormones, and
environmental factors. Treatments are typically geared toward reducing the predisposing risk factors and
include facial cleansers, hormone therapy and vitamin A analogues, and antibiotic therapy (both oral and
topical).
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Alopecia and Hair Disorders
Alopecia can be the result of hair follicle loss, loss of the hair shaft, or a combination of both. There are
three phases of hair growth: anagen, telogen, and catagen. Identifying hair follicles in their phases and
any disruption in this cycle can help lead to a diagnosis and treatment.
Androgenic alopecia represents one of the most common acquired forms of hair loss and is known to be
genetically driven in the presence of androgen. In genetically susceptible hair follicles, there is
miniaturization of hairs in a symmetric pattern (on the crown, vertex, or frontal region) in response to
normal levels of circulating androgens. Antiandrogen medications have been helpful in treating this
condition.
Telogen effluvium represents an increase in shedding of otherwise normal telogen hairs in response to a
pathologic or physiologic change. This is, for example, seen in the postpartum period, after some
medications, and there will be time of shedding usually around 3 months after the event.
Alopecia areata is a form of noncicatricial alopecia that is thought to be from hair-specific autoimmune
disorder. Clinically, there are often circular patches of hair loss but can involve the entire scalp in some
cases. Topical and intralesional steroids are often first-line therapy in smaller areas.
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Nail Disorders
The nail serves many purposes including protection of the finger, counterpressure for the pulp, and
utility in fine object manipulation and scratching. The nail is composed of the nail bed (germinal and
sterile matrices), hyponychium, and the nail plate. The nail matrix produces the nail plate through
keratinization and this is occurs continuously. The nail grows approximately 0.1 mm/d. Nail disorders
are a wide range of clinical disorders, and presentations vary depending on what part of the nail is
affected and how it manifests. Trauma to the underlying matrix can lead to a wide assortment of
disorders depending on the severity of damage to the nail bed (e.g., nail ridge, split nail, onycholysis
[nonadherence]). Pitting and clubbing represent two aberrant nail presentations that can be indicative of
systemic processes.
Melanonychia is caused by melanin production of nail matrix melanocytes. It presents as a longitudinal
pigmented band starting at the proximal nail fold, and in adults without a history of trauma, the clinician
should consider a matrix biopsy to rule out melanoma.
Infections are also common and can be acute as in a paronychial infection usually bacterial in origin or
chronic with bacterial and often fungal.
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Hyperpigmentation and Hypopigmentation
Hypopigmentation is a general term to describe lightening of the skin, which is most often from a
decreased melanin content in the skin. It may be localized or diffuse depending on the underlying cause.
This decreased melanin production (e.g., albinism) can be from the melanocytes not synthesizing melanin
or from destruction of the melanocytes, which may be hereditary or the result of trauma or autoimmune
attack (e.g., vitiligo). Inflammation can also cause a state of hypomelanosis that may resolve once the
cause of inflammation is treated. Tyrosinase inhibitors and hydroquinone work by preventing tyrosinase,
which is essential in melanogenesis, and have been used to prevent hyperpigmentation in patients
seeking resurfacing procedures.
Hyperpigmentation disorders are usually the result of increase in melanin production but rarely can be
from an increase in the melanocyte number. It may be diffuse, circumscribed, linear, or more rarely
reticulated. If the hyperpigmentation is acquired, removal of the inciting stimulus may help ameliorate
the issue.
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Nonmelanoma Skin Cancers (Keratinocyte Cancers)
NMSCs are the most common form of cancer in the United States with the incidence estimated to be 5.5
million in 2012. 3 The most important risk factor for NMSC is the skin phenotype, but it is also influenced
by UV radiation exposure. For basal cell carcinoma (BCC), especially, intermittent intense episodes of UV
exposure appear to increase the risk, whereas a history of childhood sunburns, especially severe burns,
gives an increased risk for actinic keratosis (AK) and squamous cell carcinoma (SCC). Another well-
established risk factor is immunosuppression. Patients with human immunodeficiency syndrome are
known to have a 1.8- and 5.4-fold increase in the risk for developing BCC and SCC, respectively,
compared with the general population. 20 Patients on immunosuppressive therapy also exhibit a greater
incidence of NMSC development.
The standard for diagnosis of NMSC remains a thorough physical examination followed by conventional
biopsy with histopathology for definitive diagnosis. Dermoscopy and confocal microscopy, cross-
polarized light, and fluorescence photography have all been used as adjunct screening tools to identify at-
risk lesions before proceeding with biopsy. In terms of biopsy technique, there are several techniques but
no one standard method. Options for biopsy include shave, excisional, incisional, and punch biopsy. All
have advantages and disadvantages with the goal of identifying cancerous cells for eventual destruction
without significant tissue distortion.
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Basal Cell Carcinoma
Basal cell cancer represents the most common form of skin cancer and malignancy in the Caucasian
population. They arise from the pluripotent stem cells within the epidermis and hair follicles. BCC is well
known to be locally aggressive, and the biggest risk for recurrence is locally rather than with metastasis.
Because of its propensity to occur in sun-exposed areas, particularly on the face, head, and neck, they can
cause great disfigurement. There is no role for lymph node sampling in BCC because it stays local.
Factors in BCC that are known to be prognostic include location with high-risk regions being on the face,
forehead, scalp, neck, and pretibial regions, where lesions in these areas that are >10 mm are considered
high risk. Other factors that increase the risk for recurrence include poorly defined borders, recurrent
cancer, perineural invasion, immunosuppression, and prior XRT at the site.
There are 26 listed subtypes of BCC. A general schematic for breakdown include dividing them based on
their histopathologic pattern, which is more important than the differentiation. The two subtypes are
circumscribed BCC and the diffuse subtypes of BCC. In the circumscribed group, nodular represents the
most common form of BCC and accounts for about 50% of all BCC. Its appearance is a pink/red papule
that has a pearly appearance. Other examples that would fall in the circumscribed group include adenoid
cystic, keratotic, fibroepithelioma of Pinkus.
Diffuse basal cell cancers include superficial, micronodular, infiltrating, and morpheaform (sclerosing).
Morpheaform is the most aggressive type and typically has the appearance of a firm depressed plaque in
a scar. Typically, there is invasion beyond the visible edges of the lesion that will often extend into the
deep dermis.
Treatment of BCC can be broken down into three categories: surgical, destructive, and medical. Surgical
is either primary surgical excision or Mohs surgical excision. Surgical margins in primary excision
depend on risk factors including location, tumor size, and histologic subtype. Mohs surgical incision uses
saucer-like layers to remove all tumor, creating a map for the surgeon to mark areas of tumor for further
excisions. Mohs excision is recommended for most recurrent basal cell and squamous cell cancers (see
Table 20.1). Mohs has the advantage of preserving normal tissue, and this technique is used in the face or
for other lesions that may be more aggressive. Destructive therapy aims to destroy the tissue and is only
indicated for superficial lesions. Techniques include electrodissection, cryotherapy, and radiotherapy.
Medical therapy includes 5-FU and imiquimod but is inferior to surgical and destructive techniques.
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Squamous Cell Carcinoma
AK represents an intradermal early stage SCC and is most commonly seen in areas of prolonged UV
exposure in fair-skinned and elderly patients. It has a rough erythematous papule appearance and is
typically located in sun-exposed areas (helices of ear, upper forehead, nasal bridge, bald scalp, etc.).
Lesions may be small or very large and broad. They are characterized as precancerous because they have
atypical keratinocytes confined to the epidermis. Their risk of transformation to invasive carcinoma is up
to 0.06% per year. 21
SCC in situ is commonly referred to as Bowen disease. It typically presents as a scaly elevated plaque
often in sun-exposed areas but in younger patients, may be in sun-protected sites. SCC in situ and AK can
be difficult to distinguish from psoriasis papules and plaques that may resemble these processes.
Keratoacanthomas are considered by many to be a variant of SCC. They typically present as rapidly
enlarging papules over a few months that are sharply circumscribed and have a keratotic core.
Sometimes, they spontaneously resolve, but this can take months and given similar appearance to SCC
most advocate excision. 22 They often present as a solitary lesion but may be in multiple locations as part
of a syndrome.
Invasive SCC often develops in sun-exposed areas such as the scalp, face, neck, dorsal hands, skin and
extensor forearms, with the risk factor being more related to the cumulative effect. It can have a variable
presentation with some becoming hyperkeratotic and having crusting, erosions, and ulcerations. The
growth history is variable, but signs of paresthesia, anesthesia, and pain are indicative of perineural
invasion (at least T3). Diagnosis of SCC is with tissue biopsy and also clinical examination of draining
lymph node basins.
SCC is staged using the AJCC TNM with recent changes in 2017 to reflect the clinicohistopathologic
features that increase the risk for recurrence. Sites where the tumor behaves more aggressively include
the ear, lips, and mucosal sites. When evaluating patients, palpation of regional lymph nodes should be
performed to assess for the presence of palpable nodes as well as the size. Any palpable nodes should be
biopsied with fine needle aspiration. Risk factors that increase risk for metastasis are listed in Table 20.2.
TABLE 20.2
High-Risk Features of Squamous Cell Carcinoma
Features on History and Physical
Borders: poorly defined
Diameter: Area L ≥ 20 mm; Area M ≥ 10 mm
Recurrent
Arising within a scar, prior RT site or other chronic inflammatory process
Immunosuppression
Features on Pathology
Poorly differentiated or undifferentiated, developing within Bowen disease
Acantholytic, adenosquamous, desmoplastic, or metaplastic subtypes
Tumor thickness: ≥2 mm or Clark IV, V
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Perineural, lymphatic, or vascular involvement
Adapted with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Squamous Cell Carcinoma
V.2.2018. © 2018 National Comprehensive Cancer Network, Inc. All rights reserved. The NCCN Guidelines® and illustrations herein may not
be reproduced in any form for any purpose without the express written permission of NCCN. To view the most recent and complete version of
the NCCN Guidelines, go online to NCCN.org. The NCCN Guidelines are a work in progress that may be refined as often as new significant
data become available.
Treatment of SCC depends on the stage of SCC, with some low-risk cancers being amenable to
destructive therapy similar to BCC. Direct surgical excision (primary or with Mohs) can be used for both
low- and high-risk lesions.
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Melanoma
Melanoma is the most deadly of all the skin cancers and accounts for 75% of all the deaths related to skin
cancer whereas only accounting for less than 5% of skin cancer diagnosis. Trends suggest that its
incidence continues to rise. Melanocytes that undergo a malignant transformation are most commonly in
the skin but may also be present in the eye or mucus membranes.
Melanomas arise from the melanocyte that is a dendritic cell located in the basal layer of skin. It is
responsible for producing the melanin pigment that gives the skin phenotypes. Melanocyte numbers are
equal among all skin colors; however, the production of melanin varies. Melanomas can grow in both a
radial and vertical growth pattern. The radial pattern is usually in the epidermis and some melanomas
can stay in this radial growth pattern for a long time. In the vertical growth, the growth shifts down into
the dermis and indicates a worse prognosis.
Melanomas can be broken down into five clinical and histological growth patterns. Superficial spreading
is the most common. This can occur anywhere but often occurs in regions of sun exposure. As the name
might suggest, it typically has a prolonged radial growth pattern before transforming into a more vertical.
Nodular melanoma is the second most common type and has a classic presentation of a singular lesion
with a domed-shaped dark appearance that can resemble a blood blister. It tends to develop in a vertical
growth pattern more quickly and often occurs on the trunk, and head and neck regions. Because of the
growth pattern, it is often more advanced at the time of diagnosis. Lentigo melanoma is a rare form that
presents as large tan lesions with convoluted patterns and amelanotic patterns. It has a low malignancy
potential and is more common in women, typically on the head, face, and neck. Acral-lentiginous
melanoma is the rarest in Caucasians but accounts for greater than 30% of all melanomas that occur in
dark-skinned individuals. 16 This often occurs on the palms, on soles of feet (Figure 20.9), and beneath the
nail beds. In the subungual presentation, they commonly cause a longitudinal line in the nail plate known
as Hutchinson sign. Amelanotic melanomas are responsible for 2% to 8% of invasive cases and
characterized by malignant cells that lack pigment, making them clinically difficult to identify and
leading to later identification. Desmoplastic melanomas are another rare melanoma form that typically
has an aggressive local growth pattern but less propensity to metastasize.
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FIGURE 20.9 A. Melanoma of the heel. B. Result after wide local excision and reconstruction with free radial forearm
fasciocutaneous flap.
Diagnosis of a melanoma starts with clinical examination. The ABCDE mnemonic (see Figure 20.7) can be
used as a guide for assessing pigmented lesions and can guide a clinician on when to biopsy a lesion. 23
Definitive diagnosis of melanoma is with incisional biopsy. The two classic staging classifications are the
Clark and Breslow classifications. The Clark classification is based on the anatomic level of local invasion.
Breslow classification is based on vertical depth of the invasion in millimeters. The AJCC is what is used
for staging, but part of the staging related to depth is similar to the Breslow classification because it was a
better prognosticator of disease severity and risk recurrence. 24 As part of staging workup, it is important
that the specimen is viewed with standard stains rather than frozen sectioning to prevent specimen
distortion and allow for adequate assessment of Breslow depth, which is calculated using ocular
micrometer and is in reference to the greatest depth of invasion of the tumor measured down from the
granular layer of the epidermis. This has been shown to be one of the best prognostic values for tumor
prognosis as well as lymph node metastasis. 25
Management of the primary tumor is with wide excision of the primary tumor site. Excision should
include skin and subcutaneous fat down to but not including the fascia. The National Comprehensive
Cancer Network (NCCN) has recommended surgical margins based on Breslow depth, which are listed
in Table 20.3.
TABLE 20.3
NCCN Guidelines for Tumor Margin Based on Breslow Thickness
Tumor Microstage
Thickness
Margin
Melanoma in situ (Tis)
0.5 cm
Thin (T1)
≤1.0 mm
1.0 cm
Intermediate (T2)
1.0–2 mm
1.0–2.0 cm
Intermediate (T3)
2.0–4.0 mm
2.0 cm
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Thick (T4)
>4 mm
2.0 cm
Adapted with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Squamous Cell Carcinoma
V.2.2018. © 2018 National Comprehensive Cancer Network, Inc. All rights reserved. The NCCN Guidelines® and illustrations herein may not
be reproduced in any form for any purpose without the express written permission of NCCN. To view the most recent and complete version of
the NCCN Guidelines, go online to NCCN.org. The NCCN Guidelines are a work in progress that may be refined as often as new significant
data become available.
In addition to tumor depth, ulceration and mitotic rate also play a role in staging. Mitotic rate has also
been identified as an independent predictor of survival and so is also a part of the AJCC staging. 26 The
thickness correlates with prognosis with modifications in each T category if there are mitotic figures or
ulceration indicating worse prognosis.
The sentinel lymph node is the first lymph node in the draining basin from the primary tumor site.
Because this node is usually involved, if there is regional nodal metastasis it can be used as a selective
sample marker to see if the rest of the nodal basin is affected. Sentinel lymph node sampling is advocated
in patients with stage I/II melanoma with tumor thickness 1.0 to 4.0 mm Breslow depth, or those with
depth of 0.76 to 1.0 mm with other high-risk factors, including ulceration, lymphovascular invasion,
significant vertical growth phase, and increased mitotic rate. Additionally patients with tumor >4.0 mm
depth and clinically negative nodes also benefit from SLN biopsy.
Complete surgical lymphadenectomy is recommended for any patient with clinically involved nodes
diagnosed via examination, FNA, or SLN biopsy. Node status is the most important prognostic factor in
staging melanoma.
Clinically advanced (stage IV) melanoma carries a poor prognosis, with only 10% to 15% of patients
living past 5 years.
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Merkel Cell Carcinoma
Merkel cell carcinoma is a rare form of skin cancer typically affecting older (>50) fair-skinned individuals
in sun-exposed areas. It usually presents as a solitary erythematous nodular lesion in sun-exposed areas
of the head and neck. It commonly spreads to lymph nodes with 25% to 30% of initial presenting patients
having positive nodes. It is aggressive like melanoma, and like melanoma staging depends on node
involvement with SLN biopsy. Primary surgical excision with wide margins or Mohs is standard
treatment. Local recurrence is 40% to 45%. Radiation can be used as adjuvant therapy. 27
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Questions
1. Sentinel lymph node biopsy (SLNB) would have the most benefit in which of the following
patients?
a. A 50-year-old man with a 4.0 cm diameter BCC with lymphovascular invasion
b. A 80-year-old woman with a 1.0 cm diameter melanoma with thickness of 1.0 mm and a
palpable 2 cm lymph node in the affected extremity
c. A 4-year-old boy with a 10.0 cm diameter congenital melanocytic nevus
d. A 67-year-old man with a 0.5 cm diameter melanoma with a thickness of 1.5 mm
2. Choose the most correct statement regarding retinoids.
a. Derived from vitamin C, they work by binding to nuclear receptors and modulating gene
expression.
b. Derived from vitamin A, they work by binding to transmembrane receptors and modulating
gene expression.
c. Common side effects include of topical retinoids include pruritus, peeling, photosensitivity,
and erythema.
d. Treatment results in epidermal thinning and decreased collagen in the dermis.
3. Clinically, psoriasis is a characterized by silver scaly, erythematous plaques that are often well
demarcated. Histologically, psoriasis is characterized by:
a. Vacuolar alteration of basal keratinocytes
b. Accumulation of neutrophils as spongiform pustules in the epidermis
c. Dermal changes consisting of interstitial mucin deposition and a sparse lymphocytic infiltrate
d. Basement membrane degeneration
4. Which Fitzpatrick skin type rarely burns and tans dark easily?
a. II
b. III
c. IV
d. V
5. Patients with which systemic disease are known to have a significantly increased risk for
developing a primary NMSC compared with the general population?
a. Rheumatoid arthritis
b. Hyperlipidemia
c. EBV infection
d. Human immunodeficiency syndrome
1. Answer: d. SLNB is useful in the prognostic evaluation of patients with melanoma who have stage
IB/II lesions. It allows these patients with tumor of 1 to 4 mm Breslow depth (0.8–1 mm plus
ulceration) to be evaluated for nodal spread without doing a full nodal dissection. Patients with
tumors <0.8 mm and no ulceration are not likely to have nodal involvement. Patients who have
clinically palpable lymph nodes (stage III) should have complete therapeutic lymph node dissection
in addition to wide excision of the primary tumor. There is no role or SLNB in BCC as it invades
locally and not through lymphovenous spread. Giant congenital nevi are excised for their potential
risk of malignancy and so removal of nodes is not necessary.
2. Answer: c. Retinoids are a derivative of vitamin A and are well studied for the protective effects in
the skin and reversal of photoaging. They work by binding to nuclear receptors and modulating
cellular gene expression. Clinically, this leads to epidermal thickening and increased collagen in the
dermis because of decreased breakdown and increased collagen synthesis in the dermis. Side effects
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such as pruritus, burning, erythema, and peeling are usually seen with onset of treatment and can
lead to noncompliance, especially in patients with a history of sensitive skin. Photosensitivity is
another common side effect of topical therapies, and patients are advised to avoid sun exposure
when starting therapy.
3. Answer: b. Psoriasis is a common inflammatory disease affecting the skin that causes characteristic
silver scaly, erythematous plaques that are often well demarcated. It typically affects the scalp,
extensor surface of elbow and knees, and intergluteal folds. It can also affect the nails, hands, and
trunk. The disease is thought to be caused by T-cells interacting with dendritic cells and other innate
cells of immunity. The pathognomonic pathologic finding is accumulation of neutrophils as
spongiform pustules in the epidermis. Treatment of the condition depends on disease severity with
mild forms being treated with topical steroids and other topical agents such as vitamin D analogues.
Patients with more advanced disease can be treated with phototherapy and immunomodulators,
which have shown to be effective in more severe disease forms.
4. Answer: d. Fitzpatrick skin type classifies the skin into six phenotypes based on the melanin
content of the skin (color), the inherent pigmentation of the skin, and the sensitivity of the skin to sun
damage. Lower Fitzpatrick score indicates less melanin in the skin and hence a greater sensitivity to
sun damage. Type I always burns and does not tan. Type II burns easily and tans poorly; type III tans
after an initial burn. Type IV burns minimally, tans easily. Type V rarely burns and tans dark easily.
Type VI never burns and always tans darkly.
5. Answer: d. In a matched, nationwide population-based cohort study, Omland et al. studied 4280
HIV-infected patients from a HIV cohort study with a background population cohort and found that
HIV-infected patients had an increased risk ratio of 1.79 for BCC and 5.40 for SCC compared with the
background population. 20 There was no increased risk of melanoma. Rheumatoid arthritis and
hyperlipidemia are not associated with NMSC. EBV is associated with development of
nasopharyngeal cancer and Burkitt lymphoma but not with skin cancer.
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References
Lomas, A, Leonardi-Bee, J, Bath-Hextall, F. A systematic review of worldwide incidence of nonmelanoma skin cancer. Br J Dermatol.
2012;166:1069-1080.
Guy, GP, Machlin, SR, Ekwueme, DU, Yabroff, KR. Prevalence and costs of skin cancer treatment in the U.S., 2002–2006 and 2007–2011. Am J
Prev Med. 2014;104(4):e69-e74.Using data obtained from the Medical Expenditure Panel Survey from 2002 to 2011, this study looked to estimate the
trends in NMSC prevalence and treatment costs. Although limited by relying on self or household-reported survey data, this study suggests a
significant rise in skin cancer incidence as well as the cost associated with the treatment of skin cancer.
Rogers, HW, Weinstock, MA, Feldman, SR, Coldiron, BM. Incidence estimate of nonmelanoma skin cancer (keratinocyte carcinomas) in the
US population, 2012. JAMA Dermatol. 2015;151(10):1081-1086.Using the Center for Medicare & Medicaid Services Physicians’ Claims database (to
calculate total skin cancer procedures performed) and the National Ambulatory Medical Care Survey database (to estimate the NMSC-related office
visits), these authors attempt to estimate the incidence of keratinocyte carcinomas in the United States and compared it with numbers from 2006 to
2011.
Fitzpatrick, TB. The validity and practicality of sunreactive skin types I through VI. Arch Dermatol. 1988;124:869.
Fitzpatrick, TB. Soleil et peau [Sun and skin]. J Méd Esthétique. 1975;2:33-34.
Farmer, KL, Goller, M, Lippman, SM. Prevention of nonmelanoma skin cancer. Clin Plast Surg. 1997;24(4):663.
Weissler, JM, Carney, MJ, Carreras Tartak, JA, et al. The evolution of chemical peeling and modern-day applications. Plast Reconstr Surg.
2017;140(5):920-929.This review article starts with a historical perspective of chemexfoliation in ancient times and the progress to present-day
practices. The mechanism of the peel is briefly reviewed, and there is a chemical peel classification table that offers some common peels. Indications are
listed as well as options for prepeel skin care regimens to maximize chemical peel effects. The article reviews peel application as well as posttreatment
care with a supplemental video. Through a better understanding of the mechanism of the chemical peel agents as well as modifications to the solutions,
clinicians are able to offer safe and effective resurfacing options to the patient with aesthetic concerns. Potential side effects are reviewed for peels at the
end of the paper.
Alexiades-Armenakas, MR, Dover, JS, Arndt, KA. The spectrum of laser skin resurfacing: nonablative, fractional, and ablative laser
resurfacing. J Am Acad Dermatol. 2008;58:719-737.
Raff, AB, Kroshinsky, D. Cellulitis: a review. JAMA. 2016;316(3):325-337.
Binford, GJ, Wells, MA. The phylogenetic distribution of sphingomyelinase D activity in venoms of Haplogyne spiders. Comp Biochem Physiol
B Biochem Mol Biol. 2003;135(1):25.
Hariri, S, Unger, ER, Sternberg, M, et al. Prevalence of genital human papillomavirus among females in the United States, the National
Health and Nutrition Examination Survey, 2003–2006. J Infect Dis. 2011;204:566-573.
Paavonen, J, Naud, P, Salmerón, J, et al. Efficacy of human papillomavirus (HPV)-16/18 AS04-adjuvanted vaccine against cervical infection
and precancer caused by oncogenic HPV types (PATRICIA): final analysis of a double-blind, randomized study in young women. Lancet.
2009;374:301-314.
Clark, SC, Zirwas, MJ. Management of occupational dermatitis. Dermatol Clin. 2009;27:365.
Mowad, CM, Anderson, B, Scheinman, P, et al. Allergic contact dermatitis: patient diagnosis and evaluation. J Am Acad Dermatol.
2016;74:1029-1040.
Eichenfield, LF, Tom, WL, Berger, TG, et al. Guidelines of care for the management of atopic dermatitis. Section 2: management and
treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014;71:116-132.
Bradford, PT, Goldstein, AM, McMaster, ML, Tucker, MA. Acral lentiginous melanoma incidence and survival patterns in the United States,
1986-2005. JAMA Dermatol. 2009;145(4):427-434.
Powell, FC. Rosacea. N Engl J Med. 2005;352(8):793-803.
Boehncke, WH, Schon, MP. Psoriasis. Lancet. 2015;386(9997):983-994.
Kaplan, AP. Clinical practice: chronic urticaria and angioedema. N Engl J Med. 2002;346:175-179.
Omland, SH, Ahlström, MG, Gerstoft, J, et al. Risk of skin cancer in HIV-infected patients: a Danish nationwide cohort study. J Am Acad
Dermatol. 2018;79(4):689-695. pii:S0190-9622(18) 30475-4.
Siegel, JA, Korgavkar, K, Weinstock, MA. Current perspective on actinic keratosis: a review. Br J Dermatol. 2017;177:350-358.AK is a health
concern with over $1 billion US dollars in annual cost in diagnosis and management; however, there is no universally agreed-upon diagnostic gold
standard. AK can cause significant disfigurement making it a cosmetic issue in addition to the possibility of malignant transformation. The natural
history of AK is spontaneous remission, stable existence, or malignant transformation to keratinized carcinoma with variable reported rates of 0% to
21%. Some of the discrepancy in the malignant transformation in the reported studies may be related to different definitions for AK. Further study is
needed for more universal diagnostic criteria of AK, further understanding of malignant progression and therapeutic strategies to better manage AK.
Schwartz, RA. Keratoacanthoma. J Am Acad Dermatol. 1994;30:1-19.
Abbasi, NR, Shaw, HM, Rigel, DS, et al. Early diagnosis of cutaneous melanoma. JAMA. 2004;292:2771-2776.
Breslow, A. Thickness, cross-sectional areas and depth of invasion in the prognosis of cutaneous melanoma. Ann Surg. 1970;172:902-908.In
this sentinel publication, Alexander Breslow described a technique of using an ocular micrometer to measure the depth of invasion from the skin surface
to the maximal depth of invasion. He studied 98 patients and performed 5 years of follow-up. He also looked at cross-sectional area and diameter but
found that the tumor thickness was the most significant variable and best for predicting a patient’s outcome. He also postulated it could guide which
patients should have prophylactic lymph node dissections and which group would not need them (stages I and II and stage III with thickness
<0.76 mm).
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Dzwierzynski, WW. Managing malignant melanoma. Plast Reconstr Surg. 2013;132:446e-460e.
Allen, PJ, Bowne, WB, Jaques, DP, et al. Merkel cell carcinoma: prognosis and treatment of patients from a single institution. J Clin Oncol.
2005;23(10):2300-2309.
Amin, M , Edge, SB , et al, eds. AJCC Cancer Staging Manual. 8th ed. American Joint Committee on Cancer; 2017.
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C H A P T E R 2 1
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Thermal, Chemical, and Electrical Injuries
Justin Gillenwater and Warren L. Garner
Key Points
Burn depth and size are predictive of outcomes and guide initial and definitive management.
The goal of resuscitation is maintaining tissue perfusion, specifically the skin.
Burn wounds that will not heal within 3 weeks usually should be excised and autografted.
Burn care is best provided by a multidisciplinary team working with a committed patient.
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Epidemiology
Burn injury represents a significant burden of disease. Most recent estimates indicate 486,000 people in
the United States receive medical treatment for burn injuries each year. Of these, 40,000 require inpatient
hospital admission and 3275 are fatal. 1 Burn survivors can develop lifelong deformities as a result of their
cutaneous injury with ensuing health care needs including corrective surgical procedures, therapy
sessions, and scar management. A recent systematic review estimates the average total health care cost
per burn patient is $88,218 in high-income countries. 2
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Pathophysiology
Local
A burn injury occurs when a thermal insult on the skin causes acute changes in its composition, killing
cells and denaturing proteins. Initially, burn depth is based on two extrinsic factors: intensity of heat and
duration of contact. The hotter the source or the longer the duration of contact, the deeper the burn
injury. In the area of direct thermal injury, cellular and matrix proteins are irreversibly damaged, causing
a release of cytokines such as IL-1, IL-8, and tumor necrosis factor alpha. This inflammatory cascade
causes a secondary reaction and results in local cellular apoptosis, loss of endothelial vascular integrity,
transmigration and degranulation of leukocytes, and complement activation. Although evolutionarily
advantageous from an anti-infective and hemostatic perspective, this area of inflammation causes
decreased tissue perfusion and may lead to conversion of burn wounds from smaller, superficial injuries
to larger, deeper wounds. Appropriate resuscitation and local wound care are central to limiting
reversible tissue loss and are the goal of initial burn care.
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Systemic: Burn Shock
Burns greater than 20% of total body surface area (TBSA) cause a system-wide inflammatory response
and lead to a systemic inflammatory response syndrome, sometimes called burn shock. As the local
events become systemic, the release of inflammatory mediators into the central circulation leads to leaky
microvasculature, vasodilation, decreased cardiac output, tissue hypoperfusion, and ultimately, if left
unresuscitated, death.
Similar to within burned tissue, capillary integrity becomes compromised systemically. Osmotic pressure
generated by transudate of proteins and electrolytes in addition to the low-flow state results in loss of
intravascular volume into the interstitium. Decrease in the intravascular volume causes an increase in
hematocrit and higher blood viscosity. Cell membrane alteration leads to movement of fluid into the
intracellular space. Total body edema and intravascular volume depletion is the result. Maximal fluid
shifts occur around 12 hours after burn. 3
Within 24 hours after a large burn, capillary integrity in nonburned tissue returns to near normal and
transudation of colloids out of the vascular space diminishes. By this time, the loss of plasma proteins
into burned tissue is significant enough to decrease vascular oncotic pressure. Water continues to collect
in the interstitial space even after restoration of capillary integrity and further perpetuates global tissue
edema.
Burn shock results from loss of intravascular volume, cardiac dysfunction, and vascular changes. Prior to
initiation of resuscitation when capillary leak predominates, relative hypovolemia and increased systemic
vascular resistance predominates. As resuscitation occurs and circulating blood volume is restored,
vascular tone diminishes and the systemic vascular resistance drops. Cardiac function is dynamic and
unpredictable; cytokine release and current intravascular volume status affect preload, contractility, and
afterload. 4,5 The kidney is particularly susceptible to damage from hypoperfusion, and acute kidney
injury can be perpetuated by increased blood viscosity from elevated hematocrit and myoglobinemia
from deeper tissue damage. 6,7
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Initial Management of Burns
Treatment of burn injuries, especially large burns, is resource intensive and best done by a dedicated
multidisciplinary team (Table 21.1).
TABLE 21.1
Multidisciplinary Team for the Treatment of Burns
Burn Team Member
Role in Team
The acute burn surgeon
Surgical management of burn wounds
A critical care physician
Medical management of burn shock, multiple system failure, and organ dysfunction
A reconstructive surgeon
Manage the aesthetic and functional deformities resulting from burn scars
Specially trained burn nurses
Comprehensive daily burn wound debridement and dressing changes
Physical and occupational therapists
Prevent functional disabilities and limit contracture formation
Fabricate splints
Clinical nutritionists
Assess for adequate caloric supplementation
Social workers, clinical psychologists
Manage psychosocial factors, prevent posttraumatic shock disorder
Clinical pharmacists
Manage drug dosing and interactions
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ABCs
Burn injuries are traumatic injuries, and treatment should adhere to the airway, breathing, and circulation
(ABCs) of standard trauma care. An upper airway inhalation injury can lead to early edema formation
and airway obstruction. In the event of suspected inhalation injury, securing airway patency with
endotracheal intubation is the critical first step. Patients with suspected inhalation injury that do not
exhibit signs or symptoms of impending airway obstruction may be carefully monitored in an intensive
care unit (ICU) setting. Consultation to otolaryngologist may be indicated for serial fiber optic
laryngoscopic examinations.
Patients with circumferential torso burns may need escharotomies to improve their thoracic compliance
and promote adequate ventilation—breathing—to occur. Similarly, patients with circumferential
extremity burns may need escharotomies to restore circulation distally. Although escharotomies are best
done by an experienced provider, they should not be delayed if a prolonged transport is anticipated.
Once the patient is stabilized, a full and detailed history should be obtained to determine the etiology of
the injury, obtain medical comorbidities, etc. If the patient is obtunded, then family members, emergency
medical technician providers, or witnesses can be valuable sources of information. Tetanus immunization
status should be assessed and prophylaxis administered as indicated.
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Determination of Burn Depth
After assessing for ABCs and providing initial stabilization, burn size and depth are evaluated.
Quantifying the severity of injury guides resuscitation and determines further management, including
prognosis. Nomenclature for burn wounds can be confusing, but descriptive terminology—superficial,
partial-thickness, full-thickness instead of first, second, and third degree—is advocated by the
International Society for Burn Injuries, is most represented in the burn literature, and is generally
preferred. 8 On the contrary, ICD-10 codes quantify burn depth in degrees instead of descriptive terms. 9
The clinician should be familiar with both descriptive terminology and how it corresponds to degree of
burn depth (Figure 21.1).
FIGURE 21.1 Superficial, partial-thickness (superficial and deep), and full-thickness burns.
Superficial (first-degree) burns affect the epidermis only. These are dry, erythematous, blanch with
pressure, and painful without blistering or ulceration of the skin. Sunburn is a common presentation.
They require no further management or treatment and do not lead to a systemic inflammatory response
requiring resuscitation. These can be managed as an outpatient with adequate nonopioid analgesia.
Partial-thickness (second-degree) burns extend into the dermis and are the most challenging to treat from
the perspective of the surgeon. Their appearance can be varied, and a correct diagnosis is necessary for
correct surgical management. Superficial partial-thickness burns limited to the upper layers of the dermis
will often heal without the need for grafting, whereas those extending into the deeper dermis and
involving the dermal appendages may require excision and autografting for best results. Therefore,
determining the exact depth of the partial-thickness burn on initial examination requires experience and
is important for prognostic and therapeutic reasons. Superficial partial-thickness burns generally present
with blisters that, when unroofed, reveal a pink, moist, edematous, painful blanching base (see Figure
21.1). In contrast, deep partial-thickness burns are whiter, have varying degrees of sensation and edema,
and often do not demonstrate blanching or capillary refill. Finally, it is important to remember that any
patient may have mixed areas of injury that will require different treatment.
Full-thickness (third-degree) burns are obvious in their presentation and appearance. The skin is
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contracted, dry, leathery, and insensate and can be brown, black, white, or dark red in color. There is no
moisture or exudate, and subcutaneous thrombosed veins may be visible through translucent dermis. In
most cases, full-thickness burns will require excision of the burn and grafting to achieve wound closure.
New technologies have been used to assist in assessing burn wound depth. Ultrasound, laser Doppler,
and fluorescein all attempt to assess perfusion of the burn wound and thus its depth. 10 These
technologies have not found widespread routine use yet, but they may show potential for determining
regenerative potential with more investigation.
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Assessing Burn Size
An accurate assessment of burn size is critical because triage and resuscitative efforts are based on the
TBSA affected. Overestimation or underestimations of burn size can lead to inappropriate transfers or
poor resuscitation. The Lund-Browder chart is the oldest but historically most accurate method of
assessing burn size. The rule of nines is generally the most frequently used strategy because of its
simplicity (Figure 21.2). Alternatively, the palmar method utilizes the patient’s own palm as an estimate of
1% TBSA. Computer-based applications such as the SAGE diagram can give more precise assessments.
More recently some mobile applications have been validated and can provide rapid and precise
estimations of TBSA.
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FIGURE 21.2 Common methods of estimating burn size.
(Reproduced with permission from Stout, LR. Burns and common integumentary disorders. In: Morton, PG , Fontaine, DK , eds. Critical Care Nursing: A
Holistic Approach. 11th ed. Philadelphia, PA: Wolters Kluwer; 2018:1031. A. Adapted from Anatomical Chart Company: Atlas of Pathophysiology . 3rd ed.
Springhouse, PA: Springhouse; 2010:385. Figure 32-1A and Figure 32-1B.)
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Age and body habitus affect burn size estimation. Children have disproportionately larger heads than
their legs, and this should be taken into consideration by using a pediatric chart. Obese patients have a
relatively larger proportion of skin on their trunks.
There are currently no consensus guidelines from major burn organizations to guide burn size estimation.
Consequently, the treating clinician should use the most familiar method, while understanding the
limitations of each.
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Patient Triage
Triage of the burn patient depends on the severity of the injury and the resources available to the initial
treatment team. Table 21.2 gives criteria for burn center referral from the American Burn Association
(ABA). 11
TABLE 21.2
Burn Center Referral Criteria
Partial-thickness burns greater than 10% total body surface area (TBSA)
Burns that involve the face, hands, feet, genitalia, perineum, or major joints
Third-degree burns in any age-group
Electrical burns, including lightning injury
Chemical burns
Inhalation injury
Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality
Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or
mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center
before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the
regional medical control plan and triage protocols
Burned children in hospitals without qualified personnel or equipment for the care of children
Burn injury in patients who will require special social, emotional, or rehabilitative intervention
Patients meeting criteria for transfer should have large-bore intravenous access to begin resuscitation and
be placed in clean, dry dressings. Further wound care will complicate initial management and is
unnecessary because a comprehensive evaluation will be performed when the patient arrives at the burn
unit. Normothermia must be maintained, especially for larger burns, because thermoregulation can be
impaired.
Patients who do not meet burn center referral criteria may be managed at the referring facility at the
discretion of the treating surgeon. For these patients, bedside mechanical debridement should be
performed under appropriate sedation to fully assess the depth and extent of burn injury. Blisters should
be unroofed, and broad-spectrum topical antimicrobials should be placed over the wound depending on
its depth and extent. Systemic antibiotics have no role in treated uninfected burns.
Superficial partial-thickness burns or small full-thickness burns may be taken care of as an outpatient
provided the patient meet certain criteria: One, the ability to provide adequate local wound care at home.
Two, adequate analgesia does not interfere with wound care. Three, adequate oral intake and thus
nutritional support and hydration. Four, compliance with therapeutic instructions to prevent stiffness
across joints or loss of range of motion. If these criteria are met, the patient can have close follow-up on an
outpatient basis.
If the patient does not fully satisfy criteria for management as an outpatient then consider admission to
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the hospital for provision of local wound care, analgesia, hydration, nutrition, and physical therapy.
As per ABA criteria, burns greater than 20% or greater than 10% in a child should be admitted to the ICU
for additional resuscitation and hemodynamic monitoring. ICU admissions will in general require
placement of a central venous catheter, an arterial line, a Foley catheter, and a nasogastric tube.
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Survivable Injuries
When treating large burn injuries, like any other devastating traumatic injury, the physician must first
consider primum non nocere or first, do no harm. Aggressively treating a patient with a nonsurvivable
injury leads to undue pain, anxiety, and suffering by the patient, family, and the treating team. In some
extreme cases, the best management may be simply keeping the patient comfortable and not pursuing
resuscitation. The historic prognostic indicator for burn mortality is the Baux score: the patient’s age plus
TBSA is equal to the likelihood of mortality. Twenty percent is added for inhalational injuries. Currently,
with advances in modern burn critical care and early excision of burn wounds, mortality rates have
decreased. The revised Baux score and associated nomogram are more accurate reflections of current
mortality rates. 12 The physician should work hand-in-hand with the severely burned patient’s family or
medical decision-maker in the cases of a severe burn to determine how best to proceed according to the
patient’s wishes. Preinjury designations for the patient’s desired care, such as do not resuscitate or do not
intubate, should be meticulously adhered to, based on the patient’s advanced directives.
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Resuscitation
The goal of burn resuscitation is to maintain adequate tissue perfusion—especially to the skin—during
the first 24 to 48 hours after a large burn (>20% TBSA) injury. Resuscitation must proceed carefully
because the consequences of both over or under resuscitation can be devastating. Under resuscitation
leads to hypoperfusion of critical tissues and can result in ischemic burn wounds by converting to deeper
injuries and ischemia of other organs. Over resuscitation leads to excess edema formation and its
sequelae: compartment syndromes of the extremities and abdomen, as well as organ dysfunction
including worsening respiratory function. Onset of intra-abdominal hypertension requires prompt
treatment including systemic paralysis and ultimately decompressive laparotomy if progression to
abdominal compartment syndrome develops.
Although many different formulas exist to guide burn resuscitation, all are based on the patient’s initial
weight and the size of the burn. The Parkland (4 cc × weight [kg] × % TBSA) and ABA consensus formula
(2 cc × weight [kg] × % TBSA for adults) are two common methods used to estimate the total amount of
fluids needed during the first 24 hours after a large burn injury and to set initial fluid infusion rates. 13 A
sample calculation for the Parkland formula is as follows.
Balanced, isotonic crystalloid solutions such as lactated Ringer solution are preferred, as they limit
diffusion into the interstitial space. Normal saline is generally avoided because it provides excess chloride
load and can perpetuate a metabolic acidosis. Glucose should be added when resuscitating smaller
children. There is no evidence to support the use of colloid over or in addition to crystalloid in the first
24 hours after burn injury, although this topic is still intensely debated. Early administration of colloid
may worsen burn wound edema, as large molecules leak from the intravascular space to increase the
oncotic gradient. Given the lack of evidence for its benefit, colloids have a narrow role in acute burn
resuscitation and are limited to instances when the volume of resuscitation is exceeding predicted levels.
Whatever formula is used to begin fluid infusion, adequacy of resuscitation is assessed using vital signs
and hourly urine output as a surrogate for end organ perfusion. The standard of resuscitation is to
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maintain 0.5 to 1.0 mL of urine output per kilogram per hour and mean arterial pressure greater than
65 mm Hg. The kidney is susceptible to changes in perfusion pressure, so consistent urine output
indicates globally adequate end organ perfusion. Complex algorithms to assess the end points of
resuscitation have been developed based on advanced physiologic parameters (such as central venous
pressure, pulmonary capillary wedge pressure, end diastolic volume, stroke volume variation) and
biomarkers (such as lactate, hemoglobin, base deficit, creatinine). However, there are no evidence to
demonstrate improved outcomes with these parameters over tracking urine output and vital signs.
Medically complex patients with premorbid systemic disease, for example, chronic kidney disease or
congestive heart failure, is a challenge from a resuscitative standpoint and may benefit from other
methods of goal-directed therapy such as provided with a Swan-Ganz or other cardiac monitoring
device. Initiation of vasopressor or inotropic support may be indicated, especially in the setting of fluid
resuscitation exceeding predicted amounts. Care of these patients is best left to the experienced burn
intensivist.
In a randomized controlled trial comparing ascorbic acid (vitamin C) to lactated Ringer solution alone,
Tanaka et al. in 2000 found ascorbic acid at a dose of 66 mg/kg/h for 24 hours decreased overall volume
requirements for resuscitation. 14 The authors posit vitamin C acts as an oxidative scavenger and may also
limit tissue damage from the inflammatory process of the burn. In our Unit, patients with greater than
30% TBSA are treated with ascorbate as an adjunct during the first 24 hours after burn injury.
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Analgesia and Sedation
Appropriate analgesia and sedation are critical to the care of the burn patient. From the time of
presentation to ultimate wound closure, optimizing these parameters may provide many clinical
challenges. Given the density of cutaneous nerve endings, most burn injuries are very painful and require
multiple painful procedures such as dressing changes or surgeries to treat. Moreover, many burn patients
present with substance dependence or abuse disorders that complicate the adequate provision of
analgesia or sedation.
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Analgesia
First-line agents are opioid-based analgesics such as morphine or fentanyl. These may be given orally or
intravenously depending on the circumstance and should be titrated for the desired effect. Oral
administration has, in general, a longer duration of effect and thus is preferred if possible. Analgesia in a
newly burned patient should be intravenous, as small frequent doses to define needs. Opioid side effects,
such as respiratory depression, should be balanced against inadequate analgesia. Background pain can
often be treated with a sustained-release opioid analgesic such as OxyContin or MS Contin. Breakthrough
or procedural pain can be treated with more acute agents such as morphine sulfate immediate release or
oxycodone. Nonsteroidal anti-inflammatory drugs have a role in burn pain control but are associated
with bleeding risks (both gastrointestinal and postsurgical) which can limit their use.
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Sedation
Sedation, in the form of anxiolysis, should be used in burn patients as a procedural or background
adjunct to analgesia. Although benzodiazepine use has been associated with longer ICU stays and worse
outcomes, these drawbacks may be unavoidable in a patient with a large burn undergoing frequent
anxiety provoking procedures. Other agents such as propofol or dexmedetomidine can be considered for
sedative purposes but also have drawbacks to long-term use. Ketamine is a useful alternative that does
not contribute to hemodynamic depression but may cause transient hypertension.
In the patient with a large burn and a long hospital stay, care must be taken to prevent dependence,
tolerance, and withdrawal to analgesic and anxiolytic agents.
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