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Preface

This fourth edition (4e) of Color Texbook of Pediatric Dermatology


is designed for two purposes. Firstly, 4e is intended to be a practical
University course on Pediatric Dermatology. Secondly, 4e is designed as a
rapid access reference source for the busy clinician. In both instances, 4e
is written from the perspective of what is best for the child. For the course
in pediatric dermatology, new information has been added to every chapter
and there is a major reorganization of chapters 11, 13, 15, 17 and 20.
Chapter 2 was expanded in order to add many clinical photographs of
primary and secondary lesions. For ease of interpretation, all the line
drawings are in color. The latest references were added and the
information incorporated into the text as original source information. As
for previous editions, the authors did not wish to copy other textbooks. It is
our hope that 4e will provide a format to medical educators that wish to
create a course in pediatric dermatology for their trainees.
For the reference text, the problem-oriented differential diagnosis
index was redone and will remain on the front and back of the book. By
understanding primary and secondary lesions as described in chapter two,
the clinician can rapidly create a differential diagnosis with the index. In
addition, the number of clinical photographs has increased by 30%. Our
colleagues primarily caring for children wished to have more images of the
skin conditions described. Ten new patient education sheets have been
created and the others revised..
This fourth revision was heavily dependent on comments from
primary care providers, residents and students. The Dermatology residents
at the University of Colorado systematically reviewed the previous edition
a chapter per week and made many valuable suggestions for improvement.
As with previous editions, all three editors read each revised chapter. We
emphasized the perspective of experienced clinicians in each chapter when
considering new findings and new treatments.

8
We have many to thank for this edition. As before, the encouragement
of our mentors enabled the creation of the book. This book is dedicated to
the late Dr. Alvin Jacobs who was an inspiration to us all. A special debt
is owed to Drs. Robert Goltz, the late C. Henry Kempe, W. Mitchell Sams,
Jr. and Lowell Goldsmith for their guidance, protected time, nurture and
mentorship for our careers. We also are grateful to all our colleagues in the
Society for Pediatric Dermatology who have generously used this textbook
in their institutions and provided enthusiastic support for our careers.
There has never been a medical association with such warmth and support
for each other. We are especially indebted to Claire Bonnett, our editor at
Elsevier and her colleagues at the London office.
William L. Weston, MD, Alfred T. Lane, MD, Joseph G. Morelli, MD

9
Table of Contents

Copyright
Dedication
Preface
Chapter 1: Structure and Function of the Skin
Chapter 2: Evaluation of Children with Skin Disease
Chapter 3: Acne
Chapter 4: Dermatitis
Chapter 5: Bacterial Infections (Pyodermas) and Spirochetal Infections
of the Skin
Chapter 6: Fungal and Yeast Infections of the Skin
Chapter 7: Infestations
Chapter 8: Viral Infections
Chapter 9: Papulosquamous Disorders
Chapter 10: Sun Sensitivity
Chapter 11: Bullous Diseases and Mucocutaneous Syndromes
Chapter 12: Skin Cysts and Nodules
Chapter 13: Vascular Lesions
Chapter 14: Vascular Reactions: Urticaria, Erythemas, and Purpuras
Chapter 15: Hair Disorders
Chapter 16: Nail Disorders
Chapter 17: Disorders of Pigmentation: the White Lesions and the

10
Brown Lesions
Chapter 18: Immobile and Hypermobile Skin
Chapter 19: Genodermatoses
Chapter 20: Drug Eruptions
Chapter 21: Skin Diseases in Newborns
Chapter 22: Dermatopharmacology and Topical Formulary
Index
PROBLEM-ORIENTED DIFFERENTIAL DIAGNOSIS INDEX

11
Chapter 1

Structure and Function of the Skin

A firm understanding of normal skin structure and function is necessary


for recognition and treatment of skin disease. Those providing medical care
for children should apply the principles of skin biology to the pediatric
patient and master essentials of embryology and development.

THE EPIDERMIS
Keratinization
The epidermis functions as a barrier, preventing penetration from outside
and retaining substances inside.1,2 Over 95% of epidermal cells are
keratinocytes. The process of keratinocyte replication and maturation is
called keratinization. The major keratinocyte proteins are keratins, which
provide scaffolding to determine keratinocyte shape. Keratin pairs form
intermediate filaments by combining an acidic keratin with a basic keratin.
In proliferating basal keratinocytes, keratins 5 and 14 provide the main
protein structure. As differentiation occurs, keratins 5 and 14 are replaced
by keratins 1 and 10 and the cells flatten. The process of keratinization
begins with proliferation of new keratinocytes in the region of the basal cell
layer, near the dermal–epidermal junction (Fig. 1.1). As keratinocytes
differentiate, they accumulate granules called keratohyaline granules in
their cytoplasm, and the type of keratin bundles within the cells becomes
thicker. Within the granular layer the cells lose their cylindrical and
cuboidal shapes and begin to flatten as they go through a specific process of
terminal differentiation or programmed cell death (apoptosis) called
cornification or keratinization.1,2 Cell nuclei are lost and the keratinocytes

12
flatten like stacks of plates. This final layer is called the horny layer, or
stratum corneum. The stratum corneum cells accumulate like bricks in a
wall, separated by intercellular lipids, which function like mortar. The thick
corneocyte membranes are created by the formation of an inner protein
envelope including the proteins profilaggrin, involucrin, and epiligrin. The
intercellular and cell-surface lipids are an integral part of the epidermal
barrier function.2

Fig. 1.1 Normal epidermis. The germinative layer with prominent nuclei is at
the base of the epidermis and within the same compartment as the fully
differentiated cells. As these basal cells differentiate, they migrate up toward the
skin surface, shed their nuclei, become flattened, and are shed from the skin
surface.

Individual keratinocytes are bound together by desmosomes and


adherens junctions. The desmosomes contain membrane glycoproteins
desmocollins and desmogleins, and cytoplasmic proteins desmoplakins,
periplakin, and plakoglobin.
The process of keratinization is continuous within the skin. The newly
formed keratinocytes of the basal layer mature and are shed from the skin
over an interval of approximately 28 days. Skin diseases may be associated
with variation in the speed and process of keratinization.

Epidermal Barrier
It is said that the skin is the interface between humans and their environment.
Indeed, the most important functions of the epidermis are to provide a skin
barrier against microorganisms and irritating chemicals and to impede the

13
exchange of fluids and electrolytes between the body and the environment.
This barrier function resides in the stratum corneum, where the terminally
differentiated keratinocyte develops a tough cell envelope beneath the
plasma membrane.3 The process of envelope formation involves
biochemical processing of involucrin, the major cytoplasmic protein
precursor of the cell envelope. The epidermal barrier is completed by
extracellular lipid layers surrounding the terminally differentiated
keratinocytes.
Although the skin, including the epidermis and dermis, is 1.5–4.0 mm
thick, the epidermal barrier is only 0.05–0.1 mm thick. By the daily
shedding of one to two cell layers of stratum corneum, or scale, the
epidermal barrier prevents excessive bacterial colonization of the skin
surface. In addition to continuous shedding, the flattened stratum corneum
cells are tightly adherent to each other, so that to obtain entrance into the
lower epidermis and dermis, chemicals or microorganisms must pass
between tightly compacted epidermal cells.
The water content of the environment greatly influences the epidermal
barrier (see Ch. 22). Both an excessive and an inadequate water content in
the epidermal barrier will cause microscopic and macroscopic breaks in the
barrier.
In response to friction or other forms of repeated trauma, such as
exposure to ultraviolet light (UVL) or chemical injury, stratum corneum is
formed in amounts greater than usual, as can be noted on the palms and
soles. The stratum corneum is thinnest over the eyelids and scrotum.

Pigmentation and Ultraviolet Light


Four biochromes in the skin are responsible for clinical pigmentation:
melanin, betacarotene, oxyhemoglobin, and reduced hemoglobin.1 The
brown-black pigment melanin is the dominant pigment of the skin.4,5 It is the
pigment closest to the observer’s vision and darkest in color. In dark-
skinned individuals, it is difficult to recognize yellow pigment
(betacarotene), red pigment (oxyhemoglobin), and blue pigment (reduced
hemoglobin). Melanin is produced by the pigment-forming cell, the
melanocyte, which is located in the epidermis. Different skin regions

14
contain different numbers of melanocytes. For example, three times as many
melanocytes are found in the epidermis of the forehead as in the abdominal
skin.1 Numbers of melanocytes per unit area of skin are the same despite
racial differences in pigmentation.
Each epidermal melanocyte has dendritic cytoplasmic extensions that
make contact with 35 to 45 epidermal cells. This melanocyte–keratinocyte
unit (Fig. 1.2) is responsible for clinical pigmentation. The brownish-black
polymer melanin is produced within the melanocytes in special membrane-
bound organelles called melanosomes. The genetic control of pigmentation
is extremely complex and involves more than 150 alleles spread over 90
loci. These loci direct protein products which are structural proteins,
enzymes, transcriptional regulators, transporters, growth factors, and
receptors with many cellular targets and functions.4 The enzymes, including
tyrosinase, that are crucial for melanin production are contained within the
melanosome membrane. Melanosomes develop in stages. Tyrosinase and
other enzymes convert the colorless chemical tyrosine to an oxidized
quinone compound, which in turn becomes polymerized into the brownish-
black compound melanin. Clinical pigmentation depends on the stage of the
melanosome produced and dispersion of melanosomes from melanocytes to
keratinocytes. Keratinocytes actively phagocytize the melanosomes. In black
skin, there are single units of advanced-stage melanosomes, whereas in
lighter-skinned persons, the melanosomes are aggregated and of earlier
developmental stages. Thus, the major difference in black and white skin is
the stage of melanosome development and the ability to transfer and
disperse melanin pigment, not the number of melanocytes per unit area of
skin.4

15
Fig. 1.2 Melanocyte–keratinocyte unit. The dendritic melanocyte, shown
here as a clear cell with many branches, provides melanin pigment to many
keratinocytes.

The function of melanin is to protect the deoxyribonucleic acid (DNA)


structure of epidermal cell nuclei from damage by UVL irradiation. Melanin
dispersed within the cytoplasm of keratinocytes forms a protective cap over
the keratinocyte nucleus when the keratinocytes are exposed to UVL (Fig.
1.3). Melanin pigment is lost by the daily shedding of stratum corneum cells.
Melanin within the dermis, such as that found in dermal melanocytic
birthmarks, has no such mechanism available for its elimination.

Fig. 1.3 Melanin production and transfer. Melanosomes (inset) are organelles
formed in the rough endoplasmic reticulum and Golgi area of melanocytes.

16
Their membranes contain the enzyme tyrosinase, which is responsible for the
formation of the brown-black polymer melanin. At the end of the dendrite, the
melanocytes are shown transferring pigment to the keratinocyte, where the
melanin moves to form a cap of the keratinocyte nucleus as protection against
ultraviolet injury.

UVL from the sun increases melanin pigmentation by first oxidizing


preformed melanin, increasing cross-linking of the melanin polymer and
darkening the color. This effect occurs within minutes after exposure and is
called immediate pigment darkening. During the 4–6 days after UVL
exposure, both increased melanin production and melanin transfer to
keratinocytes produce tanning.

Sunlight
The sun produces UVL of numerous wavelengths which, based on their
biologic effects, are arbitrarily divided into three groups: ultraviolet A
(UVA), ultraviolet B (UVB), and ultraviolet C (UVC) (Table 1.1). Incoming
UVL from the sun is scattered by small molecules in the atmosphere and
absorbed by the ozone layer; all UVL below 290 nm is absorbed, so that
virtually no UVC reaches the earth’s surface.

Table 1.1 Biologic effects of ultraviolet light


Ultraviolet Wavelength
Biologic effects
(UV) group (nm)
UVC 200–290 Cytotoxic (bactericidal, retinal injury)
Sunburn, sun tanning, systemic lupus erythematosus, skin
UVB 290–320
cancers
Drug photoallergies, porphyria, phyto-photodermatitis,
UVA 320–400
psoralen photoaging, PUVA therapy

PUVA, psoralen ultraviolet A-range.

Sunburn is caused by wavelengths of light from 290 to 320 nm. Photons


of UVL are absorbed by electrons of chemicals with double bonds and ring
structures, such as nucleic acids, DNA, and proteins, producing excited

17
electron states within these molecules or free radical formation.
Betacarotene and melanin act by stabilizing the free radicals and are natural
photoprotective chemicals found in skin. About 10% of UVB passes through
the epidermis and reaches the dermis. The erythema and pain of sunburn are
mediated via prostaglandins, free oxygen radicals, and other mediators.
The sunburn wavelengths of UVL are blocked by window glass. The
tanning and thickening of the epidermal barrier that result from exposure to
sunlight impair the penetration of UVL into the lower epidermis and dermis.
Wavelengths of light from 320 to 400nm (UVA) are responsible for the
photosensitivity seen in the many drug photoallergies and psoralen
phototoxicity. Light of these wavelengths passes through window glass and
also is emitted from fluorescent lamps such as those used as in overhead
lighting in schools.1

Epidermal Basement Membrane


The junction between the epidermis and dermis is the epidermal basement
membrane. This structure is composed of complex protein–cell and protein–
matrix interactions among the basal keratinocyte, the lamina lucida, the
lamina densa, the sublamina densa, and dermal collagens.6 Keratins in the
basal keratinocyte attach into the electron-dense plaques associated with the
hemidesmosomes. Anchoring filaments extend from the hemidesmosome to
dermal collagen fibers and have attachment sites to laminin 5 as well. The
complex basement membrane anchoring interactions resists shearing forces
to the skin and provides strength.
Bullous pemphigoid antigen 1 is associated with the cytoplasmic
portion of the basal cell hemidesmosome, and bullous pemphigoid antigen 2
is a transmembrane portion of the hemidesmosome.7 Laminins 5 and 6 are
associated with the anchoring filaments. Laminin 1, nidogen, and type IV
collagen are associated with the lamina lucida and lamina densa. The long
anchoring fibrils of the sublamina densa are composed of type VII collagen.
Integrins are extrahemidesmosomal attachments to the lamina densa.
Autoantibodies against basement membrane structures or genetic
defects of these structures cause a variety of diseases. Correlation of the
function of specific structures of the basement membrane and disease-

18
associated defects has helped to increase understanding of the epidermal–
dermal junction.

THE DERMIS
The dermis is composed predominantly of collagen fibers and elastin fibers
enclosed in a gel continuum of mucopolysaccharides.1,8,9 This fibrous
complex gives the dermis its great mechanical strength and elasticity,
allowing the skin to withstand severe frictional stress yet still be extensible
over joints. Elastin, collagen, and mucopolysaccharide gel are all produced
and secreted by fibroblasts. Types I, III, IV, and VII are the predominant
collagens in the skin. Although the principal mass of the dermis consists of
collagen fibers and is acellular, numerous other elements are present,
including mast cells, inflammatory cells, blood and lymph vessels, and
cutaneous nerves. These elements are responsible for regulation of heat
loss, the host defenses of the skin, nutrition, and other regulatory functions.

Collagen, Elastin, and Mechanical Properties


Most of the mechanical strength of the skin is derived from the fibrous
protein collagen, a macromolecule with a large hydroxyproline content.1,8
Mature collagen structure becomes rigid with cross-linking of adjacent
protein chains, and young collagen that is without significant cross-linking
fails to limit skin distention. Defective collagen results in extensive and
excessive distensibility of the skin, as seen in Ehlers-Danlos syndrome, or
severe blisters, as seen in recessive dystrophic epidermolysis bullosa.
Elastin fibers, which are composed of both an amorphous and a fibrillar
portion, are responsible for the reversible distensibility that allows the skin
to be restored to normal size after stretching.1,9 Defective elastin
production results in extreme wrinkling and redundant skin, as seen in cutis
laxa.

Cutaneous Vasculature
Cutaneous arteries course through the subcutaneous fat and give rise to two
vascular plexuses that run parallel to the epidermis. These vascular

19
plexuses contain arteriovenous shunts to divert blood from the skin and
provide nutrition to it, to regulate heat loss, and to participate in the defense
against foreign substances. The epidermis contains no blood vessels and
receives its nutrition via the diffusion of plasma into the intercellular
epidermal spaces. The stratum corneum has no such nutritive process.

Heat Regulation and Sweating


Skin is important in the control of body temperature. Heat generated in
organs and muscles is rapidly transported to the skin vasculature.1,10,11 The
cutaneous circulation acts as a radiator. Varying the rate and volume of
blood flow through the skin controls heat loss from this radiator. The blood
flow is controlled by the autonomic nervous system. Heat from the skin
surface is lost by evaporation of water in the form of eccrine sweat. Heat
loss or gain by convection or radiation depends on environmental
temperature. At comfortable temperatures, body heat can be regulated by the
cutaneous vasculature alone, without sweating. In hot, dry environments the
core body temperature may rise slightly but is stabilized by heat loss via
sweating. In hot, humid environments evaporation of water from the skin
surface is restricted, and heat gain occurs in the child’s body. If this
condition is allowed to continue, high fever, dehydration, and sodium
depletion may occur. With exercise and heat gain, sweating is critical to
maintaining body temperature.10,11 In children born with deficient numbers
of eccrine sweat glands (hypohidrotic ectodermal dysplasia), heat gain
occurs during hot weather, overheating, or exercise, and recurrent high fever
is often a presenting feature of the condition.

Cutaneous Nerves
Sensory nerve endings in the skin can elicit all of the principal sensations:
touch, pain, itch, warmth, and cold. The skin is supplied by both myelinated
and unmyelinated branches of spinal nerves.1,12,13 Nerve branches enter the
dermis from the subcutaneous fat and form both a superficial and a deep
nerve plexus. Unmyelinated branches from either plexus terminate in nerve
endings that may be simple or specialized. Terminals from a single axon
may serve an area as broad as 1 cm2 and overlap with nerve endings from

20
other axons. Inflow of cutaneous sensory information is strongly controlled
and modulated by the cerebral cortex. The skin has a high sensitivity to
rapid mechanical stimulation, with positional movements of less than 1 μm
detectable. Sensations of cold persist continuously when skin temperature is
below 30°C, and sensations of warmth persist continuously when it is above
37°C.1 Changes in temperature of 0.03°C can be detected, especially if the
skin temperature changes faster than 0.007°C/sec. Thermal sensitivity is
highest on the face. At temperatures below 18°C and above 45°C, pain is
produced. Pain may also be induced by pressure greater than 50 g/mm2 and
by disruption of skin.13 A number of chemicals injected into the skin may
also elicit pain. Itch is a sensation related to pain and is greatest close to
transitions of mucous membranes. Histamine is considered to be the most
important mediator of itch, but many other mediators are capable of
producing this sensation. Itch may be exclusively central rather than
cutaneous in some conditions, such as cholestasis.14

HOST DEFENSES OF THE SKIN


When breaks in the epidermal barrier occur, microorganisms invade the
upper epidermis. Plasma proteins, such as complement proteins and
immunoglobulins that normally bathe the intercellular epidermal space,
initiate an inflammatory response. In addition, antimicrobial peptides,
which are synthesized in the skin, provide a soluble barrier that acts as an
impediment to infection. These peptides, which include the cathelicidin and
defensin gene families, provide rapid, broad-spectrum defense against
infection by acting as natural antibiotics and by participating in host cell
processes involved in immune defense.15,16 Cutaneous vasodilation
(erythema) occurs early after this initial process, with diffusion of more
plasma proteins, followed by the migration of neutrophils, T lymphocytes, B
lymphocytes, and monocyte-macrophages into the dermis and later the
epidermis. Such cells initially accumulate around dermal blood vessels but
may migrate to the epidermis through the dermal–epidermal junction and
between epidermal cells. For example, in impetigo large numbers of
neutrophils accumulate just beneath the stratum corneum. Mast cells
containing histamine, heparin, and platelet-activating factors are located

21
around cutaneous blood vessels and play a regulatory role in the immune
response of the skin by their influence on cutaneous vascular responses.
The initial response of the skin to invasion by microorganisms consists
primarily of migration of neutrophilic leukocytes, but by 18–24 hours it is
characterized by the appearance of lymphocytes and monocyte-macrophages
in the dermis. Microorganisms or foreign substances not initially destroyed
by neutrophils are presumably further digested by macrophages or destroyed
by direct lymphocytotoxicity. A rich lymphatic system is also found in the
dermis, and foreign substances are carried to regional lymph nodes, where
specific immune responses are generated by T lymphocytes and B
lymphocytes. Some antigen recognition occurs in the skin because antigen-
processing cells (Langerhans cells) are found in the epidermis, and direct
Langerhans–T lymphocyte contact occurs that may be important in the
recognition of foreign antigens.
The epidermal barrier remains the primary defense of the skin, but
microorganisms that pass through the barrier can be destroyed within the
midepidermis as the skin defenses attempt to keep them out of deeper tissue.

EPIDERMAL APPENDAGES
Epidermal appendages, which are modifications of epithelium, include hair
follicle structures, sebaceous glands, nails, and the apocrine and eccrine
sweat glands. Hair follicles are formed through a complex developmental
process.17

Hair Growth
The hair growth cycle has three phases: the growing phase, anagen; the
regressing phase, catagen; and the resting phase, telogen.1 The cells of
anagen hairs have a high mitotic rate and are among the most rapidly
replicating cells in humans. The hair growth originates from the hair bulb,
which is located in the lower dermis.1,17 The delta and notch genes may be
involved in initiation of hair growth, along with ectodysplasin, a protein
involved in ectodermal dysplasias.18 Human scalp hair grows about 1.3 cm
per month.1 When growth of the hair ceases, the catagen phase occurs,

22
resulting in cessation of mitosis, apoptosis, and upward migration of the
hair bulb into the mid-dermis. The hair shaft becomes clubbed at the bottom,
causing the catagen hair to become a telogen hair (also called club hair).
The telogen hair remains in the follicle for 2–3 months and is pushed out
when the new hair grows.
There are great differences in the hair growth cycle among the different
hair types found in the various body regions. It is believed that fibroblast
growth factor regulates the duration of the anagen phase and the size of the
hair.19,20 Ambisexual hair follicles are common to both sexes and are
androgen dependent. At puberty, androgen converts vellus hairs to terminal
hairs in the axilla and the lower pubic triangle. Conversely, conversion of
terminal scalp hairs to vellus hairs occurs in the temporal area of the scalp
at puberty. Male sexual hair is responsive to high androgen levels, which
convert vellus hairs to terminal hairs in the beard area, ears, sternum, and
upper pubic triangle. In the occipital and bifrontal areas of the scalp,
androgen levels result in a conversion from terminal to vellus hairs,
resulting in androgenetic alopecia.
Hair cycles are asynchronous and vary within body sites. In the scalp
at any point in time, about 85% of the hairs are growing (anagen), 14% are
resting (telogen), and 1% are regressing (catagen). Newborns convert most
of their hairs to telogen hairs within the first 6 months of life. Some
newborns take several months to develop new anagen hairs, resulting in a
‘bald’ baby. Other infants develop new anagen hairs so rapidly that they
appear not to lose their hair. After acute febrile diseases, children or adults
can have many hairs convert from anagen to telogen with a subsequent
period of months with markedly thinned hair (telogen effluvium). Curly hair
is in part regulated by the transcription factor DLX (distal-less) and
fibroblast growth factors.18

Sebaceous Glands
Sebaceous glands are present everywhere on the human skin except for the
palms, soles, and dorsa of the feet. Generally, they are associated with hair
follicles and empty through a short duct into the canal of the hair follicle.1
The sebaceous glands are holocrine glands that produce sebum, a

23
semiliquid mixture of glandular cell debris containing glycerides, free fatty
acids, wax esters, squalene, cholesterol, and cholesterol esters. The largest
and most numerous sebaceous glands are found on the face, scalp, chest, and
back.
Sebum production is androgen dependent and begins at puberty in skin
regions with abundant sebaceous follicles.1 Sebaceous gland volume,
sebaceous cell size, and secretory capacity are all directly androgen
dependent. Obstruction of the sebaceous gland is associated with acne in
humans.

Eccrine Glands
Humans have two to five million eccrine glands. These glands function to
cool the body through evaporative heat loss of eccrine sweat. In addition,
these glands may help to moisten the frictional surfaces of the skin.

Apocrine Glands
Apocrine sweat glands are in the axilla, mons pubis, areola of the breast,
circumanal area, and the scalp. They are located deep in the subcutaneous
tissue and usually open into a hair follicle. Apocrine glands secrete a
yellowish, sticky fluid after puberty. The secretion is produced in response
to stress or sexual stimulation. In lower animals, these glands function as
sexual attractors and territorial markers.

Nails
Nails are formed by the fifth fetal month.1,21 The nail matrix contains
epithelial cells responsible for the production of the nail plate. The nail
matrix occupies an area beneath the proximal nail fold, a portion of which
may be seen as the lunula. Fingernails grow approximately 1 cm in 3
months, and toenails grow more slowly. Newborn nails are spoon-shaped
and thin and may remain so until 2 or 3 years of age.

SUBCUTANEOUS FAT

24
The subcutaneous fat lies just beneath the dermis and is composed
principally of lipocytes. It serves as a cushion to trauma, a heat insulator,
and a highly important source of energy and hormone metabolism. Premature
infants have poorly developed subcutaneous tissues, contributing to thermal
instability and metabolic difficulties.

DEVELOPMENT OF SKIN
Periderm
Knowledge of the structure and function of developing fetal skin is
invaluable in understanding abnormalities observed in newborn and infant
skin. The single layer of ectodermal cells overlaying the developing fetus
interacts with the mesoderm below to form the epidermis and dermis.1,21
Through this interaction the appendages develop, and the unique properties
of skin at different body sites result.
Between 4 and 5 weeks’ gestation, the single layer of ectodermal cells
of the fetal epidermis is covered by a layer of flattened cells called the
periderm. The periderm cells expand across the developing epidermis by
active mitosis, becoming rounded, bulging cells uniformly covered by
microvilli. The stratum corneum forms beneath the periderm cells during the
fifth to sixth month. At this time, periderm cells regress and become
shrunken remnants that slough into the amniotic fluid and become one
component of the vernix caseosa.
From the morphologic characteristics it is suggested that a transport
function exists for periderm cells. The periderm may transport fluids,
electrolytes, and sugars into the developing embryo.

Epidermal Development
After 8 weeks’ gestation an intermediate cell layer develops between the
basal cells and the periderm.1,21 In time, this layer stratifies and adds
additional cell layers. By 24 weeks’ gestation, granular and cornified cells
are present on almost all regions of the body. From this time until birth, the
stratum corneum matures and thickens so that at birth, the term infant’s skin

25
barrier function is comparable to that of an adult. The premature infant’s
barrier function is more deficient the earlier the prematurity of birth.
The sequence of development of the keratins, the development of the
basement membrane zone, the development of the desmosomes,
hemidesmosomes, and the antigens of the epidermis have been
catalogued.1,21 The epidermis follows a sequence of development that is
being intensively studied to understand the cellular interactions of normal
development and the errors that occur in skin diseases.

Cells That Migrate Into the Epidermis


Although the epidermis is ectodermal in origin, cells from other sources
migrate into the epidermis. Langerhans cells are present within the
epidermis by 6 weeks’ gestation, but they may not be functionally mature
until after 12 weeks’ gestation.1,21 The melanocyte is derived from the
neural crest and migrates to the epidermis before the twelfth gestational
week. By 16 weeks’ gestation melanocytes with melanosomes capable of
synthesizing melanin are noted, and by 20 weeks’ gestation the epidermis
has its full complement of melanocytes. Merkel cells appear in the
epidermis of the fingertips, glabrous skin, and nail beds by 12 weeks’
gestation and serve as special sensory organs. These cells may develop
within the epidermis rather than being an immigrant cell as previously
thought.

Epidermal Appendages
Hair follicle or sweat gland development begins earlier in the scalp, palm,
and sole than in other body areas. The hair germ begins in the scalp by 12
weeks’ gestation as a proliferation of keratinocytes above a collection of
fibroblasts.1,21 These cells proliferate and invaginate into the dermis,
forming the hair peg and the subsequent hair follicle. Granular cells are
present within the hair follicle after 14 weeks’ gestation, a full 6–10 weeks
before they are seen in the interfollicular skin. Hair grows at an oblique
angle to the skin surface such that hair will erupt caudally, causing the hair
to point downward.
Anlagen of eccrine glands may be present on the sole as early as 10

26
weeks’ gestation. The eccrine gland secretory coil forms on the sole at about
16 weeks’ gestation, and the secretory and myoepithelial cells differentiate
at 22 weeks’ gestation. The sebaceous gland primordia develop off the hair
follicle after 16 weeks’ gestation. Steroid hormone stimulation of sebaceous
glands is so great that these glands are considerably larger in the third
trimester fetus than those of a child. Apocrine glands, the last of the
appendages to develop, first appear during the sixth month of fetal
development.

Nails and volar pads


Development of the fetal nail, the volar pads, skin ridges, and sweat glands
are tied together in the developing digit.1,21 These structures form
simultaneously at 8 weeks’ gestation, just after the digits separate from one
another. By 12 weeks’ gestation the proximal and distal nail folds have
formed, and the volar pads are formed from mounds of mesenchyme and an
increased intermediate layer of the epidermis. The distal nail fold is the first
epithelial structure to keratinize, beginning at 12 weeks’ gestation. A nail
plate covers the nail bed by 17 weeks’ gestation. Primary dermal ridges
appear at 12 weeks’ gestation, and secondary dermal ridges at 16 weeks’
gestation.21 Sweat gland buds appear in the fingertips at 12 weeks’
gestation, but sweating does not occur until after 32 weeks’ gestation.

Influences of the Dermis on Epidermal Growth and


Differentiation
The fetal dermis plays a predominant role in transformation of the ectoderm
into epidermis and maintenance of controlled epidermal appendage
development. The continued interaction between the epidermis and dermis
maintains the continued presence of the thickened skin of the palms and
soles or the thinner skin of the face. The epidermal appendages are
maintained by epidermal–dermal interaction, and once full-thickness injury
occurs, the re-formed scar tissue appears unable to regenerate new
appendages. Skin diseases associated with thickening or thinning of the
epidermis may be associated with abnormal epidermal– dermal
communications.

27
The Dermis
The primordial dermis begins as a cellular mesenchyme that is watery and
without fibrous structure. By 6 weeks of age a fine meshwork of collagen
fibrils underlies the dermal–epidermal junction and adheres to the dermal
mesenchymal cell surfaces.1,21 Extracellular collagen increases with age,
and fibrils associate into collagen fiber bundles. Cells of the dermis become
spaced farther apart, and their elongated axes become oriented parallel to
the skin surface. The fine collagen network persists at the dermal–epidermal
junction and ensheaths epidermal appendages as they project downward.
The dermis increases in thickness from 0.1 mm at 7 weeks to 0.7 mm by 20
weeks of gestation. As the epidermal appendages project deeply into the
dermis at 16 weeks’ gestation, the dermis organizes two distinct regions: the
papillary dermis with fine fibrillar collagen and the reticular dermis with
large collagen bundles. By 20 weeks’ gestation, the fetal dermis is similar to
that of the adult in structure, although still less in total thickness. Preliminary
studies have demonstrated the 8-week-old fetus to contain fibronectin and
types I, III, and V collagen within the dermis. By 14 weeks, recognizable
fibroblasts, mast cells, endothelial cells, Schwann cells, and histiocytes are
found in the fetal dermis.21 By 60 days of gestation, anchoring filaments are
associated with the basal lamina at the dermal–epidermal junction. At 22
weeks, the elastin fibers form, but well-developed elastin fiber networks
are not observed until after 32 weeks, and the adult form of mature elastin
fibers does not occur until after 2 years of age.
Few rigorous studies have been performed on the other components of
the dermis, including vasculature, lymphatics, and nerves. Fat initially forms
with discrete areas within the dermis at 16–18 weeks, then demarcation of a
distinct fat layer that coincides with the development of hair follicles and
their projection into the lower dermis.
Overall, newborn epidermal, hair, sweat, and sebaceous structures are
nearly identical to adult structures. The dermis is less mature than adult
dermis, being thinner with less organization of collagen and elastin fibers,
with a less organized vascular network and cutaneous nerves.21 The
newborn dermis appears as a transition between fetal and adult structures.

28
REFERENCES

Goldsmith LA. Physiology, biochemistry, and molecular biology of the skin, 2nd
edn. New York: Oxford University Press, 1991.
Candi E, Schmidt R, Melino G. The cornified envelope: a model of cell death in
the skin. Nat Rev Mol Cell Biol. 2005;6(4):328-340.
Madison KC. Barrier function of the skin: ‘la raison d’etre’ of the epidermis. J
Invest Dermatol. 2003;121(2):231-241.
Slominski A, Tobin DJ, Shibahara S, et al. Melanin pigmentation in mammalian
skin and its hormonal regulation. Physiol Rev. 2004;84(4):1155-1228.
Slominski A, Wortsman J, Plonka PM, et al. Hair follicle pigmentation. J Invest
Dermatol. 2005;124(1):13-21.
Pai S, Marinkovich MP. Epidermolysis bullosa: new and emerging trends. Am J
Clin Dermatol. 2002;3(6):371-380.
Ghohestani RF, Li K, Rousselle P, et al. Molecular organization of the cutaneous
basement membrane zone. Clin Dermatol. 2001;19(5):551-562.
Canty EG, Kadler KE. Procollagen trafficking, processing and fibrillogenesis. J
Cell Sci. 2005;118(Pt 7):1341-1353.
Mithieux SM, Weiss AS. Elastin. Adv Protein Chem. 2005;70:437-461.
Galloway SD. Dehydration, rehydration, and exercise in the heat: rehydration
strategies for athletic competition. Can J Appl Physiol. 1999;24(2):188-200.
Armstrong LE, Maresh CM. Effects of training, environment, and host factors on
the sweating response to exercise. Int J Sports Med. 1998;19(Suppl 2):S103-
S105.
Kanda T. Pathological changes of human unmyelinated nerve fibers: a review.
Histol Histopathol. 2000;15(1):313-324.
Schmidt R, Schmelz M, Torebjork HE, et al. Mechano-insensitive nociceptors
encode pain evoked by tonic pressure to human skin. Neuroscience.
2000;98(4):793-800.
Jones EA, Bergasa NV. Evolving concepts of the pathogenesis and treatment of

29
the pruritus of cholestasis. Can J Gastroenterol. 2000;14(1):33-40.
Braff MH, Bardan A, Nizet V, et al. Cutaneous defense mechanisms by
antimicrobial peptides. J Invest Dermatol. 2005;125(1):9-13.
Larson AA, Dinulos JG. Cutaneous bacterial infections in the newborn. Curr
Opin Pediatr. 2005;17(4):481-485.
Rogers GE. Hair follicle differentiation and regulation. Int J Dev Biol. 2004;48(2–
3):163-170.
Van Steensel MA, Happle R, Steijlen PM. Molecular genetics of the hair follicle:
the state of the art. Proc Soc Exp Biol Med. 2000;223(1):1-7.
Schlake T. FGF signals specifically regulate the structure of hair shaft medulla via
IGF-binding protein 5. Development. 2005;132(13):2981-2990.
Kawano M, Komi-Kuramochi A, Asada M, et al. Comprehensive analysis of
FGF and FGFR expression in skin: FGF18 is highly expressed in hair follicles
and capable of inducing anagen from telogen stage hair follicles. J Invest
Dermatol. 2005;124(5):877-885.
Holbrook KA. Embryogenesis of the skin. In: Harper J, Arnold O, Prose N,
editors. Textbook of pediatric dermatology. 2nd edn. Malden, Massachusetts:
Blackwell Publishing; 2006:3-41.

30
Chapter 2

Evaluation of Children with Skin Disease

The language of dermatology frequently inhibits students, house


officers, and practitioners dealing with children from using the correct
terminology for skin disease.1 It is neither proper nor helpful to simply use
the term rash.1,2 This chapter describes the correct approach to the
presenting features, signs, and initial laboratory findings when evaluating
children with cutaneous disease. Morphology is the key to diagnosis of skin
problems, and the student of dermatology should become expert in
recognizing and describing morphologic features. The description of
primary lesions should be memorized. Particular attention should be paid to
the presence of vesicles, pustules, scaling, and color changes. These four
morphologic features will allow the identification of the major morphologic
groups, which is essential for proper diagnosis and differential diagnosis.3
A problem-oriented algorithm is included in this chapter to allow
determination of the morphologic groups of skin disease by their cutaneous
appearance. Mastering this information will aid in communication with
others delivering medical care to children.

MEDICAL HISTORY
The history obtained regarding a child’s skin condition should be
considered in the same fashion as a general medical history. The onset and
duration of each symptom should be recorded. Associated systemic
symptoms such as fever or joint pains should be sought, along with a
thorough review of systems. A past medical history, complete family history,
and information on recent medications should also be obtained.
Healthcare advice is primarily sought for children for three major

31
concerns regarding their skin: itching (pruritus), scaling, and cosmetic
appearance.

Pruritus
Persistent itching in the skin often provides the impetus to seek medical
attention. The examiner should note whether the itching is localized or
generalized and whether it is associated with skin lesions. Itching without
skin lesions suggests biliary obstruction, diabetes mellitus, uremia,
lymphoma, or hyperthyroidism. If the pruritus is associated with skin
lesions, dermatophytosis, scabies, and the many types of dermatitis should
be considered.

Scaling
Normally, one cell layer of stratum corneum, composed of flattened,
nonviable remnants of keratinocytes packed with protein (keratin) is shed
daily. This is not usually visible. Acute injury and resultant separation of
10–20 cell layers of stratum corneum result in clinically visible white
sheets of scale, such as that seen in desquamation after a sunburn or thermal
burn. Overproduction of stratum corneum by proliferating epidermis, as in
psoriasis, results in visible accumulation of excess surface scale. The scale
in psoriasis is thick in contrast to thin (pityriasis) scale.

Cosmetic Appearance
Parents may be concerned about the appearance of a child’s skin,
particularly any color change. A history of the time of appearance of skin
lesions, sequence of color changes, and course of skin changes should be
obtained.

EXAMINATION OF THE SKIN


The evaluation of skin lesions requires careful inspection of the entire
cutaneous surface, and many skin diseases are diagnosed only by their
morphologic appearance.1-3 Examination of the skin should consist of

32
identification of the primary lesion (the earliest lesion to appear), the size
or range of the primary lesion in millimeters, secondary changes, and a
description of the color, arrangement, and distribution of lesions. Often,
however, one sees children with secondary skin changes without primary
lesions. For correct diagnosis, a rigorous search should be made for a
primary lesion. To properly evaluate the primary lesion, both visual
inspection and palpation are required. Palpation should determine whether
the lesion is hard or soft, and whether it moves with the skin or the skin
moves over it.

Primary Skin Lesions (The Morphology of Skin)


1. A macule (Fig. 2.1A,B,C) is a color change in the skin that is flat to the
surface of the skin and not palpable (e.g. a tan macule, café-au-lait spot,
white macule, vitiligo).
2. A papule (Fig. 2.2A,B,C) is a solid, raised lesion with distinct borders 1
cm or less in diameter (e.g. lichen planus, molluscum contagiosum).
3. A plaque is a solid, raised, flat-topped lesion with distinct borders and
an epidermal change larger than 1 cm in diameter (e.g. psoriasis).
4. A nodule (Fig. 2.3A,B,C) is a raised, solid lesion with indistinct borders
and a deep palpable portion. A large nodule is termed a tumor (e.g.
rheumatoid nodule, neurofibroma). If the skin moves over the nodule, it is
subcutaneous in location; if the skin moves with the nodule, the nodule is
intradermal.
5. A wheal (Fig. 2.4A,B,C), an area of tense edema in the upper dermis,
produces a flat-topped, slightly raised lesion (e.g. urticaria).
6. A vesicle (Fig. 2.5A,B,C) is a raised lesion filled with clear fluid that is
less than 1 cm in diameter (e.g. varicella, herpes simplex).
7. A bulla (Fig. 2.5D) is a raised lesion larger than 1 cm and filled with
clear fluid.
8. A cyst (Fig. 2.6A,B,C) is a raised lesion that contains a palpable sac
filled with solid material (e.g. epidermal cyst, dermoid cyst).
9. A pustule (Fig. 2.7A,B,C) is a raised lesion filled with a fluid exudate,
giving it a yellow appearance (e.g. acne, folliculitis).

33
Fig. 2.1 (A) A macule is a color change in the skin that is flat to the surface
of the skin and not palpable (e.g. a tan macule, café-au-lait spot, white macule,
vitiligo). (B) A tan macule on the trunk of a child with neurofibromatosis I
(café-au-lait macule). (C) A white macule on a child with tuberous sclerosis
(ash-leaf macule).

34
Fig. 2.2 (A) A papule is a solid, raised lesion with distinct borders 1 cm or
less in diameter (e.g. lichen planus, molluscum contagiosum). (B) Skin-colored
papules on the forehead of a child with trichoepitheliomas. (C) A bleeding red
papule on the chin of a child (pyogenic granuloma).

35
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spelling, manifestly the attempt would be to measure the changes
which have been brought about in any group in terms of units which
are comparable. If group one shows ability ten, having advanced
during the year from ability seven, it will be considered just as
satisfactory as the advance which has been made in group two,
which has moved from ability eight to ability eleven. In other words,
the purpose of measurement is never to attempt to make all alike. It
is rather to discover differences and the reason for their existence;
but most of all to give us some adequate means of determining
progress or change.
Let us suppose again, in a matter of business administration, that
one school shows a much higher per capita cost than another. This
does not prove that one school is more efficiently managed than
another. What it does do is to suggest that some adequate reason is
to be found for the difference which exists. In like manner, one city
may show a much higher cost for janitors’ salaries than does
another. This may suggest investigation, but it does not prove that
the city with the higher cost for janitors’ service is inefficiently
managed or extravagant in its expenditures. It may be that the city
that spends a relatively large amount for janitorial service actually
gets more per dollar for the money which it spends than does the city
with the smaller cost. It is always a purpose of measurement to
discover discrepancies and to raise problems.
It has been contended that it is not important to derive scales or
units of measurement on the ground that the scientific study of
education is significant only in so far as it has to do with a careful
investigation of the processes involved in growth. Those who make
this contention seem to feel that a careful study of the way in which
children come to form habits, to grow in power of reasoning, or in
ability to appreciate, will give us the final answer concerning the
methods to be employed in teaching. The difficulty with this point of
view is that human beings, even though they be trained in
investigation, are fallible. The only final test of the success of any
method, however carefully derived, and however much of it may
depend upon a knowledge of the processes involved in growth in the
particular aspect of mental life which is involved, is to be found in the
result achieved. Theoretically a method may seem to be perfect, and
yet in terms of the results which are secured it may prove to be a
failure. If the results are not accurately measured, if we do not derive
scales of measurement, we can never be certain of our conclusions
with regard to the method to be employed in bringing about any
particular type of mental growth or development.
Possibly the one element in the situation which has operated to
retard development in the direction of accurate measurement of
results, more than any other, is the tendency in education to appeal
to authority, and the corresponding lack of devotion to scientific
investigation. It is, of course, much easier to solve the problems
which one meets by taking the opinion of those who have had
experience in the field. No one would deny the value of the judgment
of our great educational leaders. The fact remains, however, that
these same leaders would be the last ones to place their own
opinion in opposition to the results obtained from a careful scientific
investigation. Indeed, it is in no small measure due to the insistence
of these leaders that we are coming to have adequate investigations
with regard to our educational practice.
It has seemed necessary to discuss at some length the objections
which have been made against the attempt to measure results in
education, rather than to devote more space to a discussion of the
work which has already been done. All students of education are
familiar with the early work of Rice, and with the later contributions of
Thorndike, Ayres, Cornman, and many others who have contributed
to the literature of educational investigation. Possibly the most
significant piece of work that has been done is Thorndike’s scale for
measuring handwriting.[32] We may reasonably hope to have scales
derived for the measurement of abilities in other subjects.
In administration, considerable work has already been done with
reference to the cost of education, both as regards the relationship of
expenditure for education to other expenditures, the question of a
proper distribution of money within the educational budget, and of
the proper distribution of state school funds.[33] We can, of course,
hope for much more significant work in this field as more adequate
systems of accounting are introduced and more satisfactory reports
are issued. It is noteworthy that in those school systems in which an
attempt has been made to check up expenditures carefully,
remarkable savings have been made. We have not yet reached the
limit of possible reduction of expenditure without the sacrifice of our
present efficiency. Much work has been done on problems of school
organization, yet the problems of retardation and elimination will be
satisfactorily treated only as we secure more accurate records
concerning attendance, scholarship, health, promotions, and
demotions, such as are provided for by the genetic records now kept
in some of our more progressive school systems. The problems of
departmental work and individual instruction can never be
satisfactorily solved until we measure accurately the results secured
under different systems of organization.
Implicit in all of the argument which has been advanced in favor of
measuring results is the contention that education means change. If
changes are brought about in the children who are being educated,
then there must be the possibility of measurement. These changes
may take place in habit, in knowledge, in methods of work, in
interests and ideals, and in power of appreciation. Probably no one
would question the possibility of measuring the change which takes
place in the formation of habits. We have quite commonly been
willing to measure growth in knowledge by tests which demand that
students not only remember facts, but that they show some ability to
apply them. Whether or not a student commands a particular method
of work can be determined by observation of his method of
procedure as well as by the results that he secures. If interests or
ideals are changed, there necessarily follows a change in activity.
Any real power of appreciation will be accompanied by some change
in expression.
The fact that we do not yet have scales or units of measurement
which will enable us to evaluate accurately the results obtained in all
of the different forms of school activity is not an argument against the
possibility of measurement. In any field the development of units of
measurement is dependent upon careful investigation, and upon a
realization of the imperfection of the units already used. It is only as
we insist upon measurement that we can hope to have our units
refined. Take for example the problem of grades or marks which are
commonly assigned to students as a measure of their efficiency in
doing school work. Any investigation of these units will show that
there is very great variation in their application by different members
of the teaching corps.
The way to bring about a remedy is not to abolish all marks or
grades, but rather to study the problem of the proper distribution of
marks, and, if necessary, to weigh differently the marks of different
instructors. The more imperfect the unit of measure which we now
apply, the greater the need for insisting upon accurate measurement.
The first step in the development of scientific inquiry in any field is
found in accurate description of the phenomena involved. The
demand that we measure results in education is simply a demand
that the basis for scientific investigation be made available by means
of this accurate description of the situation as it exists. Some
investigators in education have already been able to take the further
steps in scientific inquiry which have enabled them to foretell with
considerable accuracy the results which might be expected in
education under given conditions. Further progress is, however,
dependent upon that sort of measurement which will discover
problems which are not now clearly defined or which have not yet
been thought of. Of course, as inferences are made in the light of the
problems suggested, there will be still further necessity for accurate
measurement. When those who are charged with the responsibility
of determining educational policy appeal to fact rather than to
opinion, when we are able to evaluate accurately that which we
achieve, educational progress will be assured and a profession of
education will have been established.
We shall always have most excellent work in teaching done by
those for whom scientific investigation, as such, means little. The
investigations made will, however, modify the practice of these same
teachers through changed demands and because of the
demonstration of the validity of the new method of work by those
who can appreciate the significance of results achieved by
investigators. It is certainly to be expected that open-minded
teachers will experiment for themselves and will aid in the work of
the expert who must use the schools as his laboratory. Much
depends upon the coöperation and good will of all who are engaged
in teaching. It is not too much to expect that the spirit of investigation
will be found in large measure to characterize those whose privilege
it is to provide the situation in which intellectual development is
stimulated.
An example of a study involving the coöperation of the pupils,
teachers, and supervisory officers of twenty-six separate schools or
school systems is Dr. C. W. Stone’s study on Arithmetical Abilities
and Some of the Factors Determining them. The following quotations
from Dr. Stone’s study indicate the type of result which we may hope
to get from such investigations.

In Reasoning
The scores for the reasoning problems were determined from the results of two
preliminary tests—one, giving one hundred 6th grade pupils all the time they
needed to do the problems as well as they could in the order as printed (see page
11); and another, giving one hundred 6th grade pupils all the time they needed to
do the problems as well as they could in the reverse order from that as printed.
The results as tabulated below in table II show that scores for reasoning problems
of Grade VI pupils can be very definitely arranged in a scale on the basis of
relative difficulty. Just what the scale should be can only be determined by
determining the form of distribution and the location of the zero point. From what is
known of these the scale of weighting shown in the last column of table II is
believed to be the best, and this is the one employed in the computations of this
study. However, in order to enable the reader to satisfy himself as to which is the
best method, the scores of the twenty-six systems were calculated on each of
three other bases—(1) counting each problem reasoned correctly a score of 1; (2)
counting each problem reasoned correctly a score based on the ratio of its
difficulty as shown in the next to the last column of table II; and (3) counting the
scores made on only the first six problems for which presumably all pupils of all
systems had ample time. See Appendix, p. 98.
In both reasoning and fundamentals the scores used as a measure of the
achievement of a system were computed by combining the scores of one hundred
pupils. Where more than one hundred pupils were tested, the papers used were
drawn at random, the number drawn from each class being determined by the ratio
of its number to the total number tested in the system. Where less than one
hundred pupils were tested, the combined scores made were raised to the basis of
one hundred pupils.

TABLE II
PRELIMINARY TESTS
Reasoning—Unlimited Time
100 Different Pupils Tested Each Time

% Reasoned % Reasoned Average % Weight According


Number of Weight Used as
Correctly as Correctly as Reasoned to Average %
Problems Probably the Best
Printed Reversed Correctly Correct
1 95 92.6 93.8 1 1
2 86 82.2 84.1 1.1 1
3 94 89 91.5 1 1
4 80 83 81.5 1.5 1
5 88 86 87 1.1 1
6 69 57.4 63.2 1.5 1.4
7 70 80 75 1.25 1.2
8 29 44 36.5 2.6 1.6
9 19 15.5 17.2 5.45 2
10 24 27.4 25.7 3.6 2
11 17 7.5 12.3 7.6 2
12 7 16.4 11.7 8 2

Precautions observed to make the Scoring Accurate


The simplicity of the tests made the scoring comparatively easy; and with the
observance of the following precautions it is believed that a high degree of
accuracy was attained. (1) In so far as practicable, all the papers were scored by a
single judge—only two persons being employed on any phase of the work for the
entire twenty-six systems; (2) each problem was scored through one hundred or
more papers, then the next followed through, etc.; (3) the score for each part of
each problem, the errors, etc., were entered on a blank provided with a separate
column for each item; (4) where there was doubt as to how the score should be
made, the scorer made a written memorandum of how the case was finally
decided and this memorandum served as the guide for all future similar cases.

What the Scores Measure


As used in this study the words achievements, products, abilities, except where
otherwise qualified, must necessarily refer to the results of the particular tests
employed in this investigation. That some systems may achieve other and possibly
quite as worth-while results from their arithmetic work is not denied; but what is
denied is that any system can safely fail to attain good results in the work covered
by these particular tests. Whatever else the arithmetic work may produce, it seems
safe to say that by the end of the sixth school year, it should result in at least good
ability in the four fundamental operations and the simple, everyday kind of
reasoning called for in these problems. It does not then seem unreasonable, in
view of the precautions previously enumerated, to claim that the scores made by
the respective systems afford a reliable measure of the products of their respective
procedures in arithmetic.

The Data
The source of the data used to help answer the above questions is some six
thousand test papers gathered from twenty-six representative school systems.
Copies of the tests may be found in Part I, pages 10 and 11; as may also a
statement of conditions under which the tests were personally given by the author,
page 13; and the method of scoring, pages 15 to 18.
The achievements are considered from two standpoints—(1) the scores and
mistakes of the systems as systems, (2) the scores of individual pupils as
individuals.
Table III gives the scores made in reasoning by each of the twenty-six systems,
counting all the problems that were solved, and weighting them according to the
last column of table II. The Roman numerals used in the left-hand column to
designate the systems are those that fell to each system by lot. As seen by the
column headed scores made, the systems are arranged according to number of
scores, i.e. system XXIII made three hundred fifty-six points, the lowest score, and
is placed first in the table; system XXIV made four hundred twenty-nine points, and
is placed second, etc. System V, having made the highest score, is placed last in
the table.
ACHIEVEMENTS OF THE SYSTEMS AS SYSTEMS
Measured by Scores Made
TABLE III[34] TABLE IV

Scores of the Twenty-six Systems in Reasoning with Scores of the Twenty-six Systems in Fundamentals
Deviations from the Median. Scores from all with Deviations from the Median. Scores from all
Problems Problems
M[35] = 551 M = 3111
Devia- Devia- Devia- Devia-
Systems in Scores tions from tions in Per Systems in Order Scores tions from tions in Per
Order of [36] the Cent of the of Achieve- ment Made the Cent of the
Achieve- ment Made
Median Median Median Median
XXIII 356 -195 -35 XXIII 1841 -1270 -41
XXIV 429 -122 -22 XXV 2167 -944 -30
XVII 444 -107 -19 XX 2168 -943 -30
IV 464 -87 -16 XXII 2311 -800 -26
XXV 464 -87 -16 VIII 2747 -364 -12
XXII 468 -83 -15 X 2749 -362 -12
XVI 469 -82 -15 XV 2779 -332 -11
XX 491 -60 -11 III 2845 -266 -8
XVIII 509 -42 -8 I 2935 -176 -6
XV 532 -19 -3 XXI 2951 -160 -5
III 533 -18 -3 II 2958 -153 -5
VIII 538 -13 -2 XVII 3042 -69 -2
VI 550 -1 -2 XIII 3049 -62 -2
I 552 1 2 VI 3173 62 2
X 601 50 9 XI 3261 150 5
II 615 64 12 IX 3404 293 9
XXI 627 76 14 XII 3410 299 10
XIII 636 85 15 XXIV 3513 402 13
XIV 661 110 19 XIV 3561 450 14
IX 691 140 20 IV 3563 452 14
VII 734 183 33 V 3569 458 15
XII 736 185 34 XXVI 3682 571 18
XI 759 208 38 XVI 3707 596 19
XXVI 791 240 44 XVIII 3758 647 21
XIX 848 297 54 VII 3782 671 22
V 914 363 66 XIX 4099 988 31

The middle column gives the deviations from the median, which is that measure
above and below which one half the cases lie. In this table the median is five
hundred fifty-one. These deviations serve to show the differences in scores made;
and they are also employed in computing the measures of variability and
relationship. The third column is the deviations in per cent of the median. It affords
another expression of the difference in size of scores made by the systems.
Table IV reads exactly as III, the scores[37] being those made on all problems of
the test in fundamentals. These two tables give some general help on the nature of
the product of the first six years of arithmetic work. One very evident fact is the
lack of uniformity among systems; another is the lack of correspondence of relative
position among the systems in the two tables. With the exception of systems XXIII
and XIV, no system occupies the same relative position in the two tables, e.g.
system XXIV stands second from the lowest in reasoning and eighteenth from the
lowest in fundamentals. This fact is more accurately summarized in the coefficients
of correlation, table XV, p. 37.
As seen from its heading, table XXII gives the systems in order of achievements.
These serial standings are derived from tables III and IV. Reading from the top,
system XXIII has an average serial standing of one, being lowest in both reasoning
and fundamentals; system XXV ranks three in average serial standing, being
fourth from lowest in reasoning and second from lowest in fundamentals; the
readings for the other systems are similar.
Column Heading Keys:
Sys = Systems
A = Average serial standing
B = Serial standing in reasoning
C = Serial standing in fundamentals
D = Serial standing in time expenditure
E = Week minutes devoted to arithmetic
F = Week minutes devoted to all subjects
G = % of time to arithmetic

TABLE XXII TABLE XXIII TABLE XXIV

Time Distribution among Grades


Comparative Comparative Time
Lower numbers show week minutes devoted to
Sys Achievements Expenditure
arithmetic; upper show % of school time devoted to
arithmetic in each grade
A B C D E F G I II III IV V VI
7 6 12 15 15 15
XXIII 1 1 1 14 1150 9675 12 100 100 200 250 250 250
7 9 10 9 13
XXV 3 4 2 2 722 8700 8 .. 100 140 155 130 197
8 8 8 7 11
XXII 4½ 5 4 1 507 7200 7 .. 90 90 90 90 147
7 10 12 14 15 15
XX 5 7 3 15 1161 8200 14 80 113 210 240 265 253
2 12 20 20 24 23
XVII 7½ 3 12 21 1283 7500 17 27 158 250 258 300 290
2 14 15 15 15 15
VIII 8 11 5 18 1258 9600 13 25 233 250 250 250 250
11 15 20 17 18
XV 8 9 7 16 1173 8025 15 .. 147 213 292 250 271
10 9 11 11 12 16
III 9 10 8 6 944 8025 12 125 125 150 150 165 229
14 17 17 17
XXIV 10 2 18 7 950 8775 11 .. .. 200 250 250 250
7 12 12 14 18
X 10 14 6 5 921 8550 11 .. 88 154 184 216 279
9 13 14 14 15
I 11 13 9 9 1068 9375 11 .. 130 213 238 238 249
28 20 20 24 20 23
IV 12 4 20 26 1854 8400 22 249 300 306 361 300 338
8 12 14 14 15 16
II 13 15 11 17 1247 9900 13 121 192 217 225 233 259
8 10 10 12 14 13
XXI 13 16 10 4 865 7650 11 80 100 100 180 210 195
8 12 18 18 19
VI 13 12 14 11 1126 9000 13 .. 127 177 266 266 290
5 8 13 18 17 16
XVI 14½ 6 23 12 1127 9000 13 75 113 187 263 251 238
26 23 18 19 19
XIII 15 17 13 25 1626 8475 19 .. 388 350 288 300 300
XVIII 6 5 15 20 20 19
16 8 24 19 1265 8700 15 75 75 225 300 300 290
13 15 18 18 18 21
IX 17½ 19 16 22 1559 9000 17 200 225 275 275 275 309
11 15 18 18 18
XI 18½ 22 15 10 1130 8575 13 .. 157 216 250 250 257
15 16 18 19 19 19
XIV 18½ 18 10 23 1560 8850 18 225 245 270 280 270 270
6 18 16 19 19
XII 19 21 17 13 1148 8400 14 .. 81 226 255 288 298
7 10 10 13 13 17
XXVI 22½ 23 22 3 837 7200 12 80 125 125 150 150 207
13 19 22 22 22 17
VII 22½ 20 25 24 1573 7800 20 175 262 300 300 300 236
8 10 11 12 13 13
V 23 25 21 8 971 8700 11 113 154 167 175 183 179
8 10 17 17 13 20
XIX 25 24 26 20 1276 9000 14 125 150 250 250 250 301

.. = no time assigned.

Tables XXIII and XXIV keep the same order of systems and show the time
expenditure. The first line of table XXIII reads,—system XXIII ranks fourteenth
from the lowest in time expenditure, with 1150 week minutes devoted to arithmetic,
9675 week minutes devoted to all subjects, the 1150 week minutes devoted to
arithmetic being 12 per cent of the 9675 week minutes devoted to all subjects.
Similarly for the other systems, e.g. system XXV with a serial standing in abilities
of three, and a serial standing in time expenditure of two, spends 722 week
minutes on arithmetic, and 8700 week minutes on all subjects, arithmetic costing 8
per cent of all the school time. The reader will recognize that the third column,
which gives the time devoted to all subjects for one week of each of the first six
years, gives the only new data of this table, column two being the same as given in
table XXI and the first and fourth columns being derived from the others.
Probably the first essential shown by this table is the lack of correspondence
between the serial standing in time cost and the serial standing in abilities; e.g. the
system with the lowest time cost is found by referring to table XIII to be system
XXII, which is seen in table XXII to rank four and one-half in average abilities.
Similarly, the system that ranks fifteenth in time cost, ranks fifth in abilities, etc.
Another noticeable showing is the wide variability in the school time of the
systems. It will be seen to vary from 7200 to 9900 week minutes. This time
includes recesses, and it means that lengths of school days vary from an average
of four hours to five and one-half hours. And if the names of the systems were
given, it would be recognized that almost invariably the longer school hours are
accompanied by the least amount of variation in program, such as physical
education, field trips, assemblies, etc. Perhaps the other most striking fact of this
table is the wide variation in the per cent of time devoted to arithmetic. It varies
from 22 per cent for system IV to 7 per cent for system XXII, a difference of more
than three to one.
As table XXIV is part of the discussion of factors in time expenditure, its sample
readings are given under that heading, page 62.

The Relation of Time Expenditure to Abilities Produced


The reader found one indication of the relation, or lack of relation, between time
cost and products in tables XXII and XXIII. Each of the three following tables
expresses these same facts.

TABLE XXV
Comparison of the Achievements of the Systems having Less than
Median Time Cost with those having More

Combined Scores of the Thirteen Systems


With less than With more With less than With more
median time than median median time than median
cost time cost cost time cost
Including home study Without home study

Reasoning 7,519 7,893 7,277 8,135


Fundamentals 40,751 40,273 37,165 43,859
TABLE XXVI
Ratio of Time Expenditures to Abilities[38]

Average Ratios Reasoning Ratios Fundamental Ratios


Time Cost to
Systems Serial Serial Serial
Reasoning and Time Cost to Time Cost to
Standing of Standing of Standing of
to Reasoning Fundamentals
Systems Systems Systems
Fundamentals
IV 1 2.26 1 3.99 4 .520
XXIII 2 1.92 2 3.22 1 .624
XVII 3 1.65 3 2.88 7 .421
XIII 4 1.54 4 2.55 3 .533
XX 5 1.45 7 2.36 2 .535
XVIII 6 1.41 5 2.48 13 .336
XIV 7 1.40 7 2.36 6 .438
VIII 8 1.39 8 2.33 5 .457
IX 9 1.353 9 2.25 5 .457
XVI 10 1.352 6 2.40 18 .304
XV 11 1.31 11 2.20 8 .422
VII 12 1.28 12 2.14 9 .415
XXIV 13 1.24 10 2.21 21 .270
II 14 1.22 14 2.02 7 .421
VI 15 1.20 13 2.04 11 .354
I 16 1.15 15 1.93 10 .363
III 17 1.05 16 1.77 16 .331
XII 18 0.943 17 1.55 13 .336
XXV 19 0.941 17 1.55 15 .333
X 20 0.93 18 1.53 14 .335
XI 21 0.913 20 1.48 12 .346
XIX 22 0.91 19 1.50 17 .311
XXI 23 0.83 21 1.37 19 .293
V 24 0.67 23 1.06 20 .272
XXII 25 0.65 22 1.08 23 .219
XXVI 26 0.64 24 1.05 22 .227

The above details are compiled from the scores of individual systems as given in
tables III and IV, the median cost being that given in table XXI. As measured by the
time used in school, the thirteen systems with less than the median cost stand
slightly the better; and as measured by the time including home study, the thirteen
systems with more than the median time cost stand somewhat the better. The time
used in school is doubtless the more exact measure, but, as shown in table XXI,
some systems depend on home study to a considerable extent. Hence both
measures are used. The lack of relation indicated in this general way is shown
more accurately in the table, page 263, in terms of coefficients of correlation.
The order of systems in this table is determined by the first column, which gives
the average serial standing as determined by the ratios of time to products. The
right-hand column under each heading gives the ratio of time expenditure to
abilities produced, and the left-hand column gives the serial order of that system
as measured by the highness of the ratio, i.e. highness of cost per unit of product;
e.g. in system IV the ratio of time to reasoning is 3.99 (see fourth column), the
highest ratio in reasoning (determined by dividing the time cost, 1854 week
minutes, by 464, the points made in reasoning). The ratio of time to fundamentals
in this system is .52; giving an average ratio of 2.26. That is to say, the ratio of time
to abilities in system IV is as 2.26 to 1, the highest among the twenty-six systems.
That there is no direct ratio between time expenditure and abilities is again
shown by this table. For example, system XXII, which spends the least amount of
time (see table XXI), ranks fourth from the lowest in abilities (see table XXII), ranks
25th, that is, next to the highest, in ratio of time cost to abilities produced; and,
what is even more striking, system XXVI, which spends third from the least amount
of time, ranks third from the highest in abilities and 26th or highest in the ratio of
time cost to abilities produced.
That a large amount of time expended is no guarantee of a high standard of
abilities may again be convincingly seen by comparing the ratios of the five
systems spending the smallest amount of time with the five spending the largest.
Of the five spending the least time, the average ratio is .80, which corresponds
with the 23d or the 3d from the best in ratio; and of the five spending the greatest
amount of time, the average ratio is 1.57, which corresponds with the 4th poorest
in ratio.
The last three tables have each shown the decided lack of relationship between
time cost and abilities produced, and hence for these systems it is evident that
there is practically no relation between time expenditure and arithmetical abilities;
and, in view of the representative nature of these twenty-six systems, it is probable
that this lack of relationship is the rule the country over.
This is not to say that a certain amount of time is not essential to the production
of arithmetical abilities; nor that, given the same other factors, operating equally
well, the product will not increase somewhat with an increased time expenditure.
What is claimed is that, as present practice goes, a large amount of time spent on
arithmetic is no guarantee of a high degree of efficiency. If one were to choose at
random among the schools with more than the median time given to arithmetic, the
chances are about equal that he would get a school with an inferior product; and
conversely, if one were to choose among the schools with less than the median
time cost, the chances are about equal that he would get a school with a superior
product in arithmetic.[39]
So far, then, as ability in arithmetic means ability to handle such foundation work
as is measured by the tests in this study, this “essential” has not necessarily
suffered by the introduction of other subjects and the consequent reduction of its
time allotment.
One would need to read the whole study to appreciate fully the
nature of the investigation. From the pages quoted, however, it must
be apparent that: (1) schools and school systems vary greatly in the
results which they secure in arithmetic; (2) the excellence of the work
done is not directly proportional to the time expended. We will find it
necessary to revise our opinions with regard to the organization of
school subjects, the allotment of time, the methods of teaching, and
the like, in proportion as we have careful investigation in these
several fields.

For Collateral Reading


E. L. Thorndike, The Principles of Teaching, Chapter XVI.
APPENDIX

I . T H E T E A C H I N G O F E N G L I S H I N E L E M E N TA RY S C H O O L S

By Franklin Thomas Baker, A.M.

I. Historical View of the Subject

1. The Choice of Reading Matter.


1. The school reader an expression of social ideals.
2. German primers and readers of the sixteenth and seventeenth centuries.
3. The “moral tales” of the eighteenth century.
4. The New England Primer.
5. The oratorical and patriotic selections of the early nineteenth century.
6. The school readers of to-day; their general characteristics.
2. Method.
1. The alphabetic method in use until modern times.
2. New ideas in the sixteenth century and later. Work of Ickelsamer, Basedow,
Pestalozzi, Comenius, and Jacotot.
3. Gradual ascendency of the analytic over the alphabetic (or synthetic)
method.
4. Recognition of the importance of phonetics, of association of ideas, etc.
References: Kehr, Geschichte des Lese-Unterrichts in der Volksschule, Gotha,
1889. Fechner, Geschichte des Volksschullesebuches, Gotha, 1889. Ford, The
New England Primer, New York, 1897. Reeder, Historical Development of the
School Reader, New York, 1900. Hall, How to Teach Reading, New York, 1886.
American Journal of Education, Vol. V., Hartford and London, 1858. Russell,
German Higher Schools, New York, 1900. Carpenter, Baker, and Scott, The
Teaching of English, New York, 1903. Huey, Psychology and Pedagogy of
Reading, New York, 1908.

II. First Steps in Instruction

1. Material.
1. Material should be (1) interesting, (2) literary, so far as possible, (3)
adapted to the capacities and tastes of children, (4) of enough difficulty and
sufficiently above their own ordinary thoughts to have value as instruction.
2. The best material (1) folk stuff, such as the classic fairy tales, Mother
Goose, etc., (2) tales of heroism and sacrifice, (3) poetry of the simpler type, like
that of Stevenson and Christina Rossetti.
3. Much of the language work should be free conversation between the
teacher and the children about their ordinary experiences.
2. Method.
1. During the first years much of the literary material must be given orally by
the teacher. Oral work is to be held of great importance.
2. Children to be encouraged to commit good things to memory.
3. All reading aloud by the pupils to be done as naturally as possible.
Importance of reading by phrases and sentences, rather than word by word.
4. Value of the dramatic element in early work.
5. The conflict between the “word method” and the “sentence method” over.
Modern teaching eclectic in method. If any name can be given to the best way, it
might be, perhaps, “thought method.”
6. Use of script and print: advantages of each as a first form. Value of printed
cards and other devices for drill.
7. Form of type for beginners’ books: not too large; letters to have all
differentiating marks distinct. Importance of right kind of paper, width of columns,
etc. Kinds of pictures most serviceable.
8. When shall writing begin? In general not to be forced on the child in the first
year. Arguments for and against this arrangement. Should there be any fixed
standard of accomplishment for the first year?
9. Phonetic drill. How many words must be known before it begins? Various
plans equally successful. The main thing, perhaps, is to have drill enough to give
the pupils certainty in their work, but to keep the drill subordinated to their
interest in reading.
10. The order of such drill. “Normal words,” chosen for their meaning, their
frequency of occurrence, and their similarity in form to other words either at their
beginning or at their end. Many words, however, must be learned without
relation to such a scheme.
11. “Normal sentences” those that partially help the reader to the recognition
of words; as, “The sun rises in the east, and sets in the west.” For young
children, sentences involving the use of repetitive phrases must also be
regarded as normal, as in “The House that Jack Built.”
12. In general, both analysis and synthesis to be used in word drill.
13. Importance of securing good habits as to intelligent reading, correct
spelling, etc., in the early years. Children can usually do better than they or their
elders think they can.
14. Emphasis to be placed upon reading many of the good things over and
over, until they are known in whole and in part.
References: Bryant, How to tell Stories to Children. Carpenter, Baker, and
Scott, The Teaching of English. Chubb, The Teaching of English. Colby, Literature
in Life and in School. Hall, How to teach Reading. Hinsdale, Teaching the
Language Art. Huey, Psychology and Pedagogy of Reading. Arnold, Reading, How
to teach it. Laurie, Language and Linguistic Method. Dewey, “The Primary
Education Fetich,” in The Forum, May, 1898. Dewey, The School and Society.
Dye, Story-Teller’s Art.

III. The Teaching of Literature

1. General Problems.
1. Can literature be taught? Or can pupils “be taught through literature”?
Examples of such educational use of literature.
2. Present aims in teaching literature: entertainment, portrayal of life,
acquaintance with the world of thought and feeling as presented in books,
cultivation of imagination and sense of beauty.
3. True interpretation implies grasping the central purpose, idea, or feeling of
the piece.
4. Various types of literature demand various treatment. Necessity of adapting
the treatment to the class.
5. Taste (sense of beauty) developed mainly by contact with good models.
Instruction plays a minor part. The love of good reading fostered by judicious
selection of material, and by example and influence.
6. How can the habit of good reading be cultivated?
2. Material.
1. The literature chosen must be suitable in its themes, its action, its feeling,
its simplicity.
2. Literary histories and biographies: their limited value in elementary work.
3. Scientific and historical material in literature. Literary use of such material
not to be confounded with science and history.
4. Pictures and other illustrative material: Sometimes give intuitive basis for
desired concepts; sometimes interfere with the imagination.
3. Method.
1. Reading aloud: its value. Means of securing good results; interest, sense of
reality, consciousness of an audience.
2. Analytic study, of content, form, and general literary effects.
a. Must be adapted to the pupil’s interest and his stage of development.
b. Must yield results of value appreciable by the pupil.
c. Effects of too much or too little such study.
3. Correlation of literature with other work possible in limited degree. A matter
of class treatment rather than of the general arrangement of the course of study.
A problem for the teacher rather than the principal.
4. Treatment of allusions, historical, literary, etc. The need of judicious
selection.
5. Treatment of figures of speech, verse forms, new words, etc.
6. Lesson plans: their function and value.
a. An outline should control and direct the work, yet be flexible enough to
allow freedom on the part of teacher and pupil.
b. Introductions: their nature and function. When necessary.
References: Carpenter, Baker, and Scott, Laurie, Chubb, Hinsdale, Arnold and
Hall, as cited. Scudder, Literature in Schools. C. A. McMurry, Special Method in
Reading. Bates, Talks on the Study of Literature. Colby, Literature in Life and in
School. Adler, Moral Instruction of Children.

IV. Study of Certain Typical Books

1. Nursery Rhymes (as Mother Goose, Stevenson’s Child’s Garden of Verses).


a. The nature of their appeal to children in sound, imagery, and ideas.
b. Their value in training the ear, the powers of speech, etc.
2. Grimm’ “Fairy Tales.”
a. Their source and relation to other folklore.
b. The marvelous, and its effect on children.
c. Action, logical sequence, local color.
d. Various types of myth.
e. The ideal element, poetic justice, etc. Need the harsher elements be
omitted?
f. Typical lessons.
3. “Alice in Wonderland.”
a. Its origin and its place in literature.
b. The nature of its reality: based upon things in the child’s world of
imagination.
c. Its value as humor, as a means of quickening the power of thought.
d. What preparation is needed for the appreciation of it?
e. Typical lessons.
4. “Robinson Crusoe.”
a. Its origin and place in literature.
b. Fundamental characteristics as a piece of fiction.
c. Elements in it that appeal to children, or fail so to appeal.
d. Justification of the abridged editions.
e. Its relation (1) to the world of romance, (2) to real life.
f. How best presented. Typical lessons.
5. Longfellow’s “Hiawatha.”
a. Its origin, form, popularity.
b. Its qualities, epic and romantic.
c. Its treatment of the myth.
d. Its value as school reading; parts best suited for this.
e. General value of reading about primitive life.
f. Relation to handwork, etc.
6. Hawthorne’s “Wonder Book” and “Tanglewood Tales.”
a. Their origin and general literary qualities.
b. Romantic coloring given to classic stories; compare Kingsley’s The
Heroes, and Bulfinch’s Age of Fable, and other versions of the
myths.
c. Different types of myth and fairy story represented.

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