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CHERYL KING, MS, CCRN • Section Editor

Epidermolysis Bullosa
A Case Study in Transport, Treatment, and Care
Webra Price-Douglas, PhD, CRNP, IBCLC, Beth Diehl-Svrjcek, MS, CRNP, CCRN, CCM, LNCC

ABSTRACT
There are skin rashes, lesions, and disorders in the neonatal period that require emergent assessment and consultation.
A neonate presented with epidermolysis bullosa and provided an opportunity for learning about this condition and var-
ious dermatologic resources, primarily DermAtlas. The neonate with suspected epidermolysis bullosa that is delivered in
a community setting usually requires transport to a neonatal intensive care unit with pediatric subspecialty care. A case
study involving the transport of a neonate with this condition is reviewed, followed by a discussion of the etiology, inci-
dence, pathogenesis, diagnosis, and nursing care before and during transport and parental considerations. The resources
available in the neonatal community, primarily DermAtlas, for the identification of epidermolysis bullosa and other der-
matological conditions is explored.
KEY WORDS: dermatologic conditions, epidermolysis bullosa, neonatal transport

ermatology is not usually the strong suit of Community Hospital Course

D most neonatal nurses. However, as a profes-

sion, nursing has made great strides with regard
to skin care, especially for the preterm neonate. A neo-
nate presented with epidermolysis bullosa and pro-
vided an opportunity for learning about this condition
and various resources concerning neonatal dermatol-
ogy, primarily DermAtlas.
CASE STUDY
Prenatal Birth History
Baby Boy C was the term product of a 35-year-old
African American woman who was a primigravida.
The mother received appropriate prenatal care. Mater-
nal lab results were negative, with no indication of
sexually transmitted diseases. The maternal history
was positive for placenta previa, anemia, and hypothy-
roidism. No history of alcohol or illicit drug use was
noted. A prenatal ultrasound showed no anomalies at
28 weeks’ gestation.
Address for correspondence: Webra Price-Douglas, PhD,
CRNP, IBCLC, Maryland Regional Neonatal Transport
Program, The Johns Hopkins Hospital, 600 North Wolfe St,
Nelson 2-133, Baltimore, MD 21287; wpdougla@jhmi.edu.
Author Affiliations: Maryland Regional Neonatal Transport
Program, and The Johns Hopkins Hospital Neonatal Intensive
Care Unit, Baltimore, Maryland.
Copyright 2007 © by the National Association of
Neonatal Nurses.
Artificial rupture of membranes was performed by
the obstetrician 15 hours prior to delivery. The neo-
nate was delivered vaginally without assistive instru-
mentation. Routine care, including treatment with
vitamin K and eye prophylaxis, was completed in
the delivery room. Apgar scores were 8 and 9 at 1 and
5 minutes, respectively. The neonate was cared for in
the mother’s room, fed without difficulty, and was
normothermic until a temperature of 100.6°F was
noted on the date of birth. Bleeding was observed at
the cord base, gums, and nail beds. The neonate was
returned to the nursery, and the pediatrician was noti-
fied of these clinical findings. Vesicles were also noted
upon physical examination. Initial management by
the pediatrician included obtainment of a complete
blood count (CBC), blood cultures, surface cultures,
and coagulation studies consisting of prothrombin
time and partial thromboplastin time. A peripheral
intravenous catheter was placed, and intravenous anti-
biotics, specifically ampicillin and gentamicin were
started. After these initial measures, a call was placed
by the community pediatrician requesting transfer to
a tertiary care facility for subspecialty care and eval-
uation related to a suspected herpes simplex virus
infection. The neonate was 18 hours of age.
When the Maryland Regional Neonatal Transport
Team arrived, acyclovir was administered by the
transport nurse/nurse practitioner per the recom-
mendation of the consulting neonatologist. Vital signs
were stable, and D5W was infusing at 80 mL/kg/day.
The infant was on room air with oxygen saturations
between 96% and 98%. Respirations were unlabored.

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On physical exam, vesicles were noted on the scalp
and buttocks, and the right thumb nail was displaced
by a vesicle. The base of the umbilical cord was mac-
erated with old blood; the cord had been painted
with Triple Dye. The infant was noted to be mildly
hypotonic. The prothrombin time and partial throm-
boplastin time results were pending at the time of
transport. He was transported to the Johns Hopkins
Hospital neonatal intensive care unit (NICU) via hel-
icopter related to the geographical distance between
the 2 hospitals.
Neonatal Intensive Care Unit Course
Upon admission to the NICU, Baby Boy C weighed
3,100 g (50th percentile) and had a head circumfer-
ence of 34 cm (50th percentile) and a length of 49 cm
(50th percentile). A lumbar puncture was done, and
vancomycin was added to the antibiotic regimen.
Additional vesicles were noted on the scalp, right and
left buttocks, and right shoulder. There was an avul-
sion of the right thumb nail with a vesicle underneath
the nail bed. His tone was decreased. A consultation
was obtained with pediatric dermatology on the day
of admission because of the suspicion of epidermol-
ysis bullosa (EB), and a tissue sample was obtained for
analysis. Results of the CBC were unremarkable, and
blood cultures were negative. The neonate was treated
with a 7-day course of IV antibiotics related to the
decreased tone, elevated temperature, and presence of
vesicles/lesions. The cerebral spinal fluid (CSF) herpes
simplex virus (HSV) polymerase chain reaction (PCR)
was negative. The neonate did receive 1 transfusion
of fresh frozen plasma for a prolonged prothrombin
time of 12.8 seconds (s) (normal, 9.3-11.5 s) and par-
tial thromboplastin time of 47.2 s (normal, 25.4-34.2
s) and a decreased fibrinogen level 131 g/L (normal,
150-450 g/L). There was one subsequent occurrence
of slight bleeding originating from the lower gum.
He progressed well with oral feedings and was dis-
charged home to the mother after an 8-day NICU
stay. The results of the tissue biopsy were pending at
the time of discharge. A follow-up pediatric derma-
tology appointment was scheduled 9 days after dis-
charge, with a pediatrician visit arranged for 2 days
after discharge. Aquaphor or Vaseline was ordered
and was to be applied by the mother for open areas
of the skin. Skilled nursing visits were arranged with
a home health agency.
Follow-up and Readmission
The first visit to pediatric dermatology indicated a new-
born with EB, the exact variant was unclear. A lack of
scarring was suggestive of a lesion in the basement
membrane zone of the epidermis. The mother was
instructed to continue to use petroleum jelly gauze and
nonstick gauze dressings. A nutritional consultation
was obtained. Baby Boy C weighed 3,345 g, reflecting
a weight gain of 255 g since birth.
A subsequent visit a month later to pediatric derma-
tology was requested by the mother because of new
blister formation on both of the legs. Treatment with
antibiotic ointment, Aquaphor, and petroleum jelly
was ongoing and combined with a topical moisturizer
and antibiotics. His weight was 4,250 g. Junctional EB
was highly suspected. A prescription for Silvadene
cream was ordered for open, weeping lesions. A 6- to
8-week return interval was suggested to the mother
pending any concerning change in clinical status.
Pediatric Intensive Care Unit Course
Baby Boy C was admitted to the pediatric intensive
care unit for meningitis and suspected sepsis 5 weeks
after his second pediatric dermatology visit. His mother
had taken him to the local community hospital ER
with seizure-like movements and accompanying pal-
lor. His blood culture grew Streptococcus pneumonia that
was penicillin-susceptible. The baby had received
Prevnar 2 weeks prior, but sufficient immunity had
not yet been achieved given the time interval. Intra-
venous antibiotics were started and head imaging stud-
ies ordered. Baby Boy C subsequently had an episode
of status epileptics necessitating intubation. He was
able to achieve extubation but within a few days again
required intubation for stridor and increased work of
breathing. Hyponatremia and hypovolemia were also
noted. His blood culture was positive for gram-negative
rods, and the urine culture was positive for Candida
albicans. Despite aggressive fluid resuscitation, antibi-
otics, blood product administration, and vasopressor
therapy, he experienced refractory hypotension, dis-
seminated intravascular coagulation (DIC), and adult
respiratory distress syndrome (ARDS). After consul-
tation with the family, a do-not-resuscitate (DNR)
decision was made, with no further escalation of care.
Baby Boy C died on day of life 107.
ETIOLOGY
To understand the etiology of EB, it is important to
review normal skin structure. The skin consists of 3
stratified layers: the epidermis, dermis, and subcuta-
neous layer (Figure 1). The epidermis is the outer layer
containing keratin-forming cells and melanocytes.
The connection between the epidermis and the der-
mis consists of undulating ridges that project into the
dermis. This connection provides mechanical support
and a partial barrier against the exchange of cells and
large molecules. The deepest layer of this connection
is the basement membrane. Immediately beneath the
basement membrane is the dermis. The dermis con-
tains connective tissue, sweat glands, sebaceous glands,
hair shafts, blood vessels, and nerves. The subcuta-
neous layer below the dermis consists of adipose tissue,
providing cushion and insulation.1,2
By definition, EB is a group of rare, inherited dis-
orders characterized by the presence of extremely
fragile skin, which results in the formation of blisters
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FIGURE 1.
Normal structure of the skin. From McGrath et al.1 Reprinted with permission.
and open sores in response to minor trauma. Specif-
ically, there are 3 main forms of EB, which are defined
by the depth of blister location within the skin layers
and the location of the dissolution of the skin.3 Most
specifically, the basement membrane zone is the area
in which the epidermis meets the dermis. Epidermol-
ysis bullosa simplex (EBS) is a disorder that occurs
above the basement membrane zone. Junctional EB
is an affliction through or within the basement zone.
Dystrophic EB is a problem under the basement mem-
brane zone4 (Table 1).
TABLE 1. Various Forms of
Epidermolysis Bullosa
There are three main forms of EB; they are defined by the
depth of blister location within the skin layers and the
location of the dissolution of the skin.3 Most specifically,
the basement membrane zone is the area in which the
epidermis meets the dermis. The inheritance pattern of
EB may be dominant or recessive. If a dominant pattern
is present, the offspring can inherit the gene from one
affected parent. The recessive pattern requires that both
parents carry the gene with subsequent submission to
the offspring. Most forms of EB are inherited, although
it may in rare instances present as an acquired, auto-
immune, bullous disease.6
EB simplex (EBS): a disorder that occurs above the base-
ment membrane zone and is usually inherited as an auto-
somal dominant disease.4,6
Junctional EB: an affliction through or within the base-
ment zone; it has an autosomal recessive inheritance.4,6
Dystrophic EB: a problem under the basement membrane
zone; both dominant and recessive forms exist.4,6
Advances in Neonatal Care • Vol. 7, No. 6
Epidermolysis Bullosa 291
Depending of the type of EB, the condition varies
in severity from minor blistering of the skin to a more
lethal form of the disease. Epidermolysis bullosa can
affect epithelial-lined organs, such as the surface of
the eye, oral cavity, gastrointestinal and genitourinary
tracts, or the bone marrow and musculoskeletal system.
The involvement of the basement membrane deter-
mines the presence of scarring. Epidermolysis bullosa
simplex and junctional EB do not usually produce
scars, whereas dystrophic EB often produces scars.5
INCIDENCE
An estimated 2 of every 100 000 live births are affected
with some form of EB. This accounts for approxi-
mately 12 000 people in the United States. The dis-
order occurs in every racial and ethnic group through-
out the world and affects both sexes equally.5
PATHOGENESIS
A family history of the disease, especially an affected
parent, is a significant risk factor. Interestingly, the
inheritance pattern may be dominant or recessive. If
a dominant pattern is present, the offspring can inherit
the gene from one affected parent. Epidermolysis bul-
losa simplex is usually inherited as an autosomal dom-
inant disease. The recessive pattern requires that both
parents must carry the gene with subsequent submis-
sion to the offspring. Junctional disease is an autosomal
recessive inheritance. Dystrophic EB can be domi-
nant or recessive. Unfortunately, the recessive forms
tend to be more severe in nature. Very severe forms
of inherited EB have a high mortality rate, as great
as 87%, during the infancy period, as a result of infec-
tion or failure to thrive. Most forms of EB are inher-
ited, although it may in rare instances present as an
acquired, autoimmune, bullous disease.6
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292 Price-Douglas and Diehl-Svrjcek
CLINICAL PRESENTATION/ASSESSMENT
Epidermolysis bullosa results in the formation of large
fluid-filled blisters that are evident at birth or develop
shortly after birth (Figure 2). Symptoms depend on the
type of EB. The localized milder form of EB simplex,
Weber-Cockayne, is associated with blisters that rarely
extend beyond the hands and feet. Other subtypes of
EB simplex present with blisters on all body areas.
Junctional EB produces large, ulcerated blisters on
the face, trunk, and lower extremities. These are eas-
ily infected and lead to loss of body fluids and subse-
quent dehydration. In addition, rough or thickened
fingernails and toenails, blistering around the mouth,
throat, eyes or nose, and a hoarse cry or cough afflict
the neonate with junctional EB. Dental anomalies,
such as poorly formed tooth enamel, and alopecia
from scarred areas on the scalp complete the clinical
constellation of findings. Junctional EB can be lethal
in infancy.7
Dystrophic EB has slightly different symptoms,
some of which are shared with EB simplex and junc-
tional EB. Interestingly, a condition called pseudosyn-
dactyly, a fusion of the fingers or toes, can occur with
the dystrophic type. Squamous cell carcinoma can
also affect the hands and feet of individuals with the
recessive form of dystrophic EB.5
For any skin disorder that presents as a lesion, rash,
or vesicle, a systematic approach of assessment is help-
ful and efficient. For the neonate, the search begins
with the maternal medical history and spans the pre-
natal, intrapartum, and postpartum periods. A deter-
mination regarding the onset of the lesion, rash, or
vesicle will ascertain if it was present at birth. This
determination will also include the clinical evolution
of the latter. Does it appear there is some new for-
mation or healing of previous dermatologic sites? Is
pruritus present? Where any drugs or immunizations
administered? A description of the distribution and
pattern is helpful. Where is the lesion, rash, or vesicle
FIGURE 2.
Typical blisters seen in epidermolysis bullosa.
TABLE 2. DermAtlas
DermAtlas is an online dermatology database. Although
it is not the first such resource in the field, it is the
largest, with more than 2 100 images (from more than
300 contributors), 645 diagnoses, and 58 categories, and
it continues to grow rapidly. DermAtlas is the second
most visited dermatology Web site in the world, behind
the Web site of the American Academy of Dermatology.
This technology provides an essential resource on a 24/7
basis to any individual with Internet access.
Contributions are accepted worldwide, including images
from patients and caregivers.
DermAtlas is available in the public domain and can be
accessed via the Internet at
http://dermatlas.med.jhmi.edu/derm. The database is able
to cross-reference images by body part and diagnosis,
along with age, race, and gender.
For example, a clinician who desires an image of psoriasis
on a boy’s leg can type in search terms regarding body
site, gender, and age. The system displays multiple close-
ups, each with a brief patient history, and offers links
from those images to all other skin diseases of the leg.
Because the same malady can look different in patients of
different races, DermAtlas sorts by pigmentation (light,
dark, medium).
located on the body anatomically? Is there a pattern?
Is there localization or generalization? What size is
the lesion, rash, or vesicle? Are there well-defined bor-
ders? Is there variation in the skin texture? Is the area
raised? Are there variations of pigmentation?8
By utilizing DermAtlas, which is similar to a der-
matologic textbook, to compare or describe the find-
ings, the clinician can perform a preliminary search
from the home page with some key words, such as
“blisters on thumb” and then retrieve images. An
advanced search option is available via specific query,
such as patient age, gender, location, texture, and
color or pigmentation. DermAtlas provides an invalu-
able resource when attempting to identify or describe
a skin condition. While nurses are not responsible
for assigning a medical diagnosis, the visual tools
provided by DermAtlas offer the nurse assistance
when describing various skin conditions9 (Table 2).
Other references that may be helpful are included
in Table 3.
DIAGNOSIS
An EB diagnosis can be accomplished in the prenatal
or postnatal periods. Prenatal diagnosis by amnio-
centesis or sampling of the chorionic villus can be done
as early as the 10th week of pregnancy. Postnatal diag-
nosis is obtained via a skin biopsy. One diagnostic test
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TABLE 3. Internet Resources/External Links:
National Society of Genetic Counselors:
National Institute of Arthritis and Musculoskeletal and Skin Diseases
Epidermolysis Bullosa Medical Research Foundation
National Information Center for Children and Youth with Disabilities
involves microscopically examining the skin tissue
via reflected light to determine if proteins needed to
form fibrils and filaments in the skin are missing. In
addition, magnification of tissue images via electron
microscope can serve as a diagnostic test.5
SUPPORTIVE/PREVENTATIVE THERAPY
To date, no cure exists for any type of EB, so treatment
is aimed at the prevention of new lesions, control of
pain, and maintenance of comfort. In many forms of
EB, blisters will form with the slightest pressure or fric-
tion. To control blister formation, it is best to lift the
neonate by supporting the buttocks and back while
cradling the infant in a soft material such as a sheep-
skin. Maintaining an optimal room temperature is
helpful because overheating may lead to blister for-
mation. Judicious use of skin lubricants will reduce
friction and maintain skin moistness. Tailored, soft
clothing that requires minimal manipulations when
dressing the infant is best. Utilization of sheepskins
on car seats or hard surfaces will also lessen the occur-
rence of blisters. Application of mittens or gloves at
bedtime will keep scratching to a minimum.4
TRANSPORT CONSIDERATIONS
In the transport environment, the diagnosis of EB is
not attainable. However, for any neonate who presents
with blister-type lesions, EB must be considered in
the differential diagnosis. In the case study, the primary
diagnosis was suspected herpes simplex infection, a
more common reason for transport. The neonatolo-
gist should be consulted regarding any pertinent trans-
port recommendations given the clinical presentation.
Prior to and during initial transport, the blister for-
mation may be minimal because the exposure to fric-
tion has been limited. Minimizing friction is essential;
this can be achieved with special consideration in mov-
ing and securing the infant in the transporter. If sub-
sequent transports are requested, the indications for
transport should be scrutinized and transport limited
to situations that are life threatening. Interfacility trans-
port for elective diagnostic testing or treatment should
be avoided, if possible, to limit skin trauma and addi-
tional blister formation. Transport carriers, such as
isolettes, car beds, or car seats, must be selected based
Advances in Neonatal Care • Vol. 7, No. 6
Epidermolysis Bullosa 293
www.nsgc.org
www.niams.nih.gov
www.ebkids.org
www.NICHCY.org
on the ability to maintain thermoregulation and min-
imize friction. Careful attention to infection control
practices is imperative with all neonates. Certainly,
concern for infection, careful handling, appropriate
hydration, and glucose homeostasis are of utmost
importance.
NURSING CARE
For the neonate with EB, the primary focus is on the
prevention of infection and maintenance of optimal
comfort. In the NICU, the infant can be premed-
icated with a mild analgesic before scheduled dress-
ing changes. If the dressings have adhered to the
wounds, soaking the area in warm water may facili-
tate less traumatic removal. Depending on the size
of the blister, it may be advantageous to lance the
blister in the early stage of formation so that the top
layer of skin is intact and covers the underlying red-
dened area. To accomplish this, the blister is lightly
patted with an alcohol pad before lancing it at the
sides with a sterile needle. The fluid from the blister
is drained into sterile gauze. After lancing, an antibi-
otic ointment is applied to the area. The area can
then be bandaged using a gauze strip or left open to
air. Bandages embedded with petroleum jelly, glyc-
erin, or moisturizing agents may also be employed
to cover open wounds.4
Optimal nutrition and meticulous skin care with
sterile materials will serve to circumvent some of the
infectious complications. However, infection is likely
to occur at some point, and the nurse should instruct
the parent to monitor for purulent drainage, exces-
sive wound crusting, and foul odor, as well as the
occurrence of generalized fever and chills. The par-
ent should be instructed to notify the physician of
these symptoms immediately, so antibiotic therapy,
as appropriate, can be initiated.
PARENTAL SUPPORT/GENETIC GUIDANCE
Given that EB can be an incredibly painful and difficult
disease to deal with on a daily basis, adults who have
the knowledge that they carry the gene may choose
not to pass the disease to future generations. Genetic
counseling can provide a couple with advice on future
childbearing. Identification of the gene mutation in
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294 Price-Douglas and Diehl-Svrjcek
TABLE 4. EB Research Association and Registry
The Dystrophic Epidermolysis Bullosa Research Association
DebRA of America, Inc.
5 West 36th Street
Suite 404
New York, NY 10018
Tel: (212) 868-1573 or (866) DEBRA76 (866-332-7276)
DebRA (http://www.debra.org)
National Epidermolysis Bullosa Registry
NEBR
c/o Vanderbilt University Medical Center
Vanderbilt University
2204 West End Avenue
Nashville, TN 37240
the family and subsequent prenatal testing can deter-
mine if the unborn fetus is affected, allowing the fam-
ily the option of elective termination of the pregnancy.
The Dystrophic Epidermolysis Bullosa Research
Association (DebRA) has an affiliated laboratory
that can test for the gene mutation as a portion of the
genetic counseling process.5
CONCLUSION
Care of the neonate with epidermolysis bullosa
requires baseline knowledge of the etiology and patho-
genesis of the disorder. Because of the severity and
chronicity of the disease process, a team approach is
of the utmost importance to meet the medical, nurs-
ing, and parental education components of care. In
addition, excellent resources exist in both the lay and
medical community (eg, the DebRA organization
and DermAtlas; Tables 2, 3, and 4).
Acknowledgments
The authors thank Bernard Cohen, MD, and Christoph
Lehmann, MD.
A National EB registry was created by the National Institutes
of Health in September 1986 and functions under the direc-
tion of Jo-David Fine, MD, with support provided by DebRA
of America. Dr. Fine is a DebRA Trustee and Scientific
Advisory Board Member. The Registry collects information
from patients with EB, characterizes the many forms of this
disease, establishes the frequency of various manifestations
of EB, and determines the risks of specific clinical outcomes
within EB types. The registry maintains a large electronic
database that provides for statistical analysis, promotion of
basic research, and clinical trials. To contact a nurse educa-
tor, please call 866-DEBRA76 Monday to Friday from 9 am to
5 pm Eastern Time or send an e-mail to nurse@debra.org.
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