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TABLE 8-1 -- Developmental Milestones in the First 2 Yr of Life

Holds head steady while sitting 2 Allows more visual interaction
Pulls to sit, with no head lag 3 Muscle tone
Brings hands together in midline 3 Self-discovery of hands
Asymmetric tonic neck reflex gone 4 Can inspect hands in midline
Sits without support 6 Increasing exploration
Rolls back to stomach 6.5 Truncal flexion, risk of falls
Walks alone 12 Exploration, control of proximity to parents
Runs 16 Supervision more difficult
Grasps rattle 3.5 Object use
Reaches for objects 4 Visuomotor coordination
Palmar grasp gone 4 Voluntary release
Transfers object hand to hand 5.5 Comparison of objects
Thumb-finger grasp 8 Able to explore small objects
Turns pages of book 12 Increasing autonomy during book time
Scribbles 13 Visuomotor coordination
Builds tower of 2 cubes 15 Uses objects in combination
Builds tower of 6 cubes 22 Requires visual, gross, and fine motor coordination
Smiles in response to face, voice 1.5 More active social participant
Monosyllabic babble 6 Experimentation with sound, tactile sense
Inhibits to no 7 Response to tone (nonverbal)
Follows one-step command with gesture 7 Nonverbal communication
Follows one-step command without gesture 10 Verbal receptive language (e.g.,Give it to me)
Says mama or dada 10 Expressive language
Points to objects 10 Interactive communication
Speaks first real word 12 Beginning of labeling
Speaks 46 words 15 Acquisition of object and personal names
Speaks 1015 words 18 Acquisition of object and personal names
Speaks 2-word sentences (e.g.,Mommy shoe) 19 Beginning grammaticization, 50+ word vocabulary
Stares momentarily at spot where object 2 Lack of object permanence (out of sight, out of mind) [e.g., yarn
disappeared ball dropped]
Stares at own hand 4 Self-discovery, cause and effect
Bangs 2 cubes 8 Active comparison of objects
Uncovers toy (after seeing it hidden) 8 Object permanence
Egocentric symbolic play (e.g., pretends to drink 12 Beginning symbolic thought
from cup)
Uses stick to reach toy 17 Able to link actions to solve problems
Pretend play with doll (e.g., gives doll bottle) 17 Symbolic thought

TABLE 8-2 -- Emerging Patterns of Behavior During the 1st Year of Life [*]
Prone: Lies in flexed attitude; turns head from side to side; head sags on ventral suspension
Supine: Generally flexed and a little stiff
Visual: May fixate face on light in line of vision;doll's-eye movement of eyes on turning of the body
Reflex: Moro response active; stepping and placing reflexes; grasp reflex active
Social: Visual preference for human face
Prone: Legs more extended; holds chin up; turns head; head lifted momentarily to plane of body on ventral suspension
Supine: Tonic neck posture predominates; supple and relaxed; head lags when pulled to sitting position
Visual: Watches person; follows moving object
Social: Body movements in cadence with voice of other in social contact; beginning to smile
Prone: Raises head slightly farther; head sustained in plane of body on ventral suspension
Supine: Tonic neck posture predominates; head lags when pulled to sitting position
Visual: Follows moving object 180 degrees
Social: Smiles on social contact; listens to voice and coos
Prone: Lifts head and chest with arms extended; head above plane of body on ventral suspension
Supine: Tonic neck posture predominates; reaches toward and misses objects; waves at toy
Sitting: Head lag partially compensated when pulled to sitting position; early head control with bobbing motion; back rounded
Reflex: Typical Moro response has not persisted; makes defensive movements or selective withdrawal reactions
Social: Sustained social contact; listens to music; says aah, ngah
Prone: Lifts head and chest, with head in approximately vertical axis; legs extended
Supine: Symmetric posture predominates, hands in midline; reaches and grasps objects and brings them to mouth
Sitting: No head lag when pulled to sitting position; head steady, tipped forward; enjoys sitting with full truncal support
Standing: When held erect, pushes with feet
Adaptive: Sees pellet, but makes no move to reach for it
Social: Laughs out loud; may show displeasure if social contact is broken; excited at sight of food
Prone: Rolls over; pivots;crawls or creep-crawls (Knobloch)
Supine: Lifts head; rolls over; squirms
Sitting: Sits briefly, with support of pelvis; leans forward on hands; back rounded
Standing: May support most of weight; bounces actively
Adaptive: Reaches out for and grasps large object; transfers objects from hand to hand; grasp uses radial palm; rakes at pellet
Language: Forms polysyllabic vowel sounds
Social: Prefers mother; babbles;enjoys mirror; responds to changes in emotional content of social contact
AT 10 MO
Sitting: Sits up alone and indefinitely without support, with back straight
Standing: Pulls to standing position;cruises or walks holding on to furniture
Motor: Creeps or crawls
Adaptive: Grasps objects with thumb and forefinger; pokes at things with forefinger; picks up pellet with assisted pincer movement; uncovers
hidden toy; attempts to retrieve dropped object; releases object grasped by other person
Language: Repetitive consonant sounds (mama, dada)
Social: Responds to sound of name; plays peek-a-boo or pat-a-cake;waves bye-bye
Motor: Walks with one hand held (48 wk); rises independently, takes several steps (Knobloch)
Adaptive: Picks up pellet with unassisted pincer movement of forefinger and thumb; releases object to other person on request or gesture
Language: Says a few words besides mama, dada

Social: Plays simple ball game; makes postural adjustment to dressing

TABLE 9-1 -- Emerging Patterns of Behavior from 1 to 5 Yr of Age [*]

15 MO
Motor: Walks alone; crawls up stairs
Adaptive: Makes tower of 3 cubes; makes a line with crayon; inserts raisin in bottle
Language: Jargon;follows simple commands; may name a familiar object (e.g., ball)
Social: Indicates some desires or needs by pointing; hugs parents
18 MO
Motor: Runs stiffly; sits on small chair; walks up stairs with one hand held; explores drawers and wastebaskets
Adaptive: Makes tower of 4 cubes; imitates scribbling; imitates vertical stroke; dumps raisin from bottle
Language: 10 words (average); names pictures; identifies one or more parts of body
Social: Feeds self; seeks help when in trouble; may complain when wet or soiled; kisses parent with pucker
24 MO
Motor: Runs well, walks up and down stairs, one step at a time; opens doors; climbs on furniture; jumps
Adaptive: Makes tower of 7 cubes (6 at 21 mo); scribbles in circular pattern; imitates horizontal stroke; folds paper once
Language: Puts 3 words together (subject, verb, object)
Social: Handles spoon well; often tells about immediate experiences; helps to undress; listens to stories when shown pictures
30 MO
Motor: Goes up stairs alternating feet
Adaptive: Makes tower of 9 cubes; makes vertical and horizontal strokes, but generally will not join them to make cross;
imitates circular stroke, forming closed figure
Language: Refers to self by pronoun I; knows full name
Social: Helps put things away; pretends in play
36 MO
Motor: Rides tricycle; stands momentarily on one foot
Adaptive: Makes tower of 10 cubes; imitates construction of bridge of 3 cubes; copies circle; imitates cross
Language: Knows age and sex; counts 3 objects correctly; repeats 3 numbers or a sentence of 6 syllables
Social: Plays simple games (in parallel with other children); helps in dressing (unbuttons clothing and puts on shoes);
washes hands
48 MO
Motor: Hops on one foot; throws ball overhand; uses scissors to cut out pictures; climbs well
Adaptive: Copies bridge from model; imitates construction of gate of 5 cubes; copies cross and square; draws man with 2 to 4
parts besides head; identifies longer of 2 lines
Language: Counts 4 pennies accurately; tells story
Social: Plays with several children, with beginning of social interaction and role-playing;goes to toilet alone
60 MO
Motor: Skips
Adaptive: Draws triangle from copy; names heavier of 2 weights
Language: Names 4 colors; repeats sentence of 10 syllables; counts 10 pennies correctly
Social: Dresses and undresses; asks questions about meaning of words; engages in domestic role-playing

TABLE 591-1 -- Screening Scheme for Developmental Delay: Upper Range
3 Supports weight on forearms Opens hands spontaneously Smiles appropriately Coos, laughs
6 Sits momentarily Transfers objects Shows likes and dislikes Babbles
9 Pulls to stand Pincer grasp Plays pat-a-cake, peek-a- Imitates sounds
12 Walks with one hand held Releases an object on Comes when called 12 meaningful
command words
18 Walks upstairs with Feeds from a spoon Mimics actions of others At least 6 words
24 Runs Builds a tower of 6 blocks Plays with others 23 word sentences

Infants regain or exceed birth weight by 2 wk of age and should grow at approximately 30 g (1 oz)/day during the 1st mo.
Crying normally peaks at about 6 wk of age, when healthy infants cry up to 3 hr/day, then decreases to 1 hr or less by 3
By the end of the 2nd year, somatic and brain growth slows, with corresponding decreases in nutritional requirements
and appetite, and the emergence of picky eating habits. Expect a gain of approximately 2 kg (45 lb) in weight and 78
cm (23 in) in height per year. Birthweight quadruples by 2 yr of age. An average 4 yr old weighs 40 lb and is 40 in
tall. The head will grow only an additional 5 cm between ages 3 and 18 yr.
Language development occurs most rapidly between 2 and 5 yr of age. Vocabulary increases from 50100 words to more
than 2,000. Sentence structure advances from telegraphic phrases (Baby cry) to sentences incorporating all of the major
grammatical components. As a rule of thumb, between the ages of 2 and 5 yr, the number of words in a typical sentence
equals the child's age (2 by age 2 yr, 3 by age 3 yr, and so on.) By 21 mo to 2 yr, most children are using possessives
(My ball), progressives (the -ing construction, as in I playing), questions, and negatives. By 4 yr of age, most
children can count to 4 and use the past tense; by 5 yr of age, they can use the future tense.

Primitive Reflexes
TABLE 591-2 -- Timing of Selected Primitive Reflexes

Palmar grasp 28 wk 32 wk 23 mo

Rooting 32 wk 36 wk Less prominent after 1 mo

Moro 2832 wk 37 wk 56 mo

Tonic neck 35 wk 1 mo 67 mo

Parachute 78 mo 1011 mo Remains throughout life

The Moro reflex is obtained by placing the infant in a semi-upright position. The head is momentarily allowed to fall
backward, with immediate resupport by the examiner's hand. The child symmetrically abducts and extends the arms and
flexes the thumbs, followed by flexion and adduction of the upper extremities. An asymmetric response may signify a
fractured clavicle, brachial plexus injury, or a hemiparesis. Absence of the Moro reflex in a term newborn is ominous,
suggesting significant dysfunction of the CNS.
The grasp response is elicited by placing a finger or object in the open palm of each hand. Normal infants grasp the
object, and with attempted removal, the grip is reinforced.
The tonic neck reflex is produced by manually turning the head to one side while supine. Extension of the arm occurs on
that side of the body corresponding to the direction of the face, while flexion develops in the contralateral extremities. An
obligatory tonic neck response, by which the infant remains locked in the fencer's position, is always abnormal
and implies a CNS disorder.
The parachute reflex is demonstrated by suspending the child by the trunk and by suddenly producing forward flexion
as if the child were to fall. The child spontaneously extends the upper extremities as a protective mechanism. The
parachute reflex appears before the onset of walking.

Skeletal Growth
TABLE 671-2 -- Skeletal Growth Considerations

Abnormal stature can be assessed as proportionate or disproportionate based on comparing the ratio of sitting height with
subischial height (lower limbs).
Normally the arm span is almost equal to standing height.
The head is disproportionately large at birth and ratio of head height to total height is approximately 1 : 4 at birth, which changes to 1
: 7.5 at skeletal maturity.
Lower extremities account for about 15% of height at birth and 30% at skeletal maturity.
The rate of height and growth increase is not constant and varies with growth spurts.
By age 5 yr, birth height usually doubles and the child is approximately 60% of adult height. The child is about 80% of final height at
9 yr. During puberty, the standing height increases by approximately 1 cm per month.
Bone age is more important than chronological age in determining future growth potential.

In the beginning of ambulation, the child usually has a wide-based gait with hyperflexion of hips and knees, no reciprocal arm swing, and an
initial contact with heel. By the age of 2 yr, the wide gait diminishes, reciprocal arm swing begins, and the initial contact is with the heel with
increased step length and velocity. Adult kinematic patterns usually start developing by 3 yr and the time-distance parameters reach adult values
by 7 yr, with development of a fully mature gait pattern.

Early walking is not associated with advanced development in other domains. Infants initially toddle with a wide-based gait, with the knees bent
and the arms flexed at the elbow; the entire torso rotates with each stride; the toes may point in or out, and the feet strike the floor flat. The
appearance is that of genu varus (bowleg). Subsequent refinement leads to greater steadiness and energy efficiency. After several months of
practice, the center of gravity shifts back and the torso stays more stable, while the knees extend and the arms swing at the sides for balance. The
feet are held in better alignment, and the child is able to stop, pivot, and stoop without toppling over .

Most children walk with a mature gait and run steadily before the end of their 3rd yr.

Adolescent Development
TABLE 12-2 -- Classification of Sex Maturity States in Girls
1 Preadolescent Preadolescent
2 Sparse, lightly pigmented, straight, medial border of Breast and papilla elevated as small mound; diameter of areola
labia increased
3 Darker, beginning to curl, increased amount Breast and areola enlarged, no contour separation
4 Coarse, curly, abundant, but less than in adult Areola and papilla form secondary mound
5 Adult feminine triangle, spread to medial surface of Mature, nipple projects, areola part of general breast contour

TABLE 12-3 -- Classification of Sex Maturity States in Boys

1 None Preadolescent Preadolescent
2 Scanty, long, slightly pigmented Minimal change/enlargement Enlarged scrotum, pink, texture
3 Darker, starting to curl, small amount Lengthens Larger
4 Resembles adult type, but less quantity; coarse, Larger;glans and breadth increase in Larger, scrotum dark
curly size
5 Adult distribution, spread to medial surface of Adult size Adult size

In girls, the first visible sign of puberty and the hallmark of SMR2 is the appearance of breast buds, between 8 and 12 yr of age. Menses
typically begins 22 yr later, during SMR34 (median age, 12 yr; normal range, 916 yr), around the peak height velocity. Less obvious
changes include enlargement of the ovaries, uterus, labia, and clitoris, and thickening of the endometrium and vaginal mucosa.

In boys, the first visible sign of puberty and the hallmark of SMR2 is testicular enlargement, beginning as early as 9 yr. This is followed by
penile growth during SMR3. Peak growth occurs when testis volumes reach approximately 910 cm3 during SMR4. Under the influence of LH
and testosterone, the seminiferous tubules, epididymis, seminal vesicles, and prostate enlarge. The left testis normally is lower than the right.
Some degree of breast hypertrophy, typically bilateral, occurs in 4065% of boys during SMR23 due to a relative excess of estrogenic
stimulation. Gynecomastia sufficient to cause embarrassment and social disability occurs in fewer than 10% of boys. Breast swelling <4 cm in
diameter has a 90% chance of spontaneous resolution within 3 yr. Gynecomastia presenting later in puberty, occurring in the prepubertal period,
or occurring in the absence of signs of pubertal development may be pathologic and requires a work-up, including a thorough medication (e.g.,
H2-blockers, psychotropics), drug (e.g., anabolic steroids), and medical history (e.g., Klinefelter syndrome, testicular failure, thyroid disease,

For both sexes, growth acceleration begins in early adolescence, but peak growth velocities are not reached until SMR34. Boys typically peak
23 yr later than girls, begin this growth at a later SMR stage, and continue their linear growth for approximately 23 yr after girls have stopped.
The asymmetric growth spurt begins distally, with enlargement of the hands and feet, followed by the arms and legs, and finally, the trunk and
chest, giving young adolescents a gawky appearance. Rapid enlargement of the larynx, pharynx, and lungs leads to changes in vocal quality,
typically preceded by vocal instability (voice cracking). Elongation of the optic globe often results in nearsightedness. Dental changes include
jaw growth, loss of the final deciduous teeth, and eruption of the permanent cuspids, premolars, and finally, molars. Orthodontic appliances may
be needed.

TABLE 110-3 -- Developmental Tasks of Adolescence

Early Early puberty (girls: breast bud and pubic Concrete thinking but early moral concepts, Emotional separation from parents,
adolescence hair development, start of growth spurt; progression of sexual identity development start of strong peer identification,
boys: testicular enlargement, start of (sexual orientation), possible homosexual peer early exploratory behaviors
genital growth) interest, reassessment of body image (smoking, violence)
Mid- Girls: mid-late puberty and end of growth Abstract thinking but self still seen as bullet Emotional separation from parents,
adolescence spurt; menarche; development of female proof, growing verbal abilities, identification strong peer identification,
body shape with fat deposition; boys:mid- of law with morality, start of fervent ideology increased health risk (smoking,
puberty, spermarche and nocturnal (religious, political) alcohol, etc.), heterosexual peer
emissions; voice breaks; start of growth interest, early vocational plans
Late Boys:end of puberty, continued increase Complex abstract thinking, identification of Development of social autonomy,
adolescence in muscle bulk and body hair difference between law and morality, increased intimate relationships,
impulse control, further development of development of vocational
personal identity, further development or capability and financial
rejection of religious and political ideology independence

TABLE 14-2 -- Formulas for Approximate Average Height and Weight of Normal Infants and Children
At birth 3.25 (7)
312 mo (age [mo] + 11)

16 yr Age (yr) 2 + 8 (age [yr] 5 + 17)

712 yr (age [yr] 7 + 5)


At birth 50 (20)
At 1 yr 75 (30)
212 yr age (yr) 6 + 77 (age [yr] 2 + 30)
TABLE 14-3 -- Severity of Malnutrition: Stunting and Wasting
0, normal >90 >95 >90
1, mild 7590 9095 8190
2, moderate 6074 8589 7080
3, severe <60 <85 <70


Body proportions follow a predictable sequence of changes with development. The head and trunk are relatively large at birth, with progressive
lengthening of the limbs throughout development, particularly during puberty. The lower body segment is defined as the length from the
symphysis pubis to the floor, and the upper body segment is the height minus the lower body segment. The ratio of upper body segment
divided by lower body segment (U/L ratio) equals approximately 1.7 at birth, 1.3 at 3 yr of age, and 1.0 after 7 yr of age. Higher U/L ratios are
characteristic of short-limb dwarfism or bone disorders, such as rickets.


Reference standards for bone maturation facilitate estimation of bone age. Bone age correlates well with stage of pubertal development and can
be helpful in predicting adult height in early- or late-maturing adolescents. In familial short stature, the bone age is normal (comparable to
chronological age). In constitutional delay, endocrinologic short stature, and undernutrition, the bone age is low and comparable to the height
age. Skeletal maturation is linked more closely to sexual maturity rating than to chronological age. It is more rapid and less variable in girls than
in boys.


Dental development includes mineralization, eruption, and exfoliation. Initial mineralization begins as early as the 2nd trimester (mean age for
central incisors, 14 wk) and continues through 3 yr of age for the primary (deciduous) teeth and 25 yr of age for the permanent teeth.
Mineralization begins at the crown and progresses toward the root. Eruption begins with the central incisors and progresses laterally. Exfoliation
begins at about 6 yr of age and continues through 12 yr of age. Eruption of the permanent teeth may follow exfoliation immediately or may lag
by 45 mo. The timing of dental development is poorly correlated with other processes of growth and maturation. Delayed eruption is usually
considered when there are no teeth by approximately 13 mo of age (mean + 3 standard deviations). Common causes include hypothyroid,
hypoparathyroid, familial, and (the most common) idiopathic. Individual teeth may fail to erupt because of mechanical blockage (crowding, gum

fibrosis). Causes of early exfoliation include histiocytosis X, cyclic neutropenia, leukemia, trauma, and idiopathic factors. Nutritional and
metabolic disturbances, prolonged illness, and certain medications (tetracycline) commonly result in discoloration or malformations of the dental
enamel. A discrete line of pitting on the enamel suggests a time-limited insult.

The Feeding of Infants and Children
TABLE 42-2 -- Important Principles for Weaning
Begin at 6 mo of age
Avoid foods with high allergenic potential (cow's milk, eggs, fish, nuts, soybeans).
At the proper age, encourage a cup rather than a bottle.
Introduce 1 food at a time.
Energy density should exceed that of breast milk.
Iron-containing foods (meat, iron-supplemented cereals) are required.
Zinc intake should be encouraged with foods such as meat, dairy products, wheat, and rice.
Phytate intake should be low to enhance mineral absorption.
Breast milk should continue to 12 mo; formula or cow's milk is then substituted.Give no more than 24 oz/day of cow's
Fluids other than breast milk, formula, and water should be discouraged. Give no more than 46 oz/day of fruit
juices. No soda.
Allergy prevention: promotion of breast-feeding with maternal exclusion of peanut and nut products from the mother's
diet and delay in introducing major allergenic foods: cow's milk until 1 yr of age; egg until 1824 mo of age; and peanut,
tree nuts, and seafood until 3 yr of age

Overweight and Obesity

TABLE 44-3 -- Body Mass Index (BMI) Classification of Children and Adolescents
<5th percentile Underweight
5th84th percentile Normal weight
85th94th percentile At risk for overweight
95th percentile Overweight

Vitamin Deficiencies and Excess

TABLE 45-1 -- Vitamins A, B Complex, and C
Retinol (vitamin A1); Fat-soluble;heat- In vision, as retinal, for synthesis of Nyctalopia;photophobia, xerophthalmia, Anorexia, slow growth, Liver, fish liver oils, dairy
stable;destroyed oxidation, the visual pigments rhodopsin and Bitot spots, conjunctivitis, keratomalacia drying and cracking of products, except skim
1 g retinol = 3.3 IU by vitamin A = drying; bile necessary for iodopsin; in growth, reproduction, leading to blindness; faulty epiphyseal bone skin, enlargement of liver milk; egg yolk, fortified
1 RAE. absorption; stored in liver; embryonic and fetal development, formation; defective tooth enamel; and spleen, swelling and margarines and fortified
Provitamins A:the plant pigments -, protected by vitamin E bone growth, immune and epithelial keratinization of mucous membranes and pain of long bones, bone skim milk; carotenoids
-, and -carotenes and functions, via retinoic acid as a skin; retarded growth; impaired resistance fragility, increased from plants: green
cryptoxanthin have partial retinol ligand for specific nuclear to infection, anemia, reproductive failure, intracranial pressure, vegetables, yellow fruits
activity: 12 g -carotene, or 24 g transcription factors, regulating fetal abnormalities alopecia, carotenemia; and vegetables
of other provitamin A carotenoids = genes involved in many fundamental fetal abnormalities
1 g retinol cellular processes

Thiamin:vitamin B1; (antiberiberi Water and alcohol soluble; fat- Component of thiamine Beriberi, fatigue, irritability, anorexia, None from oral intake Meat, especially pork;
vitamin) insoluble;stable in slightly acid pyrophosphate involved in oxidative constipation, headache, insomnia, whole-grain or enriched
solution; labile to heat, alkali, decarboxylation of -keto acids, tachycardia, polyneuritis, cardiac failure, cereals; legumes; nuts,
sulfites such as pyruvate, and in edema, elevated pyruvic acid in blood wheat germ; liver
transketolation reactions
Riboflavin:vitamin B2 Sparingly soluble in water; Constituent of flavoprotein enzymes Ariboflavinosis;photophobia blurred vision, Not harmful Milk, cheese; whole-grain
sensitive to light and alkali; important in oxidation-reduction burning and itching of eyes, corneal or enriched grains; meat,
stable to heat, alkali, oxidation, reactions: amino acid, fatty acid, and vascularization, poor growth, cheilosis fish; eggs;green leafy
acid carbohyrate metabolism and cellular vegetables; liver and other
respiration organ meats
Niacin:nicotinamide;nicotinc acid Water- and alcohol- Constituent of NAD and NADP, Pellagra, multiple B-vitamin deficiency Nicotinic acid (not the Meat, fish, poultry; whole-
(antipellagra vitamin) soluble;stable to acid, alkali, coenzymes in numerous oxidation- syndrome, diarrhea, dementia, dermatitis amide) is vasodilator; grain and enriched cereals;
light, heat, oxidation reduction reactions Irritability, convulsions, hypochromic skin flushing and itching; green vegetables; peanuts;
anemia; peripheral neuritis in patients hepatopathy liver;also from conversion
receiving isoniazid; oxaluria of trytophan to niacin
Vitamin B6 active forms: pyridoxine, Water-soluble;destroyed by Constituent of coenzymes for Sensory neuropathy Meat, fish, poultry; whole-
pyridoxal, pyridoxamine ultraviolet light and by heat decarboxylation, transamination, (from high-dose grain and fortified cereals;
trans-sulfuration;fatty acid supplements, not food) soybeans;nuts; potatoes;
metabolism; heme synthesis; noncitrus fruits; liver and
homocysteine metabolism kidney
Biotin Crystallized from yeast; soluble Coenzyme carboxylases; involved in Dermatitis, seborrhea; inactivated by avidin Unknown Widely distributed in
in water CO2 transfer in raw egg white foods; animal products,
yeast, liver
Pantothenic acid Limited data on stability during Component of coenzyme A and acyl Experimentally produced deficiency in Unknown Widely distributed in
cooking and food processing carrier protein involved in fatty acid humans: irritability, fatigue, gastric foods; beef, poultry, whole
metabolism complaints, numbness, paresthesias, muscle grains, liver and kidney,
cramps yeast, egg yolks

Folate:folic acid, folacin; a group of Slightly soluble in water: labile Concerned with formation and Megaloblastic anemia (infancy, pregnancy) Unknown Green vegetables, enriched
related compounds containing to heat, light, acid metabolism of 1-carbon units; usually secondary to malabsorption disease, grain products, oranges
pteridine ring, para-amino benzoic participates in synthesis of purines, glossitis, pharyngeal ulcers, impaired and other fruits, legumes,
acid, and glutamic acid; pyrimidines, nucleoproteins, immunity nuts, liver, yeast
pteroylglutamic acid homocysteine metabolism
Vitamin B12:cyanocobalamin Slightly soluble in water; stable Transfer of 1-carbon units in purine Pernicious anemia due to defect in Unknown Animal foods: muscle and
to heat in neutral solution; and labile methyl group metabolism; absorption rather than dietary lack; also organ meats, fish;
labile in acid or alkaline ones; essential for maturation of red blood secondary to gastrectomy, celiac disease, eggs;milk;cheese; fortified
destroyed by light; castle cells in bone marrow; metabolism of inflammatory lesions of small bowel, long- cereal products; fortified
intrinsic factor of the stomach nervous tissue; homocysteine term drug therapy (PAS, neomycin); soy products
required for absorption metabolism; Adenosylcobalamin is methylmalonic aciduria; homocystinuria
coenzyme for methylmalonyl
coenzyme A mutase
Ascorbic acid, antiscorbutic vitamin Water-soluble;easily oxidized, As an antioxidant, maintains Fe and Scurvy:poor wound healing, bleeding gums, Adverse effects usually Citrus fruits, tomatoes,
accelerated by heat, light, Cu ions in reduced state in petechiae, ecchymoses, follicular not serious; may include berries, cantaloupe,
alkali, oxidative enzymes, hydroxylases involved in collagen hyperkeratosis, arthralgia osmotic diarrhea, other cabbage, broccoli,
traces of copper or iron synthesis, metabolism of cholesterol gastrointestinal cauliflower, spinach,
and neurotransmitters; may be symptoms; oxaluria potatoes; cooking has
needed to maintain folate in a destructive effect
reduced form; facilitates non-heme
Fe absorption and Fe transfer from
tansferritin to ferritin
NAD(P), Nicotinamide adenine dinucleotide (phosphate); PAS, para-aminosalicylic acid

TABLE 48-1 -- Physical and Metabolic Properties and Food Sources of the Vitamins (D, E, and K)
Vitamin D3 (3-cholecalciferol), Fat-soluble, stable to heat, acid alkali, Necessary for gastrointestinal Rickets in growing Hypercalcemia, which may cause Exposure to sunlight
which is synthesized in the skin, and oxidation; bile necessary for absorption of calcium; also increases children; osteomalacia; emesis, anorexia, pancreatitis, (ultraviolet light); fish
and vitamin D2 (from plants or absorption; hydroxylation in the liver and absorption of phosphate; direct hypocalcemia may cause hypertension, arrhythmias, central oils, fatty fish, egg yolks,
yeast) are biologically equivalent; 1 kidney necessary for actions on bone, including mediating tetany and seizures nervous system effects, polyuria, and vitamin Dfortified
g = 40 IU vitamin D biologic resorption nephrolithiasis, and renal failure formula, milk, cereals,
activity and bread
Group of related compounds with Fat-soluble;readily oxidized by oxygen, Antioxidant;protection of cell Red cell hemolysis in Unknown Vegetable oils, seeds,
similar biologic activities; - iron, rancid fats; bile acids necessary for membranes from lipid peroxidation premature infants; nuts, green leafy
tocopherol is the most potent and absorption and formation of free radicals posterior column and vegetables, and
the most common form cerebellar dysfunction; margarine
pigmentary retinopathy

Group of naphthoquinones with Natural compounds are fat-soluble; Vitamin Kdependent proteins Hemorrhagic Not established; analogues (no Green leafy vegetables,
similar biologic activities; K1 stable to heat and reducing agents; labile include coagulation factors II, VII, manifestations; long-term longer used) caused hemolytic liver, and certain legumes
(phylloquinone) from diet; K2 to oxidizing agent, strong acids, alkali, IX, and X;proteins C, S, Z; matrix Gla bone and vascular health anemia, jaundice, kernicterus, and and plant oils; widely
(menaquinones) from intestinal light; bile salts necessary for intestinal protein, osteocalcin death distributed
bacteria absorption

TABLE 51-1 -- Trace Elements

Chromium Potentiates the action of insulin Impaired glucose tolerance, peripheral neuropathy and Unknown Meat, brewer's yeast
Copper Absorbed via specific intestinal transporter; Microytic anemia, osteoporosis, neutropenia, neurologic Acute:nausea, emesis, abdominal pain, coma, and hepatic Oysters, nuts, liver,
circulates bound to ceruloplasmin; enzyme cofactor symptoms, depigmentation of hair and skin necrosis; chronic toxicity (liver and brain injury) occurs margarine, legumes, corn
(superoxide dismutase, cytochrome oxidase, and in Wilson disease and another genetic disorder (see oil
enzymes involved in iron metabolism and Chapters 354.2 and 354.3 ) and secondary to excess
connective tissue formation) intake (see Chapter 354.4 )
Fluoride Incorporated into bone Dental caries (see Chapter 309 ) Chronic:dental fluorosis water (see Chapter 304 ) Toothpaste, fluoridated
Iodine Component of thyroid hormone (see Chapter 565 ) Hypothyroidism (see Chapters 567 and 569.2 ) Hypothyroidism and goiter (see Chapters 566 and 568 ); Saltwater fish, iodized
maternal excess may cause congenital hypothyroidism salt
and goiter (see Chapter 569.1 )
Iron Component of hemoglobin, myoglobin, Anemia (see Chapter 455 ), decreased alertness, Acute (see Chapter 58 ): nausea, vomiting, diarrhea, Deficiency may also
cytochromes, and other enzymes impaired learning abdominal pain, and hypotension; chronic excess usually result from blood loss
secondary to hereditary disorders (see Chapter 462.9 and (hookworm infestation,
354.5 ); causes organ dysfunction menorrhagia)
Manganese Enzyme cofactor Hypercholesterolemia, weight loss, decreased clotting Neurologic manifestations, cholestatic jaundice Nuts, grains, tea
Molybdenum Enzyme cofactor (xanthine oxidase and others) Tachycardia, tachypnea, night blindness, irritability, Hyperuricemia and increased risk of gout Legumes, grains, liver
Selenium Enzyme cofactor (prevents oxidative damage) Cardiomyopathy (Keshan disease), myopathy Nausea, diarrhea, neurologic manifestations, nail and hair Meat, seafood, whole
changes, garlic odor grains, garlic
Zinc Enzyme cofactor; constituent of zinc finger Decreased growth, dermatitis of extremities and around Abdominal pain, diarrhea, vomiting; may worsen copper Meat, shellfish, whole
proteins, which regulate gene transcription orifices, impaired immunity, poor wound healing, deficiency grains, legumes, cheese
hypogonadism, diarrhea; supplements beneficial in
diarrhea and improve neurodevelopmental outcomes

Fluids, Electrolytes, and Acid Base
Acid-Base Disorders
TABLE 52-11 -- Appropriate Compensation During Simple Acid-Base Disorders
Metabolic acidosis PCO2 = 1.5 [HCO3-] + 8 2
Metabolic alkalosis PCO2 increases by 7 mm Hg for each 10 mEq/L increase in serum
[HCO3 ]
Respiratory acidosis
Acute [HCO3-] increases by 1 for each 10-mm Hg increase in PCO2
Chronic [HCO3-] increases by 3.5 for each 10-mm Hg increase in PCO2
Respiratory alkalosis
Acute [HCO3-] falls by 2 for each 10-mm Hg decrease in PCO2
[HCO -
Chronic 3 ] falls by 4 for each 10-mm Hg decrease in PCO2

TABLE 52-12 -- Normal Values of Arterial Blood Gas

pH 7.357.45
[HCO3-] 2028 mEq/L
PCO2 3545 mm Hg

TABLE 54-1 -- Clinical Evaluation of Dehydration
Mild dehydration (<5% in an infant; <3% in an older child or adult): normal or increased pulse; decreased urine
output; thirsty; normal physical findings
Moderate dehydration (510% in an infant; 36% in an older child or adult): tachycardia; little or no urine output;
irritable/lethargic;sunken eyes and fontanel; decreased tears; dry mucous membranes; mild delay in elasticity (skin
turgor); delayed capillary refill (>1.5 sec); cool and pale
Severe dehydration (>10% in an infant; >6% in an older child or adult): rapid and weak or absent peripheral
pulses; decreased blood pressure; no urine output; very sunken eyes and fontanel; no tears; parched mucous
membranes; delayed elasticity (poor skin turgor); very delayed capillary refill (>3 sec); cold and mottled; limp,
depressed consciousness

TABLE 54-2 -- Fluid Management of Dehydration

Restore intravascular volume
Normal saline: 20 mL/kg over 20 min
Repeat as needed

Rapid volume repletion: 20 mL/kg normal saline or Ringer Lactate (maximum = 1 L) over 2 hr
Calculate 24-hr fluid needs: maintenance + deficit volume
Subtract isotonic fluid already administered from 24 hr fluid needs
Administer remaining volume over 24 hr using D5 normal saline + 20 mEq/L KCl
Replace ongoing losses as they occur

Ludans Method


< 2 y/o
Mild 5% wt loss 50 ml/kg
Mod 10% wt loss 100 ml/kg
Severe 15% wt loss 150 ml/kg

Fluid volume in 6-8 hours D50.3NaCL / D5LR

older kids > 2 y/o

Mild 30 ml/kg
Mod 60 ml/kg
Sev 90 ml/kg

active hydration 10-20 cc / kg FD (max 60 cc)

TABLE 58-2 -- Historical and Physical Findings in Poisoning
Bitter almonds Cyanide
Acetone Isopropyl alcohol, methanol, paraldehyde, salicylates
Alcohol Ethanol
Wintergreen Methyl salicylate
Garlic Arsenic, thallium, organophosphates
Miosis Narcotics (except meperidine), organophosphates, muscarinic mushrooms, clonidine, phenothiazines, chloral hydrate,
barbiturates (late), PCP
Mydriasis Atropine, alcohol, cocaine, amphetamines, antihistamines, cyclic antidepressants, cyanide, carbon monoxide
Nystagmus Phenytoin, barbiturates, ethanol, carbon monoxide
Lacrimation Organophosphates, irritant gas or vapors
Retinal hyperemia Methanol
Poor vision Methanol, botulism, carbon monoxide
Needle tracks Heroin, PCP, amphetamines
Bullae Carbon monoxide, barbiturates
Dry, hot skin Anticholinergic agents, botulism

Diaphoresis Organophosphates, nitrates, muscarinic mushrooms, aspirin, cocaine
Alopecia Thallium, arsenic, lead, mercury
Erythema Boric acid, mercury, cyanide, anticholinergics
Salivation Organophosphates, salicylates, corrosives, strychnine
Dry mouth Amphetamines, anticholinergics, antihistamine
Burns Corrosives, oxalate-containing plants
Gum lines Lead, mercury, arsenic
Dysphagia Corrosives, botulism
Cramps Arsenic, lead, thallium, organophosphates
Diarrhea Antimicrobials, arsenic, iron, boric acid
Constipation Lead, narcotics, botulism
Hematemesis Aminophylline, corrosives, iron, salicylates
Tachycardia Atropine, aspirin, amphetamines, cocaine, cyclic antidepressants, theophylline
Bradycardia Digitalis, narcotics, mushrooms, clonidine, organophosphates, blockers, calcium channel blockers
Hypertension Amphetamines, LSD, cocaine, PCP
Hypotension Phenothiazines, barbiturates, cyclic antidepressants, iron, blockers, calcium channel blockers
Depressed Alcohol, narcotics, barbiturates
Increased Amphetamines, aspirin, ethylene glycol, carbon monoxide, cyanide
Pulmonary edema Hydrocarbons, heroin, organophosphates, aspirin
Ataxia Alcohol, antidepressants, barbiturates, anticholinergics, phenytoin, narcotics
Coma Sedatives, narcotics, barbiturates, PCP, organophosphates, salicylates, cyanide, carbon monoxide, cyclic antidepressants,
Hyperpyrexia Anticholinergics, quinine, salicylates, LSD, phenothiazines, amphetamines, cocaine
Muscle fasciculation Organophosphates, theophylline
Muscle rigidity Cyclic antidepressants, PCP, phenothiazines, haloperidol
Paresthesia Cocaine, camphor, PCP, MSG
Peripheral Lead, arsenic, mercury, organophosphates
Altered behavior LSD, PCP, amphetamines, cocaine, alcohol, anticholinergics, camphor

TABLE 58-3 -- Recognizable Poison Syndromes

Increased sympathetic nervous Pyrexia Cough and decongestant
system activity preparations
Pupillary constriction

Anticholinergic activity Similar clinical picture to sympathomimetics Tricyclic antidepressants

Clinical differences include: pupillary dilation, dry mouth, Antiparkinsonian drugs
hot, dry skin


Atropine and nightshade

Mushroom poisoning (Amanita
Cyclopentolate eyedrops

Increased parasympathetic Pupillary constriction Organophosphate insecticides

nervous system activity:
cholinergic crisis Diarrhea Drugs for myasthenia gravis
(e.g., pyridostigmine)
Urinary incontinence
Carbamate insecticides
Excessive salivation
Muscle weakness

Metabolic acidosis Tachyopnea Ethanol

Kussmaul breathing (sighing respiration) Carbon monoxide
Diabetic medication
Tricyclic antidepressants

Chemical pneumonitis Cough Stoddard solvent (white spirit)

Respiratory distress Turpentine
Central nervous system depression Essential oils
A history of vomiting after ingestion need not be a feature

Acute ataxia or nystagmus Antihistamines

Anticonvulsants (especially
phenytoin and carbamazepine)
Carbon monoxide
Organic solvents

Methemoglobinemia Cyanosis resistant to oxygen therapy Alanine dyes

Sulphonamides and
metoclopramide (in neonates)

Renal failure Oliguria or anuria Carbon tetrachloride
Hematuria Ethylene glycol
Myoglobinuria Methanol

Violent emesis Aspirin

Boric acid

Generalized muscle rigidity Seizure-like, generalized muscle contractions or painful Strychnine

spasms (neck and limbs) and usually tachycardia and
Intact sensorium

Oropharyngeal pain and Lip, mouth, and pharyngeal ulcerations and burning pain Paraquat[*]
Dyspnea and hemoptysis secondary to pulmonary edema or Diquat
hemorrhage; can progress to pulmonary fibrosis over days to
weeks Caustics (i.e., acids and alkalis)
Inorganic mercuric salts
Mustards (e.g., sulfur)

Cellular hypoxia Mild: Nausea, vomiting, and headache Cyanide[*] (e.g., hydrogen
cyanide gas or sodium cyanide)
Severe: Altered mental status, dyspnea, hypotension,
seizures, and metabolic acidosis Sodium monofluoroacetate
[] (SMFA)[*]
Bitter almond odor
Carbon monoxide
Hypocalcemia or hypokalemia
Hydrogen sulfide
Sodium azide
Methemoglobin-causing agents

Peripheral neuropathy and/or Peripheral neuropathy signs and symptoms: Muscle Mercury (organic)[*]
neurocognitive effects weakness and atrophy,glove and stocking sensory loss,
and depressed or absent deep tendon reflexes Arsenic (inorganic)[*]

Neurocognitive effects: Memory loss, delirium, ataxia, Thallium

and/or encephalopathy Lead
Visual disturbances, paresthesias, and/or ataxia Acrylamide
Delirium and/or peripheral neuropathy
Encephalopathy and/or peripheral neuropathy

Severe gastrointestinal illness, Abdominal pain, vomiting, profuse diarrhea (possibly Arsenic[*]
dehydration bloody), and hypotension, possibly followed by multisystem
organ failure Ricin[*]

Inhalation an additional route of exposure; severe respiratory Colchicine

illness possible Barium
Hypokalemia common

Serotonin Altered mental status (agitation, confusion, coma), autonomi SSRIs, antidepressants, some opioids
instability (tachycardia, hyper- or hypotension), hyperkinetic (meperidine), tramadol, St. John's wort,
neuromuscular (tremor, clonus, hyperreflexia), mydriasis, MAOIs
diaphoresis, increased bowel motility
Withdrawal Abdominal cramps, diarrhea, lacrimation, sweating,goose flesh, Cessation of alcohol, barbiturates,
yawning, tachycardia, restlessness, hallucinations benzodiazepines, narcotics

TABLE 58-4 -- Screening Laboratory Clues Chloral hydrate
Methanol,[*] carbon monoxide
Cyclic antidepressants
Diabetes mellitus[*]
Paraldehyde,[*] phenformin
Isoniazid, iron Physostigmine
Ethanol,[*] ethylene glycol[*] Propranolol
Salicylates, starvation, seizures Quinine, quinidine


Isoniazid Alcohol
Insulin Anticholinergics

Propranolol Antihistamines
Oral hypoglycemic agents
Carbon monoxide
Salicylates Cyclic antidepressants
Isoniazid Hypoglycemic agents

Iron Lead

Phenothiazines Lithium
Oxalate Phencyclidine
Ethylene glycol Phenothiazines
Fluoride Salicylates



Chloral hydrate, calcium carbonate Camphor

Heavy metals (lead, zinc, barium, arsenic, lithium, bismuth, as Carbamazepine

in Pepto-Bismol) Carbon monoxide
Iron Cocaine
Phenothiazines Cyanide
Play-Doh, potassium chloride Aminophylline
Enteric-coated pills Amphetamine
Dental amalgam Anticholinergics
Antidepressants (cyclic)

TABLE 58-5 -- Major Modes of Presentation Pb (lead) [also lithium]

Antiarrhythmics Phenol
Anticholinergics Phenothiazines
Antihistamines Propoxyphene
Arsenic Salicylates
Carbon monoxide Strychnine

Causes of methemoglobinemia: amyl nitrite, aniline dyes, TABLE 709-4 -- Summary of Recommendations for Children
benzocaine, bismuth subnitrate, dapsone, primaquone, quinones, with Confirmed (Venous) Elevated Blood Lead Concentrations
1014 g/dL Lead education
TABLE 58-6 -- Common Antidotes for Poisoning
N-Acetylcysteine Acetaminophen;carbon tetrachloride and Environmental
(Mucomyst) chloroform (experimental) Follow-up blood lead monitoring in 13 mo
N-Acetylcysteine Acetaminophen 1519 g/dL Lead education
(Acetodote) Dietary
Atropine Organophosphate and carbamate Environmental
pesticides; bradycardia due to
atrioventricular conduction defects, - Follow-up blood lead monitoring in 12 mo
blocking agents
Proceed according to actions for 2024 g/dL
BAL in oil (dimercaprol) Arsenic, mercury, other metals if A follow-up blood lead concentration is in
this range at least 3 mo after initial venous
Benztropine (Cogentin) Acute dystonic reactions test; or Blood lead concentration increases
Cyanide antidote kit Cyanide 2044 g/dL Lead education
Hydrogen sulfide (nitrites only) Dietary
Deferoxamine (Desferal) Iron Follow-up blood lead monitoring in 1 wk1
mo (sooner if higher)
Complete history and physical examination
Digoxin-specific Digitalis glycosides (synthetic or natural) Laboratory studies
Fab antibodies (Digibind) Hemoglobin or hematocrit
Iron status
Dimercaptosuccinic acid Lead and probably mercury, arsenic, and
(succimer, DMSA, perhaps other metals Environmental investigation
Chemet) Lead hazard reduction
Diphenhydramine Extrapyramidal symptoms, acute dystonic Neurodevelopmental monitoring
(Benadryl) reactions, allergic reactions
Abdominal radiography (if particulate lead
EDTA, calcium (calcium Lead, manganese, nickel, zinc, and ingestion is suspected) with bowel
disodium, Versenate) perhaps chromium decontamination if indicated
Ethanol (ethyl alcohol) Methanol, ethylene glycol 4569 g/dL Lead education
Flumazenil (Romazicon) Benzodiazepines Dietary
Follow-up blood lead monitoring
Fomepizole (4- Ethylene glycol, methanol Complete history and physical examination
methylpyrazole, Antizole)
Laboratory studies
Hemoglobin or hematocrit
Glucagon Blockers, calcium channel blockers,
Iron status
hypoglycemic agents
Free EP or ZPP
Methylene blue Methemoglobinemia
Environmental investigation
Naloxone (Narcan) Narcotics
Lead hazard reduction
Clonidine (inconsistent response) Neurodevelopmental monitoring
Octreotide Sulfonylureas Abdominal radiography with bowel
decontamination if indicated Chelation
Physostigmine Anticholinergic agents
70 g/dL Hospitalize and commence chelation therapy
Proceed according to actions for 4569 g/dL
Pralidoxime (2-PAM, Organophosphate insecticides
Pyridoxine (Vitamin B6) Isoniazid, Gyromitra mushrooms
Searching for gingival lead lines
Ethylene glycol (investigational)
Evaluation of renal function (except during chelation with
Oxygen Carbon monoxide CaNa2EDTA)
Vitamin K Coumarin Testing of hair, teeth, or fingernails for lead
BAL, British antilewisite; DMSA, dimercaptosuccinic acid; EDTA, Radiographic imaging of long bones
ethylene diamine tetraacetic acid; ET, endotracheal; IM, intramuscular;
IV, intravenous; max, maximum; NS, normal saline; PO, Oral. X-ray fluorescence of long bones

TABLE 58-9 -- Classic Stages in the Clinical Course of Acetaminophen Toxicity
I 0.524 hr Anorexia, nausea, vomiting, malaise, pallor, diaphoresis
II 2448 hr Resolution of earlier symptoms; right upper quadrant abdominal pain and tenderness; elevated bilirubin,
prothrombin time, hepatic enzymes; oliguria
III 7296 hr Peak liver function abnormalities; anorexia, nausea, vomiting, and malaise may reappear
IV 4 days2 wk Resolution of hepatic dysfunction or complete liver failure

The Acutely Ill Child

Injury Control
TABLE 61-4 -- Recommended Child Restraint Methods
Recommended Birth to 1 yr; up to 2022 Older than 1 yr and 2040 lb >40 lb and under 4 9; generally between 4 and 8 years
age/weight lb of age, 4080 lb
Type of seat Infant only or rear-facing Convertible/forward-facing Belt positioning booster seat
convertible harness seat
Seat position Rear-facing only Can be rear-facing until 30 lb if Forward-facing
seat allows; generally forward-
Notes Children should use rear- Harness straps should be at or Belt positioning booster seats must be used with both
facing seat until 1 yr and above shoulder level lap and shoulder belts
at least 20 lb
Harness straps should be Most seats require top slot for Make sure the lap belt fits low and tightly across the
at or below shoulder level forward-facing use lap/upper thigh area and the shoulder belt fits snugly,
crossing the chest and shoulder to avoid abdominal
Children weighing <20 lb may use an infant seat or be placed in a convertible infant-toddler child restraint device. Infants younger than 1 yr or
weighing <20 lb should be placed in the rear seat facing backward; older toddlers and children can be placed in the rear seat in a forward-facing
child harness seat. Emphasis must be placed on the correct use of these seats, including placing the seat in the right direction, routing the belt
properly, and ensuring that the child is buckled into the seat correctly. Government regulations have made the fit between car seats and the car
easier, quicker, and less prone to error. Children younger than age 13 yr should never sit in the front seat, especially if an airbag is present.
Inflating airbags can be lethal to infants in rear-facing seats and to small children in the front passenger seat.

Pediatric Emergencies and Resuscitation

TABLE 66-3 -- Vital Signs at Various Ages TABLE 68-3 -- Age-specific Vital Signs and Laboratory Variables












Premature 120170[*] 5575/3545[] 4070[]



03 mo 100150[*] 6585/4555 3555

36 mo 90120 7090/5065 3045
0 day1 wk >180 <100 >50 >34 <65
612 mo 80120 80100/5565 2540
1 wk1 mo >180 <100 >40 >19.5 or <75
13 yr 70110 90105/5570 2030 <5
36 yr 65110 95110/6075 2025 1 mo1 yr >180 <90 >34 >17.5 or <100
612 yr 6095 100120/60 1422
75 25 yr >140 NA >22 >15.5 or <94
12 yr 5585 110135/65 1218
85 612 yr >130 NA >18 >13.5 or <105
1318 yr >110 NA >14 >11 or <117

TABLE 66-5 -- Glasgow Coma Scale
Spontaneous 4
To voice 3
To pain 2
None 1
Older Children Infants and Young Children
Oriented 5 Appropriate words; smiles, fixes, and follows 5
Confused 4 Consolable crying 4
Inappropriate 3 Persistently irritable 3
Incomprehensible 2 Restless, agitated 2
None 1 None 1
Obeys 6
Localizes pain 5
Withdraws 4
Flexion 3
Extension 2
None 1

TABLE 66-6 -- Clinical Staging of Encephalopathy

1 2 3 4 5
Lethargic Combative Comatose Comatose Comatose
Follows Inconsistent following of Occasional response to Responds only to pain No response to pain
commands commands commands
Reactive pupils Sluggish pupils Eyes may deviate Weak pupillary No pupillary response
Normal breathing May hyperventilate Irregular breathing Very irregular Requires mechanical
breathing ventilation
Normal muscle Inconsistent reflexes Decorticate posturing Decerebrate posturing Tendon reflexes absent
tone flaccid

Neurologic Emergencies and Stabilization

TABLE 67-1 -- Age-specific Criteria for Brain Death[*]

Children 1 wk2 mo of age: fulfillment of the criteria listed in Table 67-2 in 2 separate examinations at least 48 hr apart, or 1 clinical
examination followed by an isoelectric EEG at least 48 hr later
Children 2 mo1 yr: fulfillment of the clinical criteria described in Table 67-2 in 2 separate examinations, at least 24 hr apart, or 1
clinical examination followed by an isoelectric EEG or negative results of a cerebral blood flow study at least 24 hr later
Children >1 yr: fulfillment of the clinical criteria described in Table 67-2 in 2 separate examinations at 12 hr apart

TABLE 67-2 -- Diagnosis of Brain Death


1. A recognized cause of coma, sufficient to explain the History, clinical examination, laboratory, technical investigations
irreversible cessation of all brain function
2. Potentially reversible causes of coma must be


a. Sedatives and neuromuscular blocking

b. Hypothermia
c. Metabolic and endocrine disturbances:
Severe electrolyte disturbances
Severe hypo- or hyperglycemia

d. Uncontrolled hypotension
e. Surgically remediable intracranial
f. Any other sign that suggests a potentially
reversible cause of coma


1. Absence of higher brain function Lack of consciousness, voluntary movement or responsiveness except for
spinal reflexes (stimuli applied to any body region may not elicit a motor
response within the cranial nerve distribution); preferably test in a cranial
(trigeminal) dermatome rather than a spinal dermatome; no decorticate or
decerebrate posturing, no convulsions

2. Absence of brainstem function

a. Absence of sympathetic and parasympathetic regulation of the Pupils in midposition or dilated, showing neither direct nor indirect reaction
pupils to light
b. Disruption of the pathways controlling eye movement in the Absence of spontaneous eye movement, absence of reaction to injection of
brainstem iced water into the ear (vestibulo-ocular reflex), absence of doll's eye
phenomenon (oculocephalic reflexes)
c. Disruption of the afferent trigeminal and efferent facial nerve Absence of blink response to (careful) corneal stimulation
d. Disruption of afferent and efferent pathways of cranial nerves Absence of gag response to stimulation of the posterior pharynx, absence of
IX and X in the medulla oblongata cough on suctioning of the trachea
e. Absence of vagal efferent activity No significant increase of heart rate on administration of intravenous
atropine or on pressure applied to the eyeballs (oculocardiac reflex)
f. Disruption of the respiratory control centers of the medulla No respiratory movement (as assessed by observation capnography) at a
oblongata PaCO2 above a set limit during standardized apnea testing

1. Confirmation of absence of higher brain function Electrocerebral silence on EEG during at least 30 min

2. Confirmation of complete infarction of the brain and Four-vessel contrast angiography or radionuclide imaging
brainstem by confirmation of absence of blood flow

Confirmation of irreversibility Observation during a set time, repeat formal physical examination and
confirmatory tests

+2 +1 -1
Size >20 kg 1020 kg <10 kg
Airway Normal Maintainable Unmaintainable
Systolic BP >90 mm Hg 9050 mm Hg <50 mm Hg
CNS Awake Obtunded/LOC Coma/decerebrate
Open wound None Minor Major/penetrating
Skeletal None Closed fracture Open/multiple fractures

Genetics and Metabolism
TABLE 81-7 -- Microdeletion/Contiguous Gene Syndromes and Their Clinical Manifestations
7q11.23 Williams Round face with full cheeks and lips, stellate pattern in iris,
strabismus, supravalvular aortic stenosis and other cardiac
malformations, varying degrees of mental retardation, friendly
11p13 WAGR Hypernephroma (Wilms tumor), aniridia, male genital hypoplasia of
varying degrees, gonadoblastoma, long face, upward slanting
palpebral fissures, ptosis, beaked nose, low-set poorly formed
auricles, mental retardation
15q11-q13 Prader-Willi Severe hypotonia at birth, obesity, short stature (responsive to growth
(pat) hormone), small hands and feet, hypogonadism, mental retardation
15q11-q13 Angelman Hypotonia, fair hair, midface hypoplasia, prognathism, seizures,
(mat) jerky ataxic movements, uncontrollable bouts of laughter, severe
mental retardation
20p12 Alagille syndrome Bile duct paucity with cholestasis;heart defects, particularly
pulmonary artery stenosis;ocular abnormalities (posterior embryo
toxin);skeletal defects such as butterfly vertebrae;long nose with
broad mid-nose
22q11.2 Velocardiofacial-
Hypoplasia or agenesis of the thymus and parathyroid glands,
DiGeorge syndrome
hypoplasia of auricle and external auditory canal, conotruncal cardiac
anomalies, cleft palate, short stature, behavioral problems
TABLE 84-3 -- Inborn Errors of Amino Acid Metabolism Associated with Peculiar Odor
Glutaric acidemia (type II) Sweaty feet, acrid
Hawkinsinuria Swimming pool
Isovaleric acidemia Sweaty feet, acrid
Maple syrup urine disease Maple syrup
Hypermethioninemia Boiled cabbage
Multiple carboxylase deficiency Tomcat urine
Oasthouse urine disease Hops-like
Phenylketonuria Mousey or musty
Trimethylaminuria Rotting fish
Tyrosinemia Boiled cabbage, rancid butter

The Fetus
TABLE 6-4 -- Milestones of Prenatal Development
1 Fertilization and implantation; beginning of embryonic period
2 Endoderm and ectoderm appear (bilaminar embryo)
3 First missed menstrual period; mesoderm appears (trilaminar embryo); somites begin to form
4 Neural folds fuse; folding of embryo into human-like shape; arm and leg buds appear; crown-rump
length 45 mm
5 Lens placodes, primitive mouth, digital rays on hands
6 Primitive nose, philtrum, primary palate; crown-rump length 2123 mm
7 Eyelids begin
8 Ovaries and testes distinguishable
9 Fetal period begins; crown-rump length 5 cm; weight 9 g
10 External genitals distinguishable
20 Usual lower limit of viability; weight 460 g; length 19 cm
25 Third trimester begins; weight 900 g; length 25 cm
28 Eyes open; fetus turns head down; weight 1,000 g
38 Term

By 12 wk, the gender of the external genitals becomes clearly distinguishable. Lung development
proceeds, with the budding of bronchi, bronchioles, and successively smaller divisions. By 2024 wk,
primitive alveoli have formed and surfactant production has begun; before that time, the absence of alveoli
renders the lungs useless as organs of gas exchange.
Muscle contractions first appear around 8 wk, soon followed by lateral flexion movements. By 1314 wk,
breathing and swallowing motions appear and tactile stimulation elicits graceful movements. The grasp reflex
appears at 17 wk and is well developed by 27 wk. Eye opening occurs around 26 wk.
If a single ultrasound examination is performed, the most information can be obtained with a scan at 1820
wk, when both gestational age and fetal anatomy can be evaluated.
Determination of the extent of calcification by ultrasound (placental maturity index), detection of the 1st
audible fetal heart tones (1618 wk), and observation of the initial fetal movements (1820 wk) may also aid
in evaluating the maturity of a fetus.
Second-trimester screening (1518 wk) of maternal serum -fetoprotein (MSAFP) levels is used to screen
for open neural tube defects. About 90% of affected pregnancies can be detected by an elevated MSAFP level.
Gastroschisis, omphalocele, congenital nephrosis, twins, and other abnormal conditions can also be identified.
Low MSAFP is associated with incorrect gestational age estimates, trisomy 18 or 21, and intrauterine growth

Neonatal Jaundice
TABLE 102-2 -- Risk Factors for Development of Severe
Hyperbilirubinemia in Infants of 35 or More Week's
Gestation (in Approximate Order of Importance)
Necrotizing Enterocolitis
Major risk factors The clinical syndrome has been classified into stages by
Predischarge TSB or TcB level in the high-risk zone Walsh and Kliegman (1986) to include systemic, intestinal,
and radiographic findings.
Jaundice observed in the first 24 hr
Blood group incompatibility with positive direct antiglobulin A. Stage I: suspected NEC
test, other known hemolytic disease (G6PD deficiency), 1. Systemic signs are nonspecific, including apnea,
elevated ETCOc bradycardia, lethargy, and temperature instability.
2. Intestinal findings include feeding intolerance, recurrent
Gestational age 3536 wk gastric residuals, and guaiacpositive stools.
Previous sibling received phototherapy 3. Radiographic findings are normal or nonspecific.

Cephalohematoma or significant bruising B. Stage IIA: mild NEC

1. Systemic signs are similar to those in stage I.
Exclusive breastfeeding, particularly if nursing is not going
2. Intestinal findings include prominent abdominal distention
well and weight loss is excessive
with or without tenderness, absent bowel sounds, and gross
East Asian race[*] blood in the stools.
3. Radiographic findings include ileus, with dilated loops
Minor risk factors
with focal areas of pneumatosis intestinalis.
Predischarge TSB or TcB level in the high intermediate-risk
zone C. Stage IIB: moderate NEC
1. Systemic signs include stage 1 signs plus mild acidosis and
Gestational age 3738 wk thrombocytopenia.
Jaundice observed before discharge 2. Intestinal findings include increasing distention, abdominal
wall edema, and tenderness with or without a palpable mass.
Previous sibling with jaundice 3. Radiographic findings include extensive pneumatosis and
Macrosomic infant of a diabetic mother early ascites. Intrahepatic portal venous gas may be present.

Maternal age 25 yr D. Stage IIIA: advanced NEC

Male gender 1. Systemic findings include respiratory and metabolic
acidosis, assisted ventilation for apnea, decreasing blood
Decreased risk (these factors are associated with decreased pressure and urine output, neutropenia, and coagulopathy.
risk of significant jaundice, listed in order of decreasing 2. Intestinal findings include spreading edema, erythema or
importance) discoloration, and induration of the abdominal wall.
3. Radiographic findings include prominent ascites, paucity
TSB or TcB level in the low-risk zone ( Fig 102-8 )
of bowel gas, and possibly a persistent sentinel loop.
Gestational age 41 wk
E. Stage IIIB: advanced NEC
Exclusive bottle feeding
1. Systemic findings reveal generalized edema, deteriorating
Black race vital signs and laboratory indices, refractory hypotension,
shock syndrome, disseminated intravascular coagulation
Discharge from hospital after 72 hr (DIC), and electrolyte imbalance.
2. Intestinal findings reveal a tense, discolored abdomen and
3. Radiographic findings commonly show absent bowel gas
and often evidence of intraperitoneal free air.

Blood Disorders
TABLE 103-4 -- Hemorrhagic Disease of the Newborn
Age 024 hr 27 days 16 mo
Site of Cephalohematoma Gastrointestinal Intracranial
Subgaleal Ear-nose-throatmucosal Gastrointestinal
Intracranial Intracranial Cutaneous
Gastrointestinal Circumcision Ear-nose-throatmucosal
Umbilicus Cutaneous Injection sites
Intra-abdominal Gastrointestinal Thoracic
Injection sites
Etiology/risks Maternal drugs (phenobarbital, Vitamin K deficiency Cholestasismalabsorption
phenytoin, warfarin, rifampin, of vitamin K (biliary atresia,
isoniazid) that interfere with cystic fibrosis, hepatitis)
vitamin K
Inherited coagulopathy Breast-feeding Abetalipoprotein deficiency
Idiopathic in Asian breast-
fed infants
Warfarin ingestion
Prevention Posible vitamin K at birth or to Prevented by parenteral Prevented by parenteral and
mother (20 mg) before birth vitamin K at birth. Oral high-dose oral vitamin K
vitamin K regimens require during periods of
repeated dosing over time malabsorption or cholestasis
Avoid high-risk medications
Incidence Very rare 2% if not given vitamin K Dependent on primary
The swallowed blood syndrome, in which blood or bloody stools are passed, usually on the 2nd or 3rd day of
life, may be confused with hemorrhage from the gastrointestinal tract. The blood may be swallowed during
delivery or from a fissure in the mother's nipple. Differentiation from gastrointestinal hemorrhage is based on
the fact that the infant's blood contains mostly fetal hemoglobin, which is alkali-resistant, whereas swallowed
blood from a maternal source contains adult hemoglobin, which is promptly changed to alkaline hematin after
the addition of alkali. Apt devised the following test for this differentiation: (1) Rinse a blood-stained diaper or
some grossly bloody (red) stool with a suitable amount of water to obtain a distinctly pink supernatant
hemoglobin solution. (2) Centrifuge the mixture and decant the supernatant solution. (3) To five parts of the
supernatant fluid add one part of 0.25 N (1%) sodium hydroxide. Within 12 min a color reaction takes place: A
yellow-brown color indicates that the blood is maternal in origin; a persistent pink indicates that it is from the
infant. A control test with known adult or infant blood, or both, is advisable.
A physiologic decrease in hemoglobin content is noticed at 812 wk in term infants (hemoglobin, 11 g/dL)
and at about 6 wk in premature infants (710 g/dL).
Early ultrasonographic signs of hydrops include organomegaly (liver, spleen, heart), the doublebowel wall sign
(bowel edema), and placental thickening. Progression to polyhydramnios, ascites, pleural or pericardial
effusions, and skin or scalp edema may then follow.

Nervous System Disorders
Convulsions should be distinguished from the jitteriness that may be present in normal newborns, in infants of diabetic
mothers, in those who experienced birth asphyxia or drug withdrawal, and in polycythemic neonates. Jitteriness
resembling simple tremors may be stopped by holding the infant's extremity; it often depends on sensory stimuli and
occurs when the infant is active, and it is not associated with abnormal eye movements. Tremors are often more rapid
with a smaller amplitude than are tonic clonic seizures. Seizures in premature infants are often subtle and associated with
abnormal eye (fluttering, deviation, stare) or facial (chewing, tongue thrusting) movements; the motor component is often
that of tonic extension of the limbs, neck, and trunk. Term infants may have focal or multifocal, clonic or myoclonic
movements, but they may also have more subtle seizure activity. Apnea may be the 1st manifestation of seizure activity,
particularly in a premature infant.

Intracranial bleeding may be associated with disseminated intravascular coagulopathy, isoimmune thrombocytopenia, and
neonatal vitamin K deficiency, especially in infants born to mothers receiving phenobarbital or phenytoin.
TABLE 99-4 -- Hypoxic-Ischemic Encephalopathy in Term Infants
Level of consciousness Hyperalert Lethargic

Muscle tone Normal Hypotonic

Posture Normal Flexion

Tendon reflexes/clonus Hyperactive Hyperactive

Myoclonus Present Present

Moro reflex Strong Weak Absent

Pupils Mydriasis Miosis Unequal, poor light reflex

Seizures None Common Decerebration

Electroencephalographic Normal Low voltage changing to Burst suppression to

seizure activity isoelectric

Duration <24 hr if progresses; otherwise, may 24 hr to 14 days Days to weeks

remain normal

Outcome Good Variable Death, severe deficits

A low Apgar score at 20 min, absence of spontaneous respirations at 20 min of age, and persistence of abnormal
neurologic signs at 2 wk of age also predict death or severe cognitive and motor deficits.
Spinal cord injury occurs most commonly at the level of the 4th cervical vertebra with cephalic presentations and the
lower cervicalupper thoracic vertebrae with breech presentations.
In Erb-Duchenne paralysis, the injury is limited to the 5th and 6th cervical nerves. The infant loses the power to abduct
the arm from the shoulder, rotate the arm externally, and supinate the forearm. The characteristic position consists of
adduction and internal rotation of the arm with pronation of the forearm. Power to extend the forearm is retained, but
the biceps reflex is absent; the Moro reflex is absent on the affected side.
Klumpke paralysis is a rare form of brachial palsy; injury to the 7th and 8th cervical nerves and the 1st thoracic nerve
produces a paralyzed hand and ipsilateral ptosis and miosis (Horner syndrome) if the sympathetic fibers of the 1st thoracic
root are also injured.

The Umbilicus
The umbilical cord usually dries and separates within 68 days after birth. The raw surface becomes covered by a thin layer
of skin; scar tissue forms, and the wound is usually healed within 1215 days. The presence of saprophytic organisms delays
separation of the cord and increases the possibility of invasion by pathogenic organisms. Mild infection or incomplete
epithelialization may result in a moist granulating area at the base of the cord with a slight mucoid or mucopurulent discharge.
Good results are usually obtained by cleansing with alcohol several times daily.
Most umbilical hernias that appear before the age of 6 mo disappear spontaneously by 1 yr of age. Even large hernias (56 cm
in all dimensions) have been known to disappear spontaneously by 56 yr of age. Strangulation is extremely rare. It is
generally agreed that strapping is ineffective. Surgery is not advised unless the hernia persists to the age of 45 yr, causes
symptoms, becomes strangulated, or becomes progressively larger after the age of 12 yrj. Defects exceeding 2 cm are less
likely to close spontaneously.

Evaluation of immune function should be initiated for children with clinical manifestations of a specific immune
disorder or with unusual, chronic, or recurrent infections such as (1) one or more systemic bacterial infections (sepsis,
meningitis); (2) two or more serious respiratory or documented bacterial infections (cellulitis, draining otitis media,
pneumonia, lymphadenitis) within 1 yr; (3) serious infections occurring at unusual sites (liver, brain abscess); (4)
infections with unusual pathogens (Aspergillus, Serratia marcescens, Nocardia, Burkholderia cepacia); and (5)
infections with common childhood pathogens but of unusual severity. Additional clues to immunodeficiency include:
>8 ear infections per yr; >2 serious sinus infections per yr; >2 mo treatment with antibiotics with poor results; failure
to thrive with or without chronic diarrhea; and the need for intravenous antibiotics to successfully treat an infection
usually treated with oral antibiotics.

TABLE 121-1 -- Characteristic Clinical Patterns in Some Primary Immunodeficiencies

Hypocalcemia, heart disease, unusual facies DiGeorge anomaly
Delayed umbilical cord detachment, leukocytosis, recurrent infections Leukocyte adhesion defect
Diarrhea, pneumonia, thrush, failure to thrive Severe combined immunodeficiency
Maculopapular rash, alopecia, lymphadenopathy Severe combined immunodeficiency with graft-versus-
host disease
Bloody stools, draining ears, eczema Wiskott-Aldrich syndrome
Mouth ulcers, neutropenia, recurrent infections XL-Hyper IgM syndrome
Severe progressive infectious mononucleosis X-linked lymphoproliferative syndrome
Recurrent cutaneous and/or systemic staphylococcal abscesses, coarse Hyper-IgE syndrome
facial features
Persistent thrush, nail dystrophy, endocrinopathies Chronic mucocutaneous candidiasis
Short stature, fine hair, severe varicella Cartilage hair hypoplasia with short-limbed dwarfism
Oculocutaneous albinism, recurrent infection Chdiak-Higashi syndrome
Lymphadenopathy, dermatitis, pneumonia, osteomyelitis Chronic granulomatous disease
Progressive dermatomyositis with chronic enterovirus encephalitis X-linked agammaglobulinemia
Sinopulmonary infections, neurologic deterioration, telangiectasia Ataxia-telangiectasia
Recurrent neisserial meningitis C6, C7, or C8 deficiency
Sinopulmonary infections, malabsorption, splenomegaly, Common variable immunodeficiency
Candidiasis with raw egg ingestion Biotin-dependent cocarboxylase deficiency
Chronic mucocutaneous candidiasis
Associated primarily with T-cell dysfunction
Endocrinopathies are commonly associated with this
Cyclic neutropenia: recurrent aphthous ulcers and stomatitis during the periods of neutropenia
Leukocyte adhesion defect: delayed cord separation

TABLE 121-3 -- Characteristic Features of Primary Immunodeficiency
Age at the onset of Early onset, usually 26 mo of age Onset after maternal antibodies diminish, Early onset Onset at any age
infection usually after 57 mo of age, later childhood
to adulthood
Specific pathogens Bacteria: mycobacteria Bacteria: streptococci, staphylococci, Bacteria: staphylococci, Bacteria: Neisseria, Escherichia
involved Haemophilus, Campylobacter Pseudomonas, Serratia, coli
Viruses: CMV, EBV, adenovirus, parainfluenza Viruses: enterovirus[*]
3, varicella, enterovirus
Fungi and parasites: Candida; opportunistic Fungi and parasites: giardia, cryptosporidia Fungi and parasites: Candida;
infection, PCP Nocardia, Aspergillus
Affected organs Failure to thrive, protracted diarrhea, extensive Recurrent sinopulmonary infections, Skin abscesses: Infections: meningitis, arthritis,
mucocutaneous candidiasis chronic gastrointestinal symptoms, dermatitis, impetigo, septicemia, recurrent
malabsorption, arthritis, enteroviral cellulitis sinopulmonary infections
Lymph nodes:
suppurative adenitis
Oral cavity:
periodontitis, ulcers
internal organs,
abscesses, osteomyelitis

Special features Graft-versus-host disease caused by maternal Autoimmunity, lymphoreticular Prolonged attachment of Rheumatoid disorders: SLE,
engraftment or nonirradiated blood transfusion; malignancy: lymphoma, thymoma; umbilical cord, poor wound vasculitis, dermatomyositis,
Postvaccination, disseminated BCG or varicella; postvaccination paralytic polio healing scleroderma, glomerulonephritis,
hypocalcemic tetany in infancy[] angioedema

Allergic Disorders
TABLE 143-8 -- Classification of Asthma Severity
FEV1 or PEF[*] % PEF Variability
Predicted Normal (%)
Severe persistent 4 Continual Frequent 60 >30
Moderate persistent 3 Daily >1/wk >60<80 >30
Mild persistent 2 >2/wk, but <1 >2/mo 80 2030
Mild intermittent 1 2/wk <2/mo 80 <20

Rheumatic Diseases
Juvenile Rhuematoid Arthritis
TABLE 154-1 -- Criteria for the Classification of Juvenile Rheumatoid Arthritis
Age at onset: <16 yr
Arthritis (swelling or effusion, or the presence of 2 or more of the following signs: limitation of range of motion, tenderness or
pain on motion, increased heat) in 1 joints
Duration of disease: 6 wk
Onset type defined by type of articular involvement in the 1st 6 mo after onset:
Polyarthritis: 5 inflamed joints
Oligoarthritis: 4 inflamed joints
Systemic disease: arthritis with a characteristic intermittent fever
Exclusion of other forms of juvenile arthritis
Oligoarthritis (pauciarticular disease) predominantly affects the joints of the lower extremities, such as the knees and ankles (
Fig. 154-3 ). Often, only a single joint is involved at onset. Isolated involvement of upper extremity large joints is not
characteristic of this type of onset. Involvement of the hip is almost never a presenting sign of JRA. Hip disease may occur later,
particularly in polyarticular JRA, and is often a component of a deteriorating functional course.

Polyarthritis (polyarticular disease) is generally characterized by involvement of both large and small joints of both upper and
lower extremities. As many as 2040 joints may be affected in the more severely involved child, although inflammation of only
5 joints is required as a criterion for classification of this type of onset. Polyarticular disease may resemble the characteristic
presentation of adult rheumatoid arthritis and the HLA profile is often similar. Rheumatoid nodules on the extensor surfaces of
the elbows and over the Achilles tendons, while unusual, are associated with a more severe course. Micrognathia reflects chronic
temporomandibular joint disease. Cervical spine involvement of the apophyseal joints occurs frequently with a risk of atlantoaxial
subluxation and potential neurologic sequelae.

Systemic-onset disease is characterized by arthritis and prominent visceral involvement that includes hepatosplenomegaly,
lymphadenopathy, and serositis, such as a pericardial effusion. It is characterized by a quotidian fever with temperatures to 39C,
sometimes followed by mildly hypothermic temperatures for 2 wk. Each febrile episode is frequently accompanied by a
characteristic faint, erythematous, macular rash; these evanescent salmon-colored lesions may be linear or circular, from 25 mm
in size, and are often distributed in groups with a linear distribution most commonly over the trunk and proximal extremities. This
rash is not pruritic. Its most diagnostic feature is its transient nature, with a group of lesions usually lasting <1 hr. The Koebner
phenomenon, which is cutaneous hypersensitivity to superficial trauma resulting in a localized recurrence of the rash, is
suggestive, but not diagnostic, of systemic-onset disease. Heat, such as a warm bath, also evokes a reappearance of the rash.

Kawasaki Disease
TABLE 165-1 -- Clinical and Laboratory Features of Kawasaki Disease
Fever persisting at least 5 days[]
Presence of at least 4 principal features:
Changes in extremities
Acute: Erythema of palms, soles; edema of hands, feet
Subacute: Periungual peeling of fingers, toes in weeks 2 and 3
Polymorphous exanthem
Bilateral bulbar conjunctival injection without exudate
Changes in lips and oral cavity: Erythema, lips cracking, strawberry tongue, diffuse injection of oral and pharyngeal mucosae
Cervical lymphadenopathy (>1.5 cm diameter), usually unilateral
Exclusion of other diseases with similar findings[]

Systemic Lupus Erythematosus
TABLE 157-2 -- 1997 Revised Classification Criteria for Systemic Lupus Erythematosus
Malar rash Fixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds
Discoid rash Erythematous raised patches with adherent keratotic scaling and follicular plugging; atrophic scarring may occur in older
Photosensitivity Rash as a result of unusual reaction to sunlight (elicited by patient history or physician observation)
Oral ulcers Oral or nasopharyngeal ulceration, usually painless, observed by a physician
Arthritis Non-erosive arthritis involving two or more peripheral joints, characterized by tenderness, swelling, or effusion
Serositis Pleuritis:convincing history of pleuritic pain or rub heard by a physician or evidence of pleural effusion
Pericarditis:documented by ECG or rub or evidence of pericardial effusion
Renal disorder Persistent proteinuria >0.5 g/day or >3-plus (+ + +) if quantitation not performed
Cellular casts: may be red blood cell, hemoglobin, granular, tubular, or mixed
Neurologic Seizures:in the absence of offending drugs or known metabolic derangements (e.g., uremia, ketoacidosis, or electrolyte
disorder imbalance)
Psychosis:in the absence of offending drugs or known metabolic derangements (e.g., uremia, ketoacidosis, or electrolyte
Hematologic Hemolytic anemia, with reticulocytosis
Leukopenia: <4,000/mm3 total on two or more occasions
Lymphopenia: <1,500/mm3 on two or more occasions
Thrombocytopenia: <100,000/mm3
Immunologic Anti-DNA antibody to native DNA in abnormal titer
Anti-Smith:presence of antibody to Smith nuclear antigen
Positive finding of antiphospholipid antibodies based on (1) an abnormal serum level of lgG or lgM anticardiolipin
antibodies;(2) a positive test result for lupus anticoagulant using a standard method, or (3) a false-positive serologic test for
syphilis known to be positive for at least 6 mo and confirmed by Treponema pallidum immobilization or fluorescent
treponemal antibody absorption test (FTA-ABS), Standard methods should be used in testing for the presence of
Antinuclear An abnormal titer of antinuclear antibody by immunofluorescence or an equivalent assay at any time and in the absence of
antibody drugs known to be associated with drug-induced lupus syndrome
An approved modification deletes the positive LE cell preparation from the immunologic disorder criteria and substitutes the presence of a
biologic false-positive test for syphilis.
The proposed classification is based on 11 criteria. For the purpose of identifying patients in clinical studies, a person shall be said to have SLE
if any 4 or more of the 11 criteria are present, serially or simultaneously, during any interval of observa-tion.

Juvenile Dermatomyositis
o Heliotrope rash, Gottron papules
rash is often florid and is usually palpable over joints, especially the metacarpal phalangeal, intercarpal
phalangeal (Gottron papules), knees, elbows, and medial malleoli of the ankles
rash often has onset in sun-exposed areas and develops as the first symptom in 50% of cases, and
concomitantly with weakness in 25% of cases. The characteristic periorbital violaceous erythema

o Nail fold and gingival margin telangiectasia

o Palmar hyperkeratosis (mechanic's hands)
o Poikilodermatosis (dyspigmentation and telangiectasia) on the shoulder girdle (shawl sign)

Infectious Disease
Vaccine types
o whole inactivated microorganisms (polio and hepatitis A)
o parts of the organism (acellular pertussis, human papillomavirus [HPV], and HepB)
o polysaccharide capsules (pneumococcal and meningococcal polysaccharide vaccines)
o polysaccharide capsules conjugated to protein carriers (Hib, pneumococcal, and meningococcal conjugate vaccines)
o live attenuated microorganisms (measles, mumps, rubella, varicella, rotavirus, and live attenuated influenza vaccines)
o toxoids (tetanus and diphtheria)
Vaccine routes
o Most inactivated vaccines, including DTaP, hepatitis A, HepB, Hib, TIV, PCV7, MCV4, and Tdap, are administered
intramuscularly (IM).
o In contrast, the commonly used live attenuated vaccines, MMR and varicella, should be dispensed subcutaneously (SC).
o IPV and PPS23 (pneumococcal polysaccharide vaccine) can be given IM or SC.
o Immunologic responsiveness and efficacy following administration of pneumococcal polysaccharide vaccines is unpredictable in
children <2 yr of age. Two licensed pneumococcal vaccines contain purified polysaccharide of 23 valent pneumococcal serotypes
(PPV23) responsible for >95% of cases of invasive disease. The clinical efficacy of these vaccines is controversial, and studies
have yielded conflicting results. Polysaccharide antigens 6A, 14, 19F, and 23F frequently produce childhood disease and are
poorly immunogenic in children <5 yr of age.
o In contrast, pneumococcal polysaccharide vaccines conjugated to various proteins (heptavalent pneumococcal polysaccharide
conjugated to CRM197) provoke protective antibody responses in 90% of infants given these vaccines at 2, 4, and 6 mo of age,
and greatly enhanced responses (immunologic memory) are apparent after booster doses given at 1215 mo of age. In addition,
protein conjugate-polysaccharide vaccines reduce nasopharyngeal carriage of vaccine serotypes by up to 6070%. The currently
available heptavalent vaccine (PCV7) contains conjugated capsular polysaccharides of serotypes 4, 6B, 9V, 14, 19F, 23F, and
18C. Adverse events after the administration of PCV7 have included local swelling and redness and slightly increased rates of
fever, when used in conjunction with other childhood vaccines.
o Immunization with PCV7 is recommended for all infants in a schedule of 4 doses administered at 2, 4, 6, and 1215 mo of age.
High-risk children 2 yr of age (see Table 181-1 ), such as those with asplenia, sickle cell disease, some types of immune
deficiency (antibody deficiencies), HIV infection, or chronic lung, heart, or kidney disease (including nephrotic syndrome), may
benefit also from PPV23 administered after 2 yr of age and following priming with the scheduled doses of PCV7. After the initial
immunization, a single supplemental dose of PPV23 may be used 3 yr after the 1st dose for children <10 yr of age at the time of
revaccination, or it may be used at 5 yr after the 1st dose for children 10 yr of age or older at the time of revaccination.
o Universal immunization with diphtheria toxoid throughout life, to provide constant protective antitoxin levels and to reduce
severity of C. diphtheriae disease, is the only effective control measure. Although immunization does not preclude subsequent
respiratory or cutaneous carriage of toxigenic C. diphtheriae, it decreases local tissue spread, prevents toxic complications,
diminishes transmission of the organism, and provides herd immunity when at least 7080% of a population is immunized.
o The higher-potency (D) formulation of toxoid is used for primary series and booster doses for children through 6 yr of age
because of superior immunogenicity and minimal reactogenicity. For individuals 7 years of age or older, dT is recommended
for the primary series and booster doses because the lower concentration of diphtheria toxoid is adequately immunogenic and
because increasing the content of diphtheria toxoid heightens reactogenicity with increasing age.
o For children from 6 wk to 7 yr of age, five 0.5-mL doses of diphtheria-containing (D) vaccine are given in a primary series,
including 3 doses at 2, 4, and 6 mo of age, with a 4th dose, an integral part of the primary series, 912 mo after the third dose. A
booster dose is given at 46 yr of age (unless the 4th primary dose was administered after the 4th birthday). For persons 7 yr of
age and older, three 0.5 mL doses of diphtheria-containing (d) vaccine are given in a primary series of 2 doses 48 wk apart and a
3rd dose 612 mo after the 2nd dose. The only contraindication to tetanus and diphtheria toxoid is a history of neurologic or
severe hypersensitivity reaction after a previous dose. For children <7 yr of age in whom pertussis immunization is
contraindicated, DT is used. Those begun with DTaP or DT before 1 yr of age should have a total of five 0.5 mL doses of
diphtheria-containing (D) vaccines by 6 yr of age. For those beginning at around 1 yr of age, the primary series is three 0.5 mL
doses of diphtheria-containing (D) vaccine, with a booster given at 46 yr, unless the 3rd dose was given after the 4th birthday.
o A booster dose, consisting of an adult preparation of Tdap, is recommended at 1112 yr of age. Adolescents 1318 yr of age
who missed the 1112 year old Td or Tdap booster dose or in whom it has been 5 yr since the Td booster dose also should
receive a single dose of Tdap if they have completed the DTP/DTaP series.
o There is no association of DT or dT with convulsions. Local adverse effects alone do not preclude continued use. Persons who
experience Arthus-type hypersensitivity reactions or a temperature >103F (39.4C) after a dose of dT, which is rare, usually
have high serum tetanus antitoxin levels and should not be given dT more frequently than every 10 yr, even if a significant
tetanus-prone injury is sustained. DT or dT preparation can be given concurrently with other vaccines. Haemophilus influenzae
conjugate vaccines containing diphtheria toxoid (PRP-D) or the variant of diphtheria toxin, CRM197 protein (HbOC), are not
substitutes for diphtheria toxoid immunization and do not affect reactogenicity.
o A quadrivalent vaccine composed of capsular polysaccharides of meningococcal groups A, C, Y, and W135 (MPSV4) was the
primary meningococcal vaccine available in the United States until January 2005, with the approval of a diphtheria toxoidbased
protein-conjugate meningococcal vaccine (MCV4) for use in persons 1155 yr of age. MPSV4 is immunogenic in adults but is
unreliable in children <2 yr of age. It remains the only approved vaccine in the United States for children 210 yr of age and
adults >55 yr of age. About 75% of meningococcal disease among persons 11 yrs of age in the United States is caused by
serogroups C, Y, or W-135, and thus is potentially vaccine preventable.

o MCV4 and MPSV4 produce similar titers of anticapsular bactericidal antibodies against each of the 4 serogroups in the vaccines
at 1 mo after vaccination (in age-appropriate patients), with 4-fold increases in titer with both in >90% of vaccinees against
serogroups A, C, and W-135 and >80% against serogroup Y. Protective titers (1 : 128) are induced in >97% of recipients of
either vaccine against all 4 serogroups in age-appropriate patients. MCV4 causes transient fever and local redness, pain, or
swelling slightly more frequently than MPSV4, which is attributed to the diphtheria toxoid component of MCV4.
o The efficacy of MPSV4 is 85% for serogroups A and C and likely similar for serogroups W-135 and Y. Efficacy of MCV4 is
expected to be similar to MPSV4 since bactericidal antibodies confer immunity and the titers of these induced by MCV4 are
noninferior to those of MPSV4. Use of a serogroup Cdiphtheria CRM197 conjugate vaccine in the United Kingdom since 1999
has reduced serogroup C disease by about 95% in children in that country, and similar results with use of this vaccine have been
reported from Quebec. Reduced nasopharyngeal carriage of serogroup C strains among serogroup Cdiphtheria CRM197
vaccinees and community immunity (herd immunity) among nonvaccinees have been demonstrated in the U.K.
o Duration of immunity from MPSV4 is at most 35 yr, such that revaccination of persons with ongoing risk of meningococcal
infections can be considered within this time frame for past MPSV4 recipients. Protection from MCV4 is expected to be longer,
but the full duration and potential need for revaccination are not yet known. Immune responses to conjugate meningococcal
vaccines are boostable (T cell dependent), whereas those to MPSV4 are not (T cell independent). Conjugate vaccines appear to be
immunogenic and safe in infants but have not yet been approved or recommended for this age group in the United States.
o MCV4, as a single dose, is the preferred vaccine in the United States for persons 1155 yr of age for whom meningococcal
vaccination is recommended. MPSV4 remains an acceptable alternative for this age range when MCV4 is unavailable and is
recommended for children 210 yr of age and adults >55 yr of age, pending further evaluation and approval of MCV4 in these
age groups. The monovalent serogroup Cdiphtheria CRM197 conjugate vaccine currently is used in much of Europe, Canada,
Australia, and Brazil. A 3 dose series of this vaccine can be given to infants starting at 2 mo of age, with 1 dose recommended for
persons 1 yr of age.
o MCV4 is routinely recommended for all adolescents at 1112 yr at the pre-adolescent visit, and adolescents at age 15 yr or
high school entry if not previously vaccinated. The goal is routine vaccination of all 11 yr old adolescents beginning in 2008.
MCV4 and the Tdap (tetanus and diphtheria toxoids and acellular pertussis booster) vaccine should be administered to
adolescents during the same visit if both vaccines are indicated. If this is not feasible, MCV4 and Tdap can be administered in
either sequence with a minimum interval of 1 mo between vaccines. MCV4 is also recommended for all incoming college
freshmen living in dormitories. Many colleges and universities, and some states, have mandated meningococcal immunization of
all matriculating freshmen. MCV4 is also indicated for other adolescents who wish to decrease their risk for meningococcal
o Tetravalent meningococcal vaccines also are recommended for U.S. children 2 yr of age who have anatomic or functional
asplenia, complement component deficiencies that prevent terminal attack complex formation, or travel plans to areas with
hyperendemic or epidemic meningococcal infection rates such as sub-Saharan Africa during the DecemberJune dry season.
o Guillain-Barr syndrome (GBS) has been reported to be temporally related to administration of meningococcal vaccine, although
the rate among vaccine recipients is similar to that among the general population (see Chapter 615 ). Persons with previously
diagnosed GBS should not receive conjugate meningococcal vaccine.
o Three (primary) doses of DTaP should be administered during the 1st year of life, generally at ages 2, 4, and 6 mo of age. A 4th
dose (1st booster) is recommended for children at 1518 mo of age, at least 6 mo after the 3rd dose, to maintain adequate
immunity during the preschool years. The 4th dose may be administered as early as 12 mo of age, provided 6 mo have elapsed
since the 3rd dose and the child is unlikely to return at 1518 mo of age. The 5th dose (2nd booster) is recommended for children
at 46 yr of age to confer continued protection against disease during the early years of schooling. A 5th dose is not necessary if
the 4th dose in the series is administered on or after the 4th birthday.
o In 2005, 2 tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine, adsorbed (Tdap) products were licensed for
use in older individuals as single-dose booster vaccines to provide protection against tetanus, diphtheria, and pertussis. The
preferred age for Tdap vaccination is 1112 yr. All adolescents 1118 yr of age who received Td, but not Tdap, should receive a
single dose of Tdap to provide protection against pertussis if they have completed the recommended childhood DTP/DTaP
vaccination series. An interval of at least 5 yr between Td and Tdap is encouraged in routine situations to reduce the risk for local
and systemic reactions after Tdap vaccination. However, an interval of <5 yr between Td and Tdap can be used. Both Tdap and
tetravalent meningococcal conjugate vaccine should be administered to adolescents 1118 yr of age during the same visit if
both vaccines are indicated and available. Adults 1964 yr of age should receive a single dose of Tdap to replace their next Td
booster dose. Priority for Tdap vaccine should be given for health care workers who have contact with children and for eligible
family contacts of neonates.
o Globally, 2 vaccines are currently available for potential use in children. An oral, live-attenuated preparation of the Ty21a strain
of S. Typhi has been shown to have good efficacy (6782%) for up to 5 years. Significant adverse effects are rare. The Vi
capsular polysaccharide can be used in people 2 yr of age. It is given as a single intramuscular dose, with a booster every 2 yr
and has a protective efficacy of 7080%.
o Immunization with the live mumps vaccine is the primary mode of prevention used in the United States. It is given as part of the
MMR 2 dose vaccine schedule, at 1215 mo of age for the 1st dose and 46 yr of age for the 2nd dose. If not given at 46 yr, the
2nd dose should be given before children enter puberty. Antibody develops in 95% of vaccinees after 1 dose. One study showed
vaccine effectiveness of 88% for 2 doses of MMR vaccine compared with 64% for a single dose. Immunity appears to be long
lasting, with existing serologic and epidemiologic evidence indicating protection for >25 yr. As a live-virus vaccine, MMR
should not be administered to pregnant women or severely immunodeficient or immunosuppressed individuals. HIV-infected
patients not severely immunocompromised may receive the vaccine since the risk for severe infection with mumps outweighs the
risk for serious reaction to the vaccine. Individuals with anaphylactoid reactions to egg or neomycin may be at risk for immediate-
type hypersensitivity reactions to the vaccine. Persons with other types of reactions to egg or reactions to other components of the
vaccine are not restricted from receiving the vaccine.
Varicella is a vaccine-preventable disease. Live virus varicella vaccine is available as a monovalent vaccine and is also available in
combination with measles, mumps, and rubella (MMRV) vaccines. Administration of varicella vaccine within 4 wk of MMR vaccine has
been associated with a higher risk for breakthrough disease; therefore, it is recommended that the vaccines either be administered

simultaneously at different sites or be given at least 4 wk apart. Simultaneous administration of the vaccines may also be accomplished by
immunizing with the MMRV vaccine.
Varicella vaccine is recommended for routine administration to children at 1218 mo and at 46 yr of age. Catch-up vaccination with the
second dose is recommended for children and adolescents who received only 1 dose. Vaccination with 2 doses, separated by at least 4 wk,
is also recommended for children, adolescents, and adults without evidence of immunity. Breakthrough disease may be more common in
children vaccinated with a single dose younger than 15 mo.
Varicella vaccine is contraindicated in children with cell-mediated immune deficiencies, although the vaccine may be administered to
children with acute lymphoblastic leukemia who are in remission and who meet enrollment criteria under a research protocol, and the
vaccine may also be considered for HIV-infected children with a CD4 count greater than 15%. Both these groups should receive 2 doses of
vaccine, 3 months apart. Specific guidelines for immunizing these children should be reviewed before vaccination. Children with isolated
humoral immune deficiencies may receive VZV vaccine.
Vaccine virus establishes latent infection; however, the risk for developing subsequent herpes zoster is lower after vaccine than after natural
VZV infection among immunocompromised children. Postlicensure data also suggest the same trend in healthy vaccinees.
A new VZV vaccine formulation was licensed in 2006 for use as a single immunization of individuals >60 yr of age for prevention of
herpes zoster reactivation and to decrease the frequency of postherpetic neuralgia. It is not indicated for the treatment of zoster or
postherpetic neuralgia.
TABLE 255-3 -- Indications for Annual Influenza Vaccination

All children 659 mo of age

Persons 65 yr of age
Persons who live in nursing homes and other long-term care facilities that house those with long-term illnesses
Adults and children 6 mo of age with chronic heart or lung conditions, including asthma
Adults and children 6 mo of age who needed regular medical care or were in a hospital during the previous year because of a
metabolic disease (like diabetes), chronic kidney disease, or weakened immune system, including immune system problems caused
by medicines or by infection with HIV/AIDS
Children 6 mo to 18 yr of age who are on long-term aspirin therapy because of the increased risk for Reye syndrome (see Chapter
Women who will be pregnant during the influenza season
Persons with any condition that can compromise respiratory function or other handling of respiratory secretions such as a condition
that makes it hard to breathe or swallow (e.g., brain injury or disease, spinal cord injuries, seizure disorders, or the nerve or muscle


Because nearly of persons 5064 yr of age in the USA have 1 or more medical conditions that place them at increased risk for serious flu
complications, vaccination is recommended for all persons 5064 yr of age
Any person in close contact with someone in a high-risk group (see above) should get vaccinated. This includes all health care workers,
household contacts and out-of-home caregivers of children 023 mo of age, and close contacts of persons 65 yr of age

Because of the decreased potential for causing febrile reactions, only the split-virus vaccine is recommended for children <12 yr of
age. Two doses of vaccine (0.25 mL for 636 mo of age; 0.5 mL for 38 yr of age) at least 1 mo apart are recommended for primary
immunization of children <9 yr of age. Live-attenuated vaccines that are administered intranasally are in clinical trials and have been
demonstrated to have an efficacy comparable with that of inactivated vaccine in adults. Trials in children have shown efficacy of 90%.
These vaccines are currently licensed for use in ages 5 and above. Their ease of administration could serve to increase influenza
vaccination among children.

Post-Exposure Prophylaxis
o Susceptible individuals exposed to measles may be protected from infection either by vaccine administration or
immunization with immunoglobulin. The vaccine is effective in prevention or modification of measles if given within 72 hr
of exposure. Immune globulin may be given up to 6 days following exposure to prevent or modify infection.
Immunocompetent children should receive 0.25 mL/kg intramuscularly and immunocompromised children should receive
0.5 mL/kg. Immune globulin is indicated for susceptible household contacts of measles patients, especially infants <6 mo of
age, pregnant women, and immunocompromised persons.
Vaccine given to normal children within 35 days after exposure (as soon as possible is preferred) is effective in preventing or modifying
varicella, especially in a household setting where exposure is very likely to result in infection. Varicella vaccine is now recommended for
postexposure use, for outbreak control. Oral acyclovir administered late in the incubation period may modify subsequent varicella in the
normal child; however, its use in this manner is not recommended until it can be further evaluated.
High-titer anti-VZV immune globulin as postexposure prophylaxis is recommended for immunocompromised children, pregnant women,
and newborns exposed to maternal varicella to be administered intramuscularly within 96 hr of exposure. Although licensed pooled

intravenous immune globulin (IVIG) preparations contain antivaricella antibodies, the titer varies from lot to lot. Newborns whose
mothers develop varicella 5 days before to 2 days after delivery should receive 1 vial of VariZIG.
o All household contacts and those who have had intimate respiratory or habitual physical contact with a patient are closely
monitored for illness through the 7 day incubation period. Cultures of the nose, throat, and any cutaneous lesions are performed.
Antimicrobial prophylaxis is presumed effective and is administered regardless of immunization status using erythromycin (40
50 mg/kg/day divided qid PO for 7 days; maximum 2 g/day) or a single injection of benzathine penicillin G (600,000 U IM for
<30 kg, 1,200,000 U IM for 30 kg). Diphtheria toxoid vaccine, in age-appropriate form, is given to immunized individuals
who have not received a booster dose within 5 yr. Children who have not received their 4th dose should be vaccinated. Those
who have received fewer than 3 doses of diphtheria toxoid or who have uncertain immunization status are immunized with an
age-appropriate preparation on a primary schedule.
o Close contacts of patients with meningococcal disease are at increased risk for infection and should be carefully monitored and
brought to medical attention if fever develops. Antibiotic prophylaxis is indicated as soon as possible for household, daycare, and
nursery school contacts and for those who have had contact with the patient's oral secretions during the 7 days before onset of
illness. Prophylaxis is not routinely recommended for medical personnel except those with intimate exposure, such as with
mouth-to-mouth resuscitation, intubation, or suctioning before antibiotic therapy was begun. Children may be given rifampin (10
mg/kg orally every 12 hr for a total of 4 doses; maximum dose 600 mg; 5 mg/kg/dose for infants <1 mo of age) or ceftriaxone
(125 mg in a single dose IM for children <12 yr of age; 250 mg in a single dose IM for those >12 yr of age). Ciprofloxacin (500
mg orally as a single dose) may be given to persons 18 yr of age. Penicillin does not eradicate nasopharyngeal carriage;
patients treated with penicillin should receive prophylaxis before hospital discharge.
H. influenza
o For prophylaxis, children should be given rifampin orally (01 mo of age, 10 mg/kg/dose; >1 mo of age, 20 mg/kg/dose, not to
exceed 600 mg/dose) once a day for 4 consecutive days. The adult dose is 600 mg once daily. Rifampin prophylaxis is not
recommended for pregnant women.
TABLE 194-2 -- Recommended Antimicrobial Treatment and Postexposure Prophylaxis for Pertussis, by Age Group

AGE GROUP Azithromycin Erythromycin Clarithromycin TMP-SMZ

<1 mo Recommended agent. 10 Not preferred. Not recommended Contraindicated for

mg/kg/day in a single dose Erythromycin is associated (safety data infants aged <2 mo (risk
for 5 days (only limited with infantile hypertrophic unavailable) for kernicterus)
safety data available) pyloric stenosis.

Use if azithromycin is
unavailable; 4050
mg/kg/day in 4 divided
doses for 14 days.

15 mo 10 mg/kg/day in a single 4050 mg/kg/day in 4 15 mg/kg/day in 2 Contraindicated at age

dose for 5 days divided doses for 14 days. divided doses for 7 <2 mo For infants aged
days 2 mo.

TMP 8 mg/kg/day,
SMZ 40 mg/kg/day in 2
divided doses for 14

Infants (aged 6 10 mg/kg in a single dose on 4050 mg/kg/day 15 mg/kg/day in 2 TMP 8 mg/kg/day,
mo) and day 1 then 5 mg/kg/day (maximum 2 g/day) in 4 divided doses SMZ 40 mg/kg/day in 2
children (maximum 500 mg) on days divided doses for 14 days. (maximum 1 g/day) divided doses for 14
25 for 7 days days

Adults 500 mg in a single dose on 2 g/day in 4 divided doses 1 g/day in 2 divided TMP 320 mg/day, SMZ
day 1 then 250 mg/day on for 14 days. doses for 7 days 1,600 mg/day in 2
days 25 divided doses for 14
From Centers for Disease Control and Prevention: Recommended antimicrobial agents for treatment and postexposure prophylaxis of
pertussis. 2005 CDC Guidelines. MMWR 2005;54:116.
* Trimethoprim-sulfamethoxazole (TMP-SMZ) can be used as an alternative agent to macrolides in patients aged
2 mo who are allergic to macrolides, who cannot tolerate macrolides, or who are infected with a rare
macrolide-resistant strain of Bordetella pertussis.

o Intermittent fever is an exaggerated circadian rhythm that includes a period of normal temperatures on most days.
o Extremely wide fluctuations may be termed septic or hectic fever.
o Sustained fever is persistent and does not vary by more than 0.5C/day.
o Remittent fever is persistent and varies by more than 0.5C/day.
o Relapsing fever is characterized by febrile periods that are separated by intervals of normal temperature; tertian
fever occurs on the 1st and 3rd days (malaria caused by Plasmodium vivax), and quartan fever occurs on the 1st
and 4th days (malaria caused by Plasmodium malariae).
o Biphasic fever indicates a single illness with 2 distinct periods (camelback fever pattern); poliomyelitis is the
classic example. A biphasic course is also characteristic of leptospirosis, dengue fever, yellow fever, Colorado tick
fever, spirillary rat-bite fever (Spirillum minus), and the African hemorrhagic fevers (Marburg, Ebola, and Lassa
o Periodic fever is used narrowly to describe fever syndromes with a regular periodicity (cyclic neutropenia, and
periodic fever, aphthous stomatitis, pharyngitis, and adenopathy [PFAPA]) or more broadly to include disorders
characterized by recurrent episodes of fever that do not follow a strictly periodic pattern (familial Mediterranean
fever, Hibernian fever, TNF-receptor-associated periodic syndrome [TRAPS], hyper-IgD syndrome, the Muckle-
Wells syndrome).

Risk factors indicating increased probability of occult bacteremia

o temperature 39C
o WBC count 15,000/L
o an elevated absolute neutrophil count, band count, erythrocyte sedimentation rate, or C-reactive protein
H. influenzae type b bacteremia is characteristically of higher grade, as determined by quantitative blood culture
techniques, and is associated with a higher risk for localized serious infection than is bacteremia due to S. pneumoniae.
Hospitalized children with H. influenzae type b bacteremia often develop focal infections, such as meningitis, epiglottitis,
cellulitis, pericarditis, or osteoarticular infection, whereas fewer than 5% of these bacteremias can be considered transient
or occult. In contrast, among all patients with pneumococcal bacteremia (occult, symptomatic, or focal), spontaneous
resolution occurs in 3040%, with a higher rate of spontaneous resolution among well-appearing children with occult
pneumococcal bacteremia.
Consensus recommendations
o empirical antimicrobial therapy for well-appearing children <36 mo of age who have not received H. influenzae type
b and S. pneumoniae conjugate vaccines who have a rectal temperature of 39C and a WBC count of 15,000/L
o infants 336 mo of age who have a temperature of <39C and who do not appear toxic can be observed as
outpatients without performing diagnostic tests or administering antimicrobial agents
Fever of unknown origin
o The term fever of unknown origin (FUO) is best reserved for children with a fever documented by a health care
provider and for which the cause could not be identified after 3 wk of evaluation as an outpatient or after 1 wk of
evaluation in hospital. Patients with fever not meeting these criteria, and specifically those admitted to the hospital
with neither an apparent site of infection nor a noninfectious diagnosis, may be considered to have fever without
localizing signs.
o JRA and systemic lupus erythematosus are the connective tissue diseases associated most frequently with FUO.
o Diagnostic clues
Drug fever is usually sustained and not associated with other symptoms. Discontinuation of the drug is
associated with resolution of the fever, generally within 72 hr, although certain drugs, such as iodides, are
excreted for a prolonged period with fever that may persist for as long as 1 mo after drug withdrawal.
Any history of pica should be elicited. Ingestion of dirt is a particularly important clue to infection with
Toxocara (visceral larva migrans) or Toxoplasma gondii (toxoplasmosis).
The ophthalmoscope should also be used to examine nailfold capillary abnormalities that are associated with
connective tissue diseases such as juvenile dermatomyositis and systemic scleroderma. Immersion oil or
lubricating jelly is placed on the skin adjacent to the nailbed, and the capillary pattern is observed with the
ophthalmoscope set on +40.
Tenderness to tapping over the sinuses or the upper teeth suggests sinusitis.
Recurrent oral candidiasis may be a clue to various disorders of the immune system.

red, weeping eyes polyarteritis nodosa

palpebral conjunctivitis measles, coxsackievirus infection, tuberculosis, infectious mononucleosis,

lymphogranuloma venereum, and cat-scratch disease
bulbar conjunctivitis Kawasaki disease or leptospirosis
petechial conjunctival hemorrhages infective endocarditis

uveitis sarcoidosis, JRA, systemic lupus erythematosus, Kawasaki disease, Behet

disease, vasculitis

chorioretinitis CMV, toxoplasmosis, and syphilis

proptosis orbital tumor, thyrotoxicosis, metastasis (neuroblastoma), orbital infection,

Wegener granulomatosis, pseudotumor

failure of pupillary constriction hypothalamic dysfunction

fever blisters pneumococcal, streptococcal, malarial, rickettsial infection; meningococcal

meningitis (rare in meningococcemia)
hyperemia of the pharynx infectious mononucleosis, CMV infection, toxoplasmosis, salmonellosis,
tularemia, Kawasaki disease, leptospirosis
point tenderness over a bone occult osteomyelitis or bone marrow invasion from neoplastic disease

tenderness over the trapezius subdiaphragmatic abscess

generalized muscle tenderness dermatomyositis, trichinosis, polyarteritis, Kawasaki disease, or mycoplasmal or

arboviral infection

perirectal lymphadenopathy or deep pelvic abscess, iliac adenitis, or pelvic osteomyelitis


occult blood loss granulomatous colitis or ulcerative colitis

hyperactive deep tendon reflexes thyrotoxicosis

Communicability / Incubation Periods

Period of communicability
Strep pharyngitis Febrile phase of the disease (24 h if treated and 12-20 days if untreated)
N. meningitidis 7 days before onset of illness to 24 hrs after initiation of effective therapy

Pertussis Until 5 days after initiation of macrolide therapy

Measles 3 days before the rash up to 4-6 days after

Rubella Viral shedding from the nasopharynx begins about 10 days after infection and may be detected up to 2
wk following onset of the rash. The period of highest communicability is from 5 days before to 6 days
following appearance of the rash.

Mumps Virus appears in the saliva from up to 7 days before to as long as 7 days after onset of parotid
swelling. The period of maximum infectiousness is 12 days before to 5 days after parotid swelling.

Polio Poliovirus has been isolated from feces for >2 wk before paralysis to several weeks after the onset of
Enterovirus Infected children, both symptomatic and asymptomatic, frequently shed enteroviruses from the
respiratory tract for <13 wk, whereas fecal shedding continues up to 711 wk postinfection.
Parvovirus B19 Children with erythema infectiosum are not likely to be infectious at presentation because the rash
and arthropathy represent immune-mediated, postinfectious phenomena. Isolation and exclusion from
school or child care are unnecessary and ineffective after diagnosis.
Children with B19-induced red cell aplasia, including the transient aplastic crisis, are infectious when
they present and demonstrate a more intense viremia. Most of these children require transfusions and
supportive care until their hematologic status stabilizes. They should be isolated in the hospital to
prevent spread to susceptible patients and staff. Isolation should continue for at least 1 wk and until
after resolution of fever. Pregnant caregivers should not be assigned to these patients. Exclusion of
pregnant women from workplaces where children with erythema infectiosum may be present (e.g.,
primary and secondary schools) is not recommended as a general policy because it is unlikely to
reduce their risk.
Varicella Patients with varicella are contagious from 24 to 48 hr before the rash appears and until vesicles are
crusted, usually 37 days after onset of rash.

Incubation periods
Diphtheria 2-7 days

Strep pharyngitis 2-5 days

Genital gonorrhea 2-5 days in men; 5-10 days in women; 1-4 days after birth in opthalmia neonatorum

Pertussis 3-12 days

Salmonella enteritis 6-72 hours (mean 24 hours)

Typhoid fever 4-14 days; usually 7-14 days (range 3-30 days)

Shigella 12 hrs to several days

Cholera 18 hrs to 5 days

Tetanus 2-14 days

Rubella 16-18 days (figure) / 14-21 days (text)

Mumps 12-25 days (usually 16-18 days)

Polio Usually 8-12 days (range 5-35 days)

Enteroviruses The incubation period of enterovirus infections is typically 36 days, except for acute
hemorrhagic conjunctivitis, which has an incubation period of 13 days.

Varicella Usually 14-16 days (range 10-21 days)

Most important respiratory tract pathogen of early childhood - RSV

Single most important cause of severe dehydrating diarrhea in early childhood - rotavirus

Gram Positive Bacteria

Staphylococcus aureus
TABLE 180-3 -- Diagnostic Criteria of Staphylococcal Toxic Shock Syndrome

Acute fever; temperature >38.8C

Hypotension (orthostatic, shock; below age-appropriate norms)
Rash (erythroderma with late desquamation)


Mucous membrane inflammation

Vomiting, diarrhea
Liver abnormalities
Renal abnormalities
Muscle abnormalities
Central nervous system abnormalities


Absence of another explanation

Negative blood cultures (except occasionally for S. aureus)

Streptococcus pneumoniae
o S. pneumoniae is the most frequent cause of bacteremia, bacterial pneumonia, and otitis media, and the second
most common cause of meningitis in children.

TABLE 181-1 -- Children at High or Moderate Risk of Invasive Pneumococcal Infection
High risk (incidence of invasive pneumococcal disease =150 cases/100,000 people per year)

Children with:
Sickle cell disease, congenital or acquired asplenia, or splenic dysfunction

Human immunodeficiency virus infection

Cochlear implants

Presumed high risk (insufficient data to calculate rates)

Children with:
Congenital immune deficiency; some B-(humoral) or T-lymphocyte deficiencies, complement deficiencies
(particularly C1, C2, C3, and C4), or phagocytic disorders (excluding chronic granulomatous disease)

Chronic cardiac disease (particularly cyanotic congenital heart disease and cardiac failure)

Chronic pulmonary disease (including asthma treated with high-dose oral corticosteroid therapy)
Cerebrospinal leaks from a congenital malformation, skull fracture, or neurologic procedure

Chronic renal insufficiency, including nephrotic syndrome

Diseases associated with immunosuppressive therapy or radiation therapy (including malignant neoplasms,
leukemias, lymphomas, and Hodgkin disease) and solid organ transplantation

Diabetes mellitus

Moderate risk (incidence of invasive pneumococcal disease =20 cases/100,000 people Per year)

All children 2435 mo of age

Children 3659 mo of age attending out-of-home child care

Children 3659 mo of age who are black or of American Indian/Alaska Native descent

o Immunization with PCV7 is recommended for all infants in a schedule of 4 doses administered at 2, 4, 6, and 1215 mo of age.
High-risk children 2 yr of age such as those with asplenia, sickle cell disease, some types of immune deficiency (antibody
deficiencies), HIV infection, or chronic lung, heart, or kidney disease (including nephrotic syndrome), may benefit also from
PPV23 administered after 2 yr of age and following priming with the scheduled doses of PCV7. After the initial immunization,
a single supplemental dose of PPV23 may be used 3 yr after the 1st dose for children <10 yr of age at the time of revaccination,
or it may be used at 5 yr after the 1st dose for children 10 yr of age or older at the time of revaccination.

Group A Streptococcus
o Severe invasive GAS infection
Varicella is the most commonly identified risk factor in children.
In most cases, portal of entry is believed to be skin or mucous membrane. Severe invasive disease rarely follows GAS

Streptococcal vs staphylococcal impetigo

Streptococcal: vesicular --> pustular --> rupture and form thick, honey colored crust
Staphylococcal: generally bullous

Scarlet fever
o The rash appears within 2448 hr after onset of symptoms, although it may appear with the 1st signs of illness . It often begins
around the neck and spreads over the trunk and extremities. It is a diffuse, finely papular, erythematous eruption producing a bright
red discoloration of the skin, which blanches on pressure. It is often more intense along the creases of the elbows, axillae, and groin.
The skin has a goose-pimple appearance and feels rough. The face is usually spared, although the cheeks may be erythematous with
pallor around the mouth.
o After 34 days, the rash begins to fade and is followed by desquamation, 1st on the face, progressing downward, and often
resembling that seen subsequent to a mild sunburn. Occasionally, sheetlike desquamation may occur around the free margins of the
fingernails, the palms, and the soles. Examination of the pharynx of a patient with scarlet fever reveals essentially the same findings
as with GAS pharyngitis.
o In addition, the tongue is usually coated and the papillae are swollen. After desquamation, the reddened papillae are prominent,
giving the tongue a strawberry appearance.

Why can glomerulonephritis occur after both throat and skin infections while rheumatic fever occurs only after throat infections?
o GAS can be subdivided into >100 serotypes on the basis of the M protein antigen, which is located on the cell surface and in
fimbriae that project from the outer edge of the cell.
o The M types commonly associated with pharyngitis rarely cause skin infections, and the M types commonly associated with skin
infections rarely cause pharyngitis.

o A few of the pharyngeal strains (M type 12) have been associated with glomerulonephritis, but far more of the skin strains (M
types 49, 55, 57, and 60) have been considered nephritogenic. A few of the pharyngeal serotypes, but none of the skin strains, have
been associated with acute rheumatic fever.
o Rheumatogenic potential is not solely dependent on the serotype but is a characteristic of specific strains within several serotypes.

Group B Streptococcus
o TABLE 183-2 -- Recommended Duration of Therapy for Manifestations of GBS Disease

Bacteremia without a focus 10 days

Meningitis 23 wk

Ventriculitis 4 wk

Osteomyelitis 4 wk

o GBS prophylaxis
Vaginorectal GBS screening cultures should be performed for all pregnant women at 3537 wk gestation.
Women whose culture status is unknown (culture not done, incomplete, or results unknown) and who deliver prematurely
(<37 wk gestation) or experience prolonged rupture of membranes (18 hr) or intrapartum fever (38.0C) should also
receive intrapartum chemoprophylaxis. If amnionitis is suspected, broad-spectrum antibiotic therapy that includes an agent
active against GBS should replace GBS prophylaxis.
Cefazolin if penicillin intolerant
Clindamycin or erythromycin for penicillin allergic at high risk for anaphylaxis

Asymptomatic Case Contacts: All household contacts and those who have had intimate respiratory or habitual physical contact with a patient are
closely monitored for illness through the 7 day incubation period. Cultures of the nose, throat, and any cutaneous lesions are performed.
Antimicrobial prophylaxis is presumed effective and is administered regardless of immunization status using erythromycin (4050 mg/kg/day
divided qid PO for 7 days; maximum 2 g/day) or a single injection of benzathine penicillin G (600,000 U IM for <30 kg, 1,200,000 U IM for
30 kg). Diphtheria toxoid vaccine, in age-appropriate form, is given to immunized individuals who have not received a booster dose within 5
yr. Children who have not received their 4th dose should be vaccinated. Those who have received fewer than 3 doses of diphtheria toxoid or who
have uncertain immunization status are immunized with an age-appropriate preparation on a primary schedule.
Asymptomatic Carriers: When an asymptomatic carrier is identified, antimicrobial prophylaxis is given for 7 days and an age-appropriate
preparation of diphtheria toxoid is administered immediately if a booster has not been given within 1 yr. Individuals are placed on droplet
precautions (respiratory tract colonization) or contact precautions (cutaneous colonization only) until at least 2 subsequent cultures obtained 24
hr apart after cessation of therapy are negative. Repeat cultures are performed about 2 wk after completion of therapy for cases and carriers, and,
if positive, an additional 10 day course of oral erythromycin should be given and follow-up cultures performed. Susceptibility testing of isolates
should be performed as erythromycin resistance is reported. Neither antimicrobial agent eradicates carriage in 100% of individuals. In 1 report,
21% of carriers failed a single course of therapy. Antitoxin is not recommended for asymptomatic close contacts or carriers, even if inadequately
immunized. Transmission of diphtheria in modern hospitals is rare. Only those with an unusual contact with respiratory or oral secretions should
be managed as contacts. Investigation of the casual contacts of patients and carriers or persons in the community without known exposure has
yielded extremely low carriage rates and is not routinely recommended.

Gram Negative Bacteria

Bordetella pertussis
o For sporadic cases, a clinical case definition of cough of 14 days' duration with at least 1 associated symptom of paroxysms,
whoop, or post-tussive vomiting has a sensitivity of 81% and specificity of 58% for culture confirmation. Pertussis should be
suspected in older children whose cough illness is escalating at 710 days and whose coughing episodes are not continuous.
Pertussis should be suspected in infants <3 mo of age with apnea, cyanosis, or an acute life-threatening event (ALTE).
o Stages
Incubation 3-12 days

Catarrhal 1-2 weeks

Paroxysmal 2-6 weeks

Convalescent 2 weeks
Salmonella typhi
o Individuals who excrete S. Typhi for 3 mo after infection are regarded as chronic carriers.
o Shigellae require very low inocula to cause illness. Ingestion of as few as 10 S. dysenteriae serotype 1 organisms can cause
dysentery in some susceptible individuals. This is in contrast to organisms such as Vibrio cholerae, which require ingestion of
1081010 organisms to cause illness. The inoculum effect explains the ease of person-to-person transmission (major
mechanism) of shigellae in contrast to V. cholerae.
o Colon is the target organ (most intense changes in the distal colon)
o Greater severity and risk for complications with S. dysenteriae serotype 1 infection (this type tends to occur in epidemics)

Viral Infections
o Koplik spots appear 1-4 days prior to the onset of the rash
o Cough is the symptom that lasts the longest (often up to 10 days)
Labs: reduced total WBC with lymphocytes more decreased than neutrophils; normal ESR and CRP
o Susceptible individuals exposed to measles may be protected from infection either by vaccine administration or immunization
with immunoglobulin. The vaccine is effective in prevention or modification of measles if given within 72 hr of exposure.
Immune globulin may be given up to 6 days following exposure to prevent or modify infection. Immunocompetent children
should receive 0.25 mL/kg intramuscularly and immunocompromised children should receive 0.5 mL/kg. Immune globulin is
indicated for susceptible household contacts of measles patients, especially infants <6 mo of age, pregnant women, and
immunocompromised persons.
o Centrifugal rash
o Labs: leukopenia, neutropenia, mild thrombocytopenia
o Most common clinical manifestations of CRS: ocular (cataracts or retinopathy in 71%) and deafness (67%)
o Patients with postnatal infection should be isolated from susceptible individuals for 7 days after onset of the rash. Standard plus
droplet precautions are recommended for hospitalized patients. Children with CRS may excrete the virus in respiratory secretions
up to 1 yr of age and should be maintained in contact precautions until then unless repeated cultures of urine and pharyngeal
secretions are negative. Similar precautions apply to CRS patients with regard to attendance in school and out-of-home child care.
o Manifestations of nonpolio enteroviruses: nonspecific febrile illness, hand-foot-mouth disease, herpangina, pleurodynia, URTI,
acute hemorrhagic conjunctivitis, myocarditis and pericarditis, diarrhea, meningitis, myositis, arthritis, pancreatitis, orchitis
o Poliovirus
In suspected cases of acute flaccid paralysis, 2 stool specimens should be collected 2448 hr apart, as soon as possible
after the diagnosis of poliomyelitis is suspected. Poliovirus concentrations are high in the stool in the 1st week after the
onset of paralysis, which is the optimal time for collection of stool specimens. Polioviruses may be isolated from 8090%
of acutely ill patients, whereas <20% may yield virus within 34 wk after onset of paralysis. Because most children with
spinal or bulbospinal poliomyelitis have constipation, rectal straws may be used to obtain specimens; ideally a minimum
of 810 g of stool should be collected.
o Coxsackievirus
Characteristic lesions, present on the anterior tonsillar pillars, soft palate, uvula, tonsils, posterior pharyngeal wall,
and, occasionally, the posterior buccal surfaces, are discrete 12 mm vesicles and ulcers that enlarge over 23 days
to 34 mm and are surrounded by erythematous rings that vary in size up to 10 mm. Typically about 5 lesions are
present, with a range of 1 to >15.
Pleurodynia (Bornholm disease) is an epidemic or sporadic illness characterized by paroxysmal thoracic pain, due
to myositis involving chest and abdominal wall muscles.
o Echovirus (enteric cytopathic human orphan virus)
Parvovirus B19
o Erythema infectiosum / fifth disease
o Arthropathy
o Transient aplastic crisis
o Myocarditis
o Papular-purpuric gloves and socks syndrome (PPGSS)
o The hallmarks of common HSV infections are skin vesicles and shallow ulcers.
o The vesicles may be more extensively distributed than typically seen with enteroviral herpangina.
o The most common site of herpes labialis is the vermilion border of the lip.
Vaccine given to normal children within 35 days after exposure (as soon as possible is preferred) is effective in preventing or modifying
varicella, especially in a household setting where exposure is very likely to result in infection. Varicella vaccine is now recommended for
postexposure use, for outbreak control. Oral acyclovir administered late in the incubation period may modify subsequent varicella in the
normal child; however, its use in this manner is not recommended until it can be further evaluated.
High-titer anti-VZV immune globulin as postexposure prophylaxis is recommended for immunocompromised children, pregnant women,
and newborns exposed to maternal varicella. Human varicella-zoster immune globulin (VariZIG) is distributed by FFF Enterprises,
California, (1-800-843-7477) to be administered intramuscularly within 96 hr of exposure. The recommended dose is 1 vial (125 units)
for each 10 kg increment (maximum 625 units) given intramuscularly as soon as possible but within 96 hr after exposure.
Although licensed pooled intravenous immune globulin (IVIG) preparations contain antivaricella antibodies, the titer varies from lot to
lot. The recommended dose of IVIG for postexposure prophylaxis is 400 mg/kg administered once within 96 hr of exposure.
Immunocompromised patients who have received high-dose IVIG (100400 mg/kg) for other indications within 23 wk before VZV
exposure can be expected to have serum antibodies to VZV.
Newborns whose mothers develop varicella 5 days before to 2 days after delivery should receive 1 vial of VariZIG. VariZIG is also
indicated for pregnant women, premature infants <28 wk of gestation (<1,000 g) who were exposed to varicella, and premature infants
>28 wk of gestation who are exposed to varicella and whose mother has no evidence of varicella immunity. If possible, adults should be
tested for VZV IgG antibodies before VariZIG administration because many adults with no clinical history of varicella are immune. Anti-
VZV antibody prophylaxis may ameliorate disease but does not eliminate the possibility of progressive disease, nor does it assure that
varicella is not transmitted to close susceptible contacts; patients should be monitored and treated with acyclovir if necessary once lesions
Close contact between a susceptible high-risk patient and a patient with herpes zoster is also an indication for VariZIG prophylaxis.
Passive antibody administration or treatment does not reduce the risk for herpes zoster or alter the clinical course of varicella or herpes
zoster when given after the onset of symptoms.

o Benign EBV-associated proliferations include oral hairy leukoplakia, primarily in adults with AIDS, and lymphoid interstitial
pneumonitis, primarily in children with AIDS. Malignant EBV-associated proliferations include nasopharyngeal carcinoma,
Burkitt lymphoma, Hodgkin disease, lymphoproliferative disorders, and leiomyosarcoma in immunodeficient states, including
o Epitrochlear LAD most suggestive.
o Splenomegaly is typical.
o "Ampicillin rash" if treated with ampicillin or amoxicillin.
Very few patients with infectious mononucleosis experience complications. The most feared complication is subcapsular splenic
hemorrhage or splenic rupture, which occurs most frequently during the 2nd week of the disease at a rate of <0.5% of cases in adults;
the rate in children is unknown but is probably much lower. Rupture is commonly related to trauma, which often may be mild, and is
rarely fatal. Swelling of the tonsils and oropharyngeal lymphoid tissue may be substantial and may cause airway obstruction that
manifests as drooling, stridor, and interference with breathing. Airway compromise with progressive symptoms occurs in <5% of cases
and is a common indication for hospitalization with infectious mononucleosis. It may be managed by elevating the head of the bed and
administration of intravenous hydration, humidified air, and systemic corticosteroids. Respiratory distress with incipient or actual
airway occlusion should be managed by tonsillo-adenoidectomy followed by endotracheal intubation for 1224 hr in an intensive care
Many uncommon and unusual neurologic conditions have been reported to be associated with EBV infectious mononucleosis.
Headache is present in about half of cases, with severe neurologic manifestations, such as seizures and ataxia, in 15% of cases.
Perceptual distortions of sizes, shapes, and spatial relationships, known as the Alice in Wonderland syndrome (metamorphopsia),
may be a presenting symptom. There may be meningitis with nuchal rigidity and mononuclear cells in the cerebrospinal fluid, facial
nerve palsy, transverse myelitis, and encephalitis.
Guillain-Barr syndrome or Reye syndrome may follow acute illness. Hemolytic anemia, often with a positive Coombs test result and
with cold agglutinins specific for red cell antigen i, occurs in 3% of cases. The onset is typically in the 1st 2 wk of illness and lasts for
<1 mo. Aplastic anemia is a rare complication that usually presents 34 wk after the onset of illness, usually with recovery in 48
days, but some cases do require bone marrow transplantation. Mild thrombocytopenia and neutropenia are common, but severe
thrombocytopenia (<20,000 platelets/L) or severe neutropenia (<1,000 neutrophils/L) are rare. Myocarditis or interstitial pneumonia
may occur, both resolving in 34 wk. Other rare complications include pancreatitis, parotitis, and orchitis.

The prodromal period of roseola is usually asymptomatic but may include mild upper respiratory tract signs, among them minimal
rhinorrhea, slight pharyngeal inflammation, and mild conjunctival redness. Mild cervical or, less frequently, occipital
lymphadenopathy may be noted. Some children may have mild palpebral edema. Physical findings during the prodromal stage have no
clear relationship to roseola, and may simply reflect an accompanying respiratory viral infection. Clinical illness is generally heralded
by high temperature, usually ranging from 37.9 to 40C (101106F), with an average of 39C (103F). Some children may become
irritable and anorexic during the febrile stage, but most behave normally despite high temperatures. Seizures may occur in 510% of
children with roseola during this febrile period. Infrequent complaints include rhinorrhea, sore throat, abdominal pain, vomiting, and
diarrhea. In Asian countries, ulcers at the uvulopalatoglossal junction (Nagayama spots) are common in infants with roseola. Fever
persists for 35 days, and then typically resolves rather abruptly (crisis). Occasionally, the fever may gradually diminish over 2436
hours (lysis). A rash appears within 1224 hr of fever resolution. In many cases, the rash develops during defervescence or within a
few hours of fever resolution. The rash of roseola is rose colored, as the name implies, and is fairly distinctive. However, it may be
confused with exanthems resulting from rubella, measles, or erythema infectiosum. The roseola rash begins as discrete, small (25
mm), slightly raised pink lesions on the trunk and usually spreads to the neck, face, and proximal extremities. The rash is not usually
pruritic, and no vesicles or pustules develop. Lesions typically remain discrete but occasionally may become almost confluent . After
13 days, the rash fades. Some children experience evanescent rashes that resolve within a few hours. Subtle differences in clinical
presentation have been noted between roseola associated with HHV-7 compared with HHV-6. These include a slightly older age,
lower mean temperature, and shorter duration of fever in HHV-7-associated cases. However, these differences are insufficient to
clinically distinguish HHV-6- from HHV-7-associated roseola. There are reports of children experiencing HHV-6-associated roseola
followed later by HHV-7-associated roseola.

TORCH Infections

Congenital infection may present as a mild or severe neonatal disease, with onset during the 1st mo of life or with sequelae or relapse of a
previously undiagnosed, and untreated, infection presenting during infancy or even later in life. There is a wide variety of manifestations of
congenital infection ranging from hydrops fetalis and perinatal death to small size for gestational age, prematurity, peripheral retinal scars,
persistent jaundice, mild thrombocytopenia, CSF pleocytosis, and the characteristic triad of chorioretinitis, hydrocephalus, and cerebral
calcifications. More than half of congenitally infected infants are considered normal in the perinatal period, but almost all such children develop
ocular involvement later in life if they are not treated during infancy. Neurologic signs such as convulsions, setting-sun sign with downward
gaze, and hydrocephalus with increased head circumference may be associated with or without substantial cerebral damage, or with relatively
mild inflammation obstructing the aqueduct of Sylvius. If affected infants are treated promptly, signs and symptoms may resolve and they may
develop normally.

All newborns infected with T. gondii should be treated whether or not they have clinical manifestations of the infection because treatment may
be effective in interrupting acute disease that damages vital organs. Infants should be treated for 1 yr with pyrimethamine (2 mg/kg/day for 2
days, then 1 mg/kg/day for 2 or 6 mo, then 1 mg/kg given on Monday, Wednesday, and Friday, or more often, PO), sulfadiazine (100 mg/kg/day
divided bid PO), and leukovorin (510 mg given on Monday, Wednesday, and Friday, PO).

TABLE 244-1 -- Pathologic Findings of Congenital Rubella Syndrome

Cardiovascular Patent ductus arteriosus

Pulmonary artery stenosis

Ventriculoseptal defect


Central nervous system Chronic meningitis

Parenchymal necrosis

Vasculitis with calcification

Eye Microphthalmia



Ciliary body necrosis



Ear Cochlear hemorrhage

Endothelial necrosis

Lung Chronic mononuclear interstitial pneumonitis

Liver Hepatic giant cell transformation


Lobular disarray

Bile stasis

Kidneys Interstitial nephritis

Andrenal glands Cortical cytomegaly

Bone Malformed osteoid

Poor mineralization of osteoid

Thinning cartilage

Spleen, lymph nodes Extramedullary hematopoiesis

Thymus Histiocytic reaction

Absence of germinal centers

Skin Erythropoiesis in dermis

o The most important risk factor for severe congenital defects is the stage of gestation at the time of infection. Maternal infection
during the 1st 8 wk of gestation results in the most severe and widespread defects. The risk for congenital defects has been
estimated at 90% for maternal infection before 11 wk of gestation, 33% at 1112 wk, 11% at 1314 wk, and 24% at 1516 wk.
Defects occurring after 16 wk of gestation are uncommon, even if fetal infection occurs.
Nerve deafness is the single most common finding among infants with CRS. Most infants have some degree of intrauterine
growth restriction. Retinal findings described as salt-and-pepper retinopathy are the most common ocular abnormality, but it
has little early effect on vision. Unilateral or bilateral cataracts are the most serious eye finding, occurring in about of infants (
Fig. 244-4 ). Cardiac abnormalities occur in half of the children infected during the 1st 8 wk of gestation. Patent ductus arteriosus
is the most frequently reported cardiac defect, followed by lesions of the pulmonary arteries and valvular disease. Interstitial
pneumonitis leading to death in some cases has been reported. Neurologic abnormalities are common and may progress following
birth. Meningoencephalitis is present in 1020% of infants with CRS and may persist for up to 12 mo. Longitudinal follow-up
through 912 yr of infants without initial retardation revealed progressive development of additional sensory, motor, and
behavioral abnormalities, including hearing loss and autism. PRP has also been recognized rarely following CRS. Subsequent
postnatal growth retardation and ultimate short stature has been reported in a minority of cases. Rare reports of immunologic
deficiency syndromes have also been described.

Figure 244-4 Bilateral cataracts in infant with congenital rubella syndrome.
A variety of late-onset manifestations of CRS have been recognized. In addition to PRP, these include diabetes mellitus (20%),
thyroid dysfunction (5%), and glaucoma and visual abnormalities associated with the retinopathy, which had previously been
considered benign.
o If pregnant woman is exposed, test for rubella IgG ASAP, and if negative, repeat at 2-3 wks and at 6 wks after exposure.
CMV: Symptomatic congenital CMV infection was originally termed cytomegalic inclusion disease. Only 5% of all congenitally infected
infants have severe cytomegalic inclusion disease, another 5% have mild involvement, and 90% are born with subclinical, but still
chronic, CMV infection. The characteristic signs and symptoms of clinically manifested infections include intrauterine growth
restriction, prematurity, hepatosplenomegaly and jaundice, blueberry muffinlike rash, thrombocytopenia and purpura, and microcephaly
and intracranial calcifications. Other neurologic problems include chorioretinitis, sensorineural hearing loss, and mild increases in
cerebrospinal fluid protein. Symptomatic newborns are usually easy to identify. The most severe symptomatic congenital infect ions and
those resulting in sequelae are more likely to be caused by primary rather than reactivated infections in pregnant women. Reinfection
with a different strain of CMV can lead to symptomatic congenital infection. Asymptomatic congenital CMV infection is likely the
leading cause of sensorineural hearing loss, which occurs in approximately 7% of all infants with congenital CMV infection, whether
symptomatic at birth or not. A randomized controlled phase III study with ganciclovir (6 mg/kg/dose every 12 hr IV for the 1st 6 wk of
life) concluded that treatment both prevents hearing deterioration and improves or maintains normal hearing function at 6 mo of age, and
may prevent the hearing deterioration that occurs after 1 yr of age.
HSV infection may be acquired in utero, during the birth process, or during the neonatal period. Intrauterine and postpartum
infections are well described but occur infrequently. Postpartum transmission may be from the mother or another adult with a
nongenital (typically HSV-1) infection such as herpes labialis. Most cases of neonatal herpes result from maternal infection and
transmission, usually during passage through a contaminated infected birth canal of a mother with asymptomatic genital herpes.
Transmission is well documented in infants delivered by cesarean section. Fewer than 30% of mothers of an infant with neonatal
herpes have a history of genital herpes. The risk for infection is higher in infants born to mothers with primary genital infection
(>30%) compared to recurrent genital infection (<2%). Use of scalp electrodes may also increase risk.
Neonatal HSV infection is almost never asymptomatic. Its clinical presentation reflects timing of infection, portal of entry, and
extent of spread. Infants with intrauterine infection typically have skin vesicles or scarring, eye findings including chorioretinitis
and keratoconjunctivitis, and microcephaly or hydranencephaly that are present at delivery. Few infants survive without therapy,
and those that do generally have severe sequelae. Infants infected during delivery or postpartum present with 1 of 3 patterns of
disease: (1) disease localized to the skin, eyes, or mouth; (2) encephalitis with or without skin, eye, or mouth (SEM) disease; or
(3) disseminated infection involving multiple organs, including the brain, lungs, liver, heart, adrenals, and skin.
Infants with SEM disease generally present at 511 days of life and typically develop a few small vesicles, particularly on the
presenting part or at sites of trauma such as with scalp electrode placement. If untreated, infants with SEM disease may progress
to develop encephalitis or disseminated disease.
Infants with encephalitis typically present at 817 days of life with clinical findings suggestive of bacterial meningitis, including
irritability, lethargy, poor feeding, poor tone, and seizures. Fever is relatively uncommon, and only about 60% have skin vesicles
( Fig. 249-3 ). If untreated, 50% will die and most survivors have severe neurologic sequelae.

Figure 249-3 Vesicular-pustular lesions on the face of a neonate with herpes simplex virus infection. See also color plates.

Infants with disseminated HSV infections generally become ill at 511 days of life. Their clinical picture is similar to bacterial
sepsis with hyper- or hypothermia, irritability, poor feeding, and vomiting. They may also exhibit respiratory distress, cyanosis,
apneic spells, jaundice, purpuric rash, and evidence of central nervous system infection; seizures are common. Skin vesicles are
seen in about 75% of cases. If untreated, the infection causes shock and disseminated intravascular coagulation; approximately
90% of these infants die, and most survivors have severe neurologic sequelae.
All infants with proven or suspected neonatal HSV infection should be begun promptly on high-dose intravenous acyclovir (60
mg/kg/day divided every 8 hr IV). Treatment may be discontinued in those infants shown by laboratory testing to not be infected.
Infants with HSV disease limited to skin, eyes, and mouth should be treated for 14 days, while those with disseminated or central
nervous system disease should receive 21 days of therapy. Patients receiving high-dose therapy should be monitored for
o The risk for transmission is greatest during a primary or nonprimary 1st infection (3050%) and much lower when the exposure is
during a recurrent infection (<2%). Infants born to mothers dually infected with HIV and HSV-2 are also at increased risk for
acquiring HIV compared with infants born to HIV-positive mothers who are not HSV-2 infected. (Nonprimary 1st infection
occurs in individuals previously infected with 1 type of HSV (HSV-1) who have become infected for the 1st time with the other
HSV type (HSV-2).)
o Syphilis
Untreated syphilis during pregnancy has a transmission rate approaching 100%. Fetal or perinatal death occurs in 40% of affected
infants. Among survivors, manifestations have traditionally been divided into early and late stages. The early signs appear during the 1st
2 yr of life, and late signs appear gradually during the 1st 2 decades. Early manifestations result from transplacental spirochetemia and
are analogous to the secondary stage of acquired syphilis. Approximately 66% of infected infants are asymptomatic at the time of birth
and are identified only by routine prenatal screening; if they are untreated, symptoms develop within weeks or months.
The early manifestations of congenital infection are varied and involve multiple organ systems ( Table 215-1 ). Hepatosplenomegaly,
jaundice, and elevated liver enzymes are common. Histologically, liver involvement includes bile stasis, fibrosis, and extramedullary
hematopoiesis. Lymphadenopathy tends to be diffuse and to resolve spontaneously, although shotty nodes may persist. Coombs negative
hemolytic anemia is characteristic. Thrombocytopenia is often associated with platelet trapping in an enlarged spleen. Characteristic
osteochondritis and periostitis ( Fig. 215-3 ) and mucocutaneous rash ( Fig. 215-4 ), pre senting with erythematous maculopapular or
bullous lesions, followed by desquamation involving hands and feet, are common. Mucous patches, rhinitis (snuffles), and
condylomatous lesions ( Fig. 215-5 ) are highly characteristic features of mucous membrane involvement in congenital syphilis. Bone
involvement occurs frequently. Roentgenographic abnormalities include multiple sites of osteochondritis at the wrists, elbows, ankles,
and knees, and periostitis of the long bones and rarely the skull. The osteochondritis is painful and often results in irritability and refusal
to move the involved extremity (pseudoparalysis of Parrot). Central nervous system (CNS) abnormalities, failure to thrive,
chorioretinitis, nephritis, and nephrotic syndrome may also be seen. Clinical manifestations of renal involvement include hypertension,
hematuria, proteinuria, hypoproteinemia, hypercholesterolemia, and hypocomplementemia. They appear to be related to glomerular

deposition of circulating immune complexes. Less common clinical manifestations of early congenital syphilis include gastroenteritis,
peritonitis, pancreatitis, pneumonia, eye involvement (glaucoma and chorioretinitis), nonimmune hydrops, and testicular masses.
TABLE 215-1 -- Clues That Suggest a Diagnosis of Congenital Syphilis[*]

Untreated early syphilis in the mother Osteochondritis, periostitis

Untreated latent syphilis in the mother Snuffles, hemorrhagic rhinitis

An untreated mother who has contact with a known Condylomata lata

syphilitic during pregnancy

Bullous lesions, palmar/plantar rash

Mother treated for syphilis during pregnancy with a drug Mucous patches
other than penicillin

Hepatomegaly, splenomegaly

Mother treated for syphilis during pregnancy without Jaundice

follow-up to delivery

Nonimmune hydrops fetalis

Generalized lymphadenopathy

Central nervous system signs; elevated cell count or protein in

cerebrospinal fluid

Hemolytic anemia, diffuse intravascular coagulation,



Nephrotic syndrome

Placental villitis or vasculitis (unexplained enlarged placenta)

Intrauterine growth restriction

Figure 215-3 Osteochondritis and periostitis in a newborn with congenital syphilis.

Figure 215-4 Papulosquamous plaques in 2 infants with syphilis.

Figure 215-5 Perianal condylomata lata.

The late manifestations result primarily from chronic inflammation of bone, teeth, and the CNS. Skeletal changes due to persistent or
recurrent periostitis and associated thickening of bone include frontal bossing, a bony prominence of the forehead(olympian brow),
unilateral or bilateral thickening of the sternoclavicular third of the clavicle (clavicular or Higoumnaki sign), an anterior bowing of the
midportion of the tibia (saber shins), and convexity along the medial border of the scapula (scaphoid scapula). Dental abnormalities are
common and include Hutchinson teeth ( Fig. 215-6 ), which are the peg or barrel-shaped upper central incisors that erupt during the 6th
yr of life; abnormal enamel, which results in a notch along the biting surface; and mulberry molars, the abnormal 1st lower (6 yr)
molars characterized by a small biting surface and an excessive number of cusps. Defects in enamel formation lead to repeated caries and
eventual tooth destruction.

Figure 215-6 Hutchinson teeth as a late manifestation of congenital syphilis.

A saddle nose ( Fig. 215-7 ), a depression of the nasal root, is a result of syphilitic rhinitis that destroys the adjacent bone and cartilage.
A perforated nasal septum may be an associated abnormality. Rhagades are linear scars that extend in a spokelike pattern from previous
mucocutaneous fissures of the mouth, anus, and genitalia. Juvenile paresis, an uncommon latent meningovascular infection, typically
presents during adolescence with behavioral changes, focal seizures, or loss of intellectual function. Juvenile tabes with spinal cord
involvement and cardiovascular involvement with aortitis are extremely rare.

Figure 215-7 Saddle nose in a newborn with congenital syphilis.

Other late manifestations of congenital syphilis may represent a hypersensitivity phenomenon. These include unilateral or bilater al
interstitial keratitis with symptoms such as intense photo phobia and lacrimation, followed within weeks or months by corneal
opacification and complete blindness. Less common ocular manifestations include choroiditis, retinitis, vascular occlusion, and optic
atrophy. Eighth nerve deafness may be unilateral or bilateral, appears at any age, presents initially as vertigo and high-tone hearing loss,
and progresses to permanent deafness. The Clutton joint represents a unilateral or bilateral synovitis involving the lower extremities
(usually the knee), which presents as painless joint swelling with sterile synovial fluid; spontaneous remission usually occurs after a
period of several weeks. Soft tissue gummas (identical to those of acquired disease) and paroxysmal cold hemoglobinuria are rare
hypersensitivity phenomena.

o Reiter syndrome - S. flexneri infection

o Ekiri syndrome - toxic encephalopathy secondary to Shigella
The rare syndrome of severe toxicity, convulsions, extreme hyperpyrexia, and headache associated with brain
edema and a rapidly fatal outcome without sepsis or significant dehydration (Ekiri syndrome or lethal toxic
encephalopathy) is not well understood.
o Fitz-Hugh-Curtis syndrome - perihepatitis due to N. gonorrhea
Dissemination from the fallopian tubes through the peritoneum to the liver capsule results in perihepatitis
(Fitz-Hugh-Curtis syndrome).
May also be caused by Chlamydia
o Ritter's disease - staphylococcal scalded skin syndrome
(+) Nikolsky sign (epidermis separates in response to gentle stroking)
Abortive type resembles scarlet fever and has a negative Nikolsky sign
o St. Anthony's fire - erysipelas (GABHS)
Superficial severe inflammation of the skin with blanched raised sharply demarcated, irregular, rapidly
advancing borders
Prominent constitutional symptoms (fever, chills, vomiting, irritability)
o Vincent angina
Vincent angina, also known as acute necrotizing ulcerative gingivitis or trench mouth, is an acute,
fulminating, mixed bacterial-spirochetal infection of the gingival margin and floor of the mouth. It is
characterized by gingival pain, foul breath, and pseudomembrane formation.
o Ludwig angina
Ludwig angina is an acute, life-threatening cellulitis of dental origin of the sublingual and submandibular
spaces. Infection spreads rapidly in the neck and may cause airway obstruction.
o Lemierre syndrome
Lemierre syndrome, or postanginal sepsis, is a suppurative infection of the lateral pharyngeal space that
usually begins as pharyngitis. It may complicate infectious mononucleosis. It presents as septic
thrombophlebitis of the jugular vein leading to multiple septic pulmonary embolizations. Clinical signs
include neck swelling and pain, trismus, and dysphagia culminating with signs of sepsis and respiratory
distress. Fusobacterium necrophorum is the most commonly involved organism, although polymicrobial
infection is frequent.
o Forchheimer spots
About the time of onset of the rash, examination of the throat may reveal tiny, rose-colored lesions
(Forchheimer spots) or petechial hemorrhages on the soft palate.

Typhoid fever
In about 25% of cases, a macular or maculopapular rash (rose spots) may be visible around the 7th10th day of
the illness, and lesions may appear in crops of 1015 on the lower chest and abdomen and last 23 days.
o Cer vicofacial actinomycosis - "lumpy jaw"
Cervicofacial actinomycosis usually presents as a painless, slow-growing, hard mass and can produce cutaneous
fistulas, a condition commonly known as lumpy jaw.
o Chancroid
painful genital ulceration and inguinal lymphadenopathy that is caused by Haemophilus ducreyi
lymphadenopathy can become fluctuant to form buboes
gram-negative coccobacilli in parallel clusters (school of fish)
o Infantile hypertrophic pyloric stenosis
Associated with treatment of pertussis with erythromycin in infants < 1 mos
o Stepladder rise in fever - typhoid
o Campylobacter jejuni - associated with GBS, Miller-Fisher syndrome (GBS variant with ataxia, areflexia and
ophthalmoplegia), and reactive arthritis (also IgA nephropathy)
o Yersinia - enterocolitica (mimics appendicitis), pseudotuberculosis (mesenteric lymphadenitis; may have a
complication similar to Kawasaki), pestis (bubonic plague or acute febrile lymphadenitis)
o Echthyma gangrenosum - characteristic skin lesion of Pseudomonas (hemorrhagic nodules --> ulcers with eschar
o Rope sign (polio) - an acute angulation between the chin and larynx caused by weakness of the hyoid muscles (the
hyoid bone is pulled posteriorly, narrowing the hypopharyngeal inlet)
o Hand foot and mouth disease - most frequently caused by coxsackievirus A16 (more severe: enterovirus 71)
o "Diseases"
First disease - measles
Second disease - scarlet fever
Third disease - rubella
Fourth disease - Filatov-Dukes disease (atypical scarlet fever)
Fifth disease - erythema infectiosum
Sixth disease - roseola infantum / exanthem subitum

o Adenovirus - Pharyngoconjunctival fever is a clinically distinct syndrome that occurs typically with type 3
adenovirus. Features include a high temperature that lasts 45 days, pharyngitis, conjunctivitis, preauricular and
cervical lymphadenopathy, and rhinitis. Nonpurulent conjunctivitis occurs in 75% of patients and is manifested by
inflammation of both the bulbar and palpebral conjunctivae of 1 or both eyes, which often persists after the fever and
other symptoms have resolved. Headache, malaise, and weakness are common, and there is considerable lethargy
after the acute stage.
o Tzanck smear
o Balloon cells and multinucleated giant cells - herpes
o Acantholytic epidermal cells - pemphigus

TABLE 303-7 -- Mechanisms of Diarrhea
Secretory Decreased Watery, normal Cholera, toxigenic E. coli; Persists during fasting;
absorption, osmolality; osmoles = 2 carcinoid, VIP, neuroblastoma, bile salt malabsorption
increased secretion, (Na+ + K+) congenital chloride diarrhea, may also increase
electrolyte transport Clostridium difficile, intestinal water secretion;
cryptosporidiosis (AIDS) no stool leukocytes
Osmotic Maldigestion, Watery, acidic, and Lactase deficiency, glucose- Stops with fasting;
transport defects reducing substances; galactose malabsorption, increased breath
ingestion of increased osmolality; lactulose, laxative abuse hydrogen with
unabsorbable osmoles >2 (Na+ + K+) carbohydrate
malabsorption; no stool
Increased motility Decreased transit Loose to normal- Irritable bowel syndrome, Infection may also
time appearing stool, thyrotoxicosis, postvagotomy contribute to increased
stimulated by gastrocolic dumping syndrome motility
Decreased Defect in Loose to normal Pseudoobstruction, blind loop Possible bacterial
motility neuromuscular appearing stool overgrowth
unit(s) Stasis
Decreased surface Decreased Watery Short bowel syndrome, celiac May require elemental
area (osmotic, functional capacity disease, rotavirus enteritis diet plus parenteral
motility) alimentation
Mucosal invasion Inflammation, Blood and increased Salmonella, Shigella, infection; Dysentery evident in
decreased colonic WBCs in stool amebiasis; Yersinia, blood, mucus, and WBCs
reabsorption, Campylobacter infections
increased motility

TABLE 337-1 -- Food-borne Illnesses (Bacterial)
Bacillus anthracis 2 days to weeks Nausea, vomiting, malaise, Weeks Insufficiently cooked Blood Penicillin is first choice
bloody diarrhea, acute abdominal contaminated meat for naturally acquired
pain gastrointestinal anthrax.
Ciprofloxacin is second

Bacillus cereus 16 hr Sudden onset of severe nausea 24 hr Improperly refrigerated Normally a clinical diagnosis. Supportive care
(preformed and vomiting. Diarrhea may be cooked or fried rice, meats Clinical laboratories do not
enterotoxin) present. routinely identify this
organism. If indicated, send
stool and food specimens to
reference laboratory for
culture and toxin
Bacillus cereus 1016 hours Abdominal cramps, watery 2448 hr Meats, stews, gravies, Testing not necessary, self- Supportive care
(diarrheal toxin) diarrhea, nausea. vanilla sauce limiting (consider testing
food and stool for toxin in
Brucella abortus, B. 721 days Fever, chills, sweating, Weeks Raw milk, goat cheese Blood culture and positive Acute: Rifampin and
melitensis, and B. suis weakness, headache, muscle and made from unpasteurized serology doxycycline daily for 6 wk.
joint pain, diarrhea, bloody stools milk, contaminated meats Infections with complications
during acute phase require combination therapy with
rifampin, tetracycline, and an
Campylobacter jejuni 25 days Diarrhea, cramps, fever, and 210 days Raw and undercooked Routine stool culture; Supportive care. For severe
vomiting; diarrhea may be poultry, unpasturized milk, Campylobacter requires cases, antibiotics such as
bloody. contaminated water special media and incubation erythromycin and quinolones
at 42C to grow. may be indicated early in the
diarrheal disease. Guillain-Barr
syndrome can be a sequela.
Clostridium 1272 hr Vomiting, diarrhea, blurred Variable (from Home-canned foods with a Stool, serum, and food can be Supportive care. Botulism
botulinum children vision, diplopia, dysphagia, and days to low acid content, tested for toxin. Stool and antitoxin is helpful if given early
and adults (preformed descending muscle weakness months). Can improperly canned food can also be cultured for in the course of the illness.
toxin) be complicated commercial foods, home- the organism. These tests can Contact the state health
by respiratory canned or fermented fish, be performed at some state department. The 24-hour number
failure and herb-infused oils, baked health department for state health departments to
death. potatoes in aluminium foil, laboratories and CDC. call is (700) 4887100.
cheese sauce, bottled

garlic, foods held warm
for extended periods of
time (e.g., in a warm oven)
Clostridium 330 days In infants <12 mo, lethargy, Variable Honey, home-canned Stool, serum, and food can be Supportive care. Botulism
botulinuminfants weakness, poor feeding, vegetables and fruits, corn tested for toxin. Stool and immune globulin can be
constipation, hypotonia, poor syrup food can also be cultured for obtained from the Infant
head control, poor gag and the organism. These tests can Botulism Prevention Program,
sucking reflex be performed at some state Health and Human Services,
health department California (510-540-2646),
laboratories and CDC. Botulinum antitoxin is generally
not recommended for infants.
Clostridium 816 hr Watery diarrhea, nausea, 2448 hr Meats, poultry, gravy, Stools can be tested for Supportive care. Antibiotics not
perfringens toxin abdominal cramps; fever is rare. dried or precooked foods, enterotoxin and cultured for indicated.
time- and/or temperature- organism. Because
abused food Clostridium perfringens can
normally be found in stool,
quantitative cultures must be
Enterohemorrhagic E. 18 days Severe diarrhea that is often 510 days Undercooked beef Stool culture; E. coli O157 : Supportive care, monitor renal
coli (EHEC) including bloody, abdominal pain and especially hamburger, H7 requires special media to function, hemoglobin, and
E. coli O157 : H7 and vomiting. Usually, little or no unpasteurized milk and grow. If E. coli O157 : H7 is platelets closely. E. coli O157 :
other Shiga toxin fever is present. More common juice, raw fruits and suspected, specific testing H7 infection is also associated
producing E. coli in children <4 yr old. vegetables (e.g., sprouts), must be requested. Shiga with hemolytic uremic syndrome
(STEC) salami (rarely), and toxin testing may be done (HUS), which can cause lifelong
contaminated water using commercial kits; complications. Studies indicate
positive isolates should be that antibiotics may promote the
forwarded to public health development of HUS.
laboratories for confirmation
and serotyping.
Enterotoxigenic E. coli 13 days Watery diarrhea, abdominal 3 to >7 days Water or food Stool culture. ETEC requires Supportive care. Antibiotics are
(ETEC) cramps, some vomiting contaminated with human special laboratory techniques rarely needed except in severe
feces for identification. If cases. Recommended antibiotics
suspected, must request include TMP-SMX and
specific testing. quinolones.
Listeria 948 hr for Fever, muscle aches, and nausea Variable Fresh soft cheeses, Blood or cerebrospinal fluid Supportive care and antibiotics;
monocytogenes gastrointestinal or diarrhea. Pregnant women unpasteurized milk, cultures. Asymptomatic fecal Intravenous ampicillin,
symptoms, 26 may have mild flu-like illness, inadequately pasteurized carriage occurs; therefore, penicillin, or TMP-SMX are
wk for invasive and infection can lead to milk, ready-to-eat deli stool culture usually not recommended for invasive
disease premature delivery or stillbirth. meats, hot dogs helpful. Antibody to disease.

Elderly or immunocompromised listerolysin O may be helpful
patients may have bacteremia or to identify outbreak
meningitis. retrospectively.
At birth and Infants infected from mother at
infancy risk for sepsis or meningitis.
Salmonella spp. 13 days Diarrhea, fever, abdominal 47 days Contaminated eggs, Routine stool cultures Supportive care. Other than for
cramps, vomiting. S. typhi and S. poultry, unpasteurized S. typhi and S. paratyphi,
paratyphi produce typhoid with milk or juice, cheese, antibiotics are not indicated
insidious onset characterized by contaminated raw fruits unless there is extra-intestinal
fever, headache, constipation, and vegetables (alfalfa spread, or the risk of extra-
malaise, chills, and myalgia; sprouts, melons). S. typhi intestinal spread, of the
diarrhea is uncommon, and epidemics are often related infection. Consider ampicillin,
vomiting is not usually severe. to fecal contamination of gentamicin, TMP-SMX, or
water supplies or street- quinolones if indicated. A
vended foods. vaccine exists for S. typhi.
Shigella spp. 2448 hr Abdominal cramps, fever, and 47 days Food or water Routine stool cultures Supportive care. TMP-SMX
diarrhea. Stools may contain contaminated with human recommended in the U. S. if
blood and mucus. fecal material. Usually organism is susceptible; nalidixic
person-to-person spread, acid or other quinolones may be
fecal-oral transmission. indicated if organism is resistant,
Ready-to-eat foods especially in developing
touched by infected food countries.
workers, e.g., raw
vegetables, salads,
Staphylococcus aureus 16 hr Sudden onset of severe nausea 2448 hrs Unrefrigerated or Normally a clinical diagnosis. Supportive care.
(preformed and vomiting. Abdominal improperly refrigerated Stool, vomitus, and food can
enterotoxin) cramps. Diarrhea and fever may meats, potato and egg be tested for toxin and
be present. salads, cream pastries. cultured if indicated.
Vibrio cholerae (toxin) 2472 hr Profuse watery diarrhea and 37 days. Contaminated water, fish, Stool culture; Vibrio cholerae Supportive care with aggressive
vomiting, which can lead to Causes life- shellfish, street-vended requires special media to oral and intravenous rehydration.
severe dehydration and death threatening food typically from Latin grow. If V. cholerae is In cases of confirmed cholera,
within hours dehydration. America or Asia suspected, must request tetracycline or doxycycline is
specific testing. recommended for adults, and
TMP-SMX for children (<8 yr).
Vibrio 248 hr Watery diarrhea, abdominal 25 days Undercooked or raw Stool cultures. Vibrio Supportive care. Antibiotics are
parahaemolyticus cramps, nausea, vomiting. seafood, such as fish, parahaemolyticus requires recommended in severe cases:
shellfish special media to grow. If V. tetracycline, doxycycline,
parahaemolyticus is gentamicin, and cefotaxime.

suspected, must request
specific testing.
Vibrio vulnificus 17 days Vomiting, diarrhea, abdominal 28 days Undercooked or raw Stool, wound, or blood Supportive care and antibiotics;
pain, bactermia, and wound shellfish, especially cultures. Vibrio vulnificus tetracycline, doxycycline, and
infections. More common in the oysters, other requires special media to ceftazidime are recommended.
immunocompromised, or in contaminated seafood, and grow. If V. vulnificus is
patients with chronic liver open wounds exposed to suspected, must request
disease (presenting with bullous seawater specific testing.
skin lesions). Can be fatal in
patients with liver disease and
the immunocompromised.
Yersinia enterocolytica 2448 hr Appendicitis-like symptoms 13 wk, usually Undercooked pork, Stool, vomitus, or blood Supportive care. If septicemia or
and Y. (diarrhea and vomiting, fever, self-limiting unpasteurized milk, tofu, culture. Yersinia requires other invasive disease occurs,
pseudotuberculosis and abdominal pain) occur contaminated water. special media to grow. If antibiotic therapy with
primarily in older children and Infection has occurred in suspected, must request gentamicin or cefotaxime
young adults. May have a infants whose caregivers specific testing. Serology is (doxycycline and ciprofloxacin
scarlitiniform rash or erythema handled chitterlings. available in research and also effective).
nodosum with Y. reference laboratories.

TABLE 337-2 -- Food-borne Illnesses (Viral)

Hepatitis A 28 days average Diarrhea, dark urine, jaundice, and flu- Variable, 2 Shellfish harvested from Increase in ALT, billirubin. Supportive care.
(1550 days) like symptoms, i.e., fever, headache, wk3 mo contaminated waters, raw produce, Positive IgM and anti Prevention with
nausea, and abdominal pain contaminated nated drinking hepatitis A antibodies. immunization.
water, uncooked foods and cooked
foods that are not reheated after
contact with infected food handler
Noroviruses (and 1248 hr Nausea, vomiting, abdominal cramping, 1260 hr Shellfish, fecally contaminated Routine RT-PCR and EM on Supportive care such
other diarrhea, fever, myalgia, and some foods, ready-to-eat foods touched fresh unpreserved stool as rehydration. Good
caliciviruses) headache. Diarrhea is more prevalent in by infected food workers (salads, samples. Clinical diagnosis, hygiene.
adults and vomiting is more prevalent in sandwiches, ice, cookies, fruit) negative bacterial cultures.
children. Prolonged asymptomatic Stool is negative for WBCs.
excretion possible.
Rotavirus 13 days Vomiting, watery diarrhea, low-grade 48 days Fecally contaminated foods. Identification of virus in stool Supportive care.

fever. Temporary lactose intolerance may Ready-to-eat foods touched by via immunoassay Severe diarrhea may
occur. Infants and children, elderly, and infected food workers (salads, require fluid and
immunocompromised are especially fruits). electrolyte
vulnerable. replacement.
Other viral agents 1070 hr Nausea, vomiting, diarrhea, malaise, 29 days Fecally contaminated foods. Identification of the virus in Supportive care,
(astroviruses, abdominal pain, headache, fever Ready-to-eat foods touched by early acute stool samples. usually mild, self-
adenoviruses, infected food workers. Some Serology. Commercial ELISA limiting. Good
parvoviruses) shellfish. kits are now available for hygiene.
adenoviruses and astroviruses.

TABLE 337-3 -- Food-borne Illnesses (Parasitic)

Angiostrongylus 1 wk to 1 mo Severe headaches, nausea, Several weeks Raw or undercooked Examination of CSF for elevated Supportive care. Repeat lumbar
cantonensis vomiting, neck stiffness, to several intermediate hosts (e.g., pressure, protein, leukocytes, and punctures and use of corticosteroid
paresthesias, hyperesthesias, months snails or slugs), infected eosinophils; serologic testing using therapy may be used for more severely ill
seizures, and other neurologic paratenic (transport) ELISA to detect antibodies to patients.
abnormalities hosts (e.g., crabs, Angiostrongylus cantonensis
freshwater shrimp),
fresh produce
contaminated with
intermediate or transport
Cryptosporidium 210 days Diarrhea (usually watery), stomach May be Any uncooked food or Request specific examination of the Supportive care, self-limited. If severe
cramps, upset stomach, slight fever remitting and food contaminated by stool for Cryptosporidium. May need consider paromomycin for 7 days. For
relapsing over an ill food handler after to examine water or food. children aged 111 yr, consider
weeks to cooking; drinking water nitazoxanide for 3 days.
Cyclospora 114 days, Diarrhea (usually watery), loss of May be Various types of fresh Request specific examination of the TMP-SMX for 7 days.
cayetanensis usually at least 1 appetite, substantial loss of weight, remitting and produce (imported stool for Cyclospora. May need to
wk stomach cramps, nausea, vomiting, relapsing over berries, lettuce) examine water or food.
fatigue weeks to
Entamoeba 23 days to 14 Diarrhea (often bloody), frequent May be Any uncooked food or Examination of stool for cysts and Metronidazole and a luminal agent
histolytica wk bowel movements, lower protracted food contaminated by parasitesmay need at least 3 (iodoquinol or paromomycin)
abdominal pain (several weeks an ill food handler after samples. Serology for long-term
to several cooking; drinking water infections.
Giardia lamblia 12 wk Diarrhea, stomach cramps, gas, Days to weeks Any uncooked food or Examination of stool for ova and Metronidazole

weight loss food contaminated by parasitesmay need at least 3
an ill food handler after samples.
cooking; drinking water.
Toxoplasma 523 days Generally asymptomatic, 20% may Months Accidental ingestion of Isolation of parasites from blood or Asymptomatic healthy, but infected,
gondii develop cervical lymphadenopathy contaminated other body fluids; observation of persons do not require treatment.
and/or a flu-like illness. In substances (e.g., soil parasites in patient specimens via Spiramycin or pyrimethamine plus
immunocompromised patients: contaminated with cat microscopy or histology. Detection sulfadiazine may be used for pregnant
central nervous system (CNS) feces on fruits and of organisms is rare; serology women. Pyrimethamine plus sulfadiazine
disease, myocarditis, or vegetables), raw or (reference laboratory needed) can be may be used for immunocompromised
pneumonitis is often seen. partly cooked meat a useful adjunct in diagnosing persons, in specific cases. Pyrimethamine
(especially pork, lamb, toxoplasmosis. However, IgM plus sulfadiazine (with or without
or venison) antibodies may persist for 618 mo steroids) may be given for ocular disease
and thus may not necessarily indicate when indicated. Folinic acid is given
recent infection. PCR of bodily with pyrimethamine plus sulfadiazine to
fluids. For congenital infection: counteract bone marrow suppression.
isolation of T. gondii from placenta,
umbilical cord, or infant blood. PCR
of white blood cells, CSF, or
amniotic fluid, or IgM and IgA
serology, performed by a reference
Toxoplasma In infants at birth Treatment of the mother may Months Passed from mother
gondii (congenital reduce severity and/or incidence of (who acquired acute
infection) congenital infection. Most infected infection during
infants have few symptoms at birth. pregnancy) to child
Later, they will generally develop
signs of congenital toxoplasmosis
(mental retardation, severely
impaired eyesight, cerebral palsy,
seizures), unless the infection is
Trichinella 12 days for Acute:nausea, diarrhea, vomiting, Months Raw or undercooked Positive serology or demonstration Supportive care plus mebendazole or
spiralis initial symptoms; fatigue, fever, abdominal contaminated meat, of larvae via muscle biopsy. Increase albendazole
others begin 28 discomfort followed by muscle usually pork or wild in eosinophils.
wk after infection soreness, weakness, and occasional game meat (e.g., bear or
cardiac and neurologic moose)

TABLE 337-4 -- Food-borne Illnesses (Noninfectious)
Antimony 5 min8 hr usually Vomiting, metallic taste Usually self- Metallic container Identification of metal in Supportive care
<1 hr limited beverage or food
Arsenic Few hours Vomiting, colic, diarrhea Several days Contaminated food Urine. May cause Gastric lavage, BAL
eosinophilia (dimercaprol)
Cadmium 5 min8 hr usually Nausea, vomiting, myalgia, increase in Usually self- Seafood, oysters, clams, Identification of metal in Supportive care
<1 hr salivation, stomach pain limited lobster, grains, peanuts food
Ciguatera fish poisoning 26 hr Gl:abdominal pain, nausea, vomiting, Days to weeks A variety of large reef fish: Radioassay for toxin in fish Supportive care, IV mannitol.
(ciguatera toxin) diarrhea to months grouper, red snapper, or a consistent history Children more vulnerable.
amberjack, and barracuda (most
3 hr Neurologic:paresthesias, reversal of hot or
cold, pain, weakness
25 days Cardiovascular:bradycardia, hypotension,
increase in T wave abnormalities
Copper 5 min8 hr usually Nausea, vomiting, blue or green vomitus Usually self- Metallic container Identification of metal in Supportive care
<1 hr limited beverage or food
Mercury 1 wk or longer Numbness, weakness of legs, spastic May be Fish exposed to organic Analysis of blood, hair Supportive care
paralysis, impaired vision, blindness, coma. protracted mercury, grains treated with
Pregnant women and the developing fetus mercury fungicides
are especially vulnerable.
Mushroom toxins, short- <2 hr Vomiting, diarrhea, confusion, visual Self-limited Wild mushrooms (cooking may Typical syndrome and Supportive care
acting (museinol, muscarine, disturbance, salivation, diaphoresis, not destroy these toxins) mushroom identified or
psilocybin, Coprius hallucinations, disulfiram-like reaction, demonstration of the toxin
artemetaris, ibotenic acid) confusion, visual disturbance.
Mushroom toxins, long- 48 hr diarrhea; 24 Diarrhea, abdominal cramps, leading to Often fatal Mushrooms Typical syndrome and Supportive care, life-
acting (amanitin) 48 hr liver failure hepatic and renal failure mushroom identified and/or threatening, may need life
demonstration of the toxin support
Nitrite poisoning 12 hr Nausea, vomiting, cyanosis, headache, Usually self- Cured meats, any contaminated Analysis of the food, blood Supportive care, methylene
dizziness, weakness, loss of consciousness, limited foods, spinach exposed to blue
chocolate-brown colored blood excessive nitrification
Pesticides (organophosphates Few min to few Nausea, vomiting, abdominal cramps, Usually self- Any contaminated food Analysis of the food, blood Atropine;2-PAM
or carbamates hours diarrhea, headache, nervousness, blurred limited (Pralidoxime) is used when
vision, twitching, convulsions, salivation atropine is not able to control
and meiosis symptoms and is rarely
necessary in carbamate
Puffer fish (tetrodotoxin) <30 min Parasthesias, vomiting, diarrhea, abdominal Death usually Puffer fish Detection of tetrodotoxin in Life-threatening, may need
pain, ascending paralysis, respiratory failure in 46 hr fish respiratory support


Scombroid (histamine) 1 min3 hr Flushing, rash, burning sensation of skin, 36 hr Fish:bluefin, tuna, skipjack, Demonstration of histamine Supportive care, antihistamines
mouth and throat, dizziness, urticaria, mackerel, marlin, escolar, and in food or clinical diagnosis
parasthesias mahi mahi
Shellfish toxins (diarrheic, Diarrheic shellfish Nausea, vomiting, diarrhea, and abdominal Hours to 23 A variety of shellfish, primarily Detection of the toxin in Supportive care, generally self-
neurotoxic, amnesic) poisoning (DSP) pain accompanied by chills, headache, and days mussels, oysters, scallops, and shellfish; high-pressure limiting. Elderly are especially
30 min to 2 hr fever shellfish from the Florida coast liquid chromatography sensitive to ASP
and the Gulf of Mexico
Neurotoxic shellfish Tingling and numbness of lips, tongue, and
poisoning (NSP) throat, muscular aches, dizziness, reversal
few min to hours of the sensations of hot and cold, diarrhea,
and vomiting
Amnesic shellfish Vomiting, diarrhea, abdominal pain and
poisoning (ASP) neurologic problems such as confusion,
2448 hr memory loss, disorientation, seizure, coma
Shellfish toxins (paralytic 30 min3 hr Diarrhea, nausea, vomiting leading to Days Scallops, mussels, clams, Detection of toxin in food Life-threatening, may need
shellfish poisoning) parasthesias of mouth, lips, weakness, cockles or water where fish are respiratory support
dysphasia, dysphonia, respiratory paralysis located; high-pressure
liquid chromatography
Sodium fluoride Few min to 2 hr Salty or soapy taste, numbness of mouth, Usually self- Dry foods (e.g., dry milk, flour, Testing of vomitus or Supportive care
vomiting, diarrhea, dilated pupils, spasms, limited baking powder, cake mixes) gastric washings. Analysis
pallor, shock, collapse contaminated with sodium of the food.
fluoridecontaining insecticides
and rodenticides
Thallium Few hours Nausea, vomiting, diarrhea, painful Several days Contaminated food Urine, hair Supportive care
parathesias, motor polyneuropathy, hair loss
Tin 5 min8 hr usually Nausea, vomiting, diarrhea Usually self- Metallic container Analysis of the food Supportive care
<1 hr limited
Vomitoxin Few min to 3 hr Nausea, headache, abdominal pain, Usually self- Grains such as wheat, corn, Analysis of the food Supportive care
vomiting limited barley
Zinc Few hours Stomach cramps, nausea, vomiting, Usually self- Metallic container Analysis of the food, blood Supportive care
diarrhea, myalgias limited and feces, saliva or urine

o Clinical manifestations (severe abdominal pain, high fever, emesis, anorexia, generalized toxicity, urgency, and
painful defecation)
The diarrhea may be watery and of large volume initially, evolving into frequent small-volume, bloody
mucoid stools; most children (>50%) never progress to the stage of bloody diarrhea, whereas in others
the 1st stools are bloody. Significant dehydration related to the fluid and electrolyte losses in both feces
and emesis can occur. Untreated diarrhea may last 12 wk; only about 10% of patients have diarrhea
persisting for more than 10 days. Persistent diarrhea occurs in malnourished infants, those with AIDS,
and occasionally previously normal children. Even nondysenteric disease can be complicated by
persistent illness.
Neurologic findings are among the most common extraintestinal manifestations of bacillary dysentery,
occurring in as many as 40% of hospitalized infected children. Enteroinvasive E. coli can cause similar
neurologic toxicity. Convulsions, headache, lethargy, confusion, nuchal rigidity, or hallucinations may
be present before or after the onset of diarrhea. The cause of these neurologic findings is not understood.
In the past, these symptoms were attributed to the neurotoxicity of Shiga toxin, but it is clear that that
explanation is wrong since the organisms isolated from children with Shigella-related seizures are
usually not Shiga toxin producers. Seizures sometimes occur when little fever is present, suggesting that
simple febrile convulsions do not explain their appearance. Hypocalcemia or hyponatremia may be
associated with seizures in a small number of patients. Although symptoms often suggest central nervous
system infection, and cerebrospinal fluid pleocytosis with minimally elevated protein levels can occur,
Shigella meningitis is rare.
The most common complication of shigellosis is dehydration. Inappropriate secretion of antidiuretic
hormone with profound hyponatremia may complicate dysentery, particularly when S. dysenteriae is the
etiologic agent. Hypoglycemia and protein-losing enteropathy may occur. Other major complications,
particularly in very young, malnourished children, include sepsis and disseminated intravascular
coagulation. Given that shigellae penetrate the intestinal mucosal barrier, these events are surprisingly
uncommon. Shigellae and sometimes other gram-negative enteric bacilli are recovered from blood
cultures in 15% of patients in whom blood cultures are taken; because patients selected for blood
cultures represent a biased sample, the risk for bacteremia in unselected cases of shigellosis is
presumably lower. Bacteremia is more common with S. dysenteriae serotype 1 than with other shigellae;
the mortality rate is high (-20%) when sepsis occurs.
Neonatal shigellosis is rare. Newborns may have only low-grade fever with mild nonbloody diarrhea.
However, complications occur more commonly than in older children and include septicemia,
meningitis, dehydration, colonic perforation, and toxic megacolon.
S. dysenteriae serotype 1 infection is commonly complicated by hemolysis, anemia, and hemolytic-
uremic syndrome. This syndrome is caused by Shiga toxinmediated endothelial injury; E. coli that
produce Shiga toxin (E. coli 0157 : H7, E. coli 0111 : NM, E. coli 026 : H11) also cause hemolytic-
uremic syndrome (see Chapter 518 ).
Rectal prolapse, toxic megacolon or pseudomembranous colitis (usually associated with S. dysenteriae),
cholestatic hepatitis, conjunctivitis, iritis, corneal ulcers, pneumonia, arthritis (usually 25 wk after
enteritis), reactive arthritis with uveitis, urethritis and rash, cystitis, myocarditis, and vaginitis (typically
with a blood-tinged discharge associated with S. flexneri) are uncommon events. Although rare, surgical
complications of shigellosis can be severe; the most common are intestinal obstruction, appendicitis, and
perforation. Death is a rare outcome in well-nourished older children; malnutrition, illness in the 1st year
of life, hypothermia, severe dehydration, thrombocytopenia, hyponatremia, renal failure, and bacteremia
are common in children who die during bacillary dysentery. The rare syndrome of severe toxicity,
convulsions, extreme hyperpyrexia, and headache associated with brain edema and a rapidly fatal
outcome without sepsis or significant dehydration (Ekiri syndrome or lethal toxic encephalopathy) is
not well understood.
o Diagnosis
Although clinical features suggest shigellosis, they are insufficiently specific to allow confident diagnosis.
Infection by Campylobacter jejuni, Salmonella, enteroinvasive E. coli, Shiga toxinproducing E. coli such as
E. coli 0157 : H7, Yersinia enterocolitica, Clostridium difficile, and Entamoeba histolytica, as well as
inflammatory bowel disease, may cause confusion. Presumptive data supporting a diagnosis of bacillary
dysentery include the finding of fecal leukocytes (confirming the presence of colitis), fecal blood, and
demonstration in peripheral blood of leukocytosis with a dramatic left shift (often with more bands than
segmented neutrophils). The total peripheral white blood cell count is usually 5,00015,000 cells/mm3,
although leukopenia and leukemoid reactions occur.
Cultures of both stool and rectal swab specimens optimize the diagnosis of Shigella infections. In children who
appear to be toxic, blood cultures should be obtained; this is particularly important in very young or
malnourished infants because of their increased risk for bacteremia.

o Treatment
As with gastroenteritis from other causes, the 1st concern about a child with suspected shigellosis should be for
fluid and electrolyte correction and maintenance (see Chapters 55 and 337 ). Nutrition is a key concern in areas
where malnutrition is common. A high-protein diet during convalescence enhances growth in the following 6
mo. A single large dose of vitamin A (200,000 IU) lessens severity of shigellosis in areas where vitamin A
deficiency is common. Drugs that retard intestinal motility (diphenoxylate hydrochloride with atropine
[Lomotil] or loperamide [Imodium]) should not be used because of the risk for prolonging the illness.
Although some authorities recommend withholding antibacterial therapy because of the self-limited nature of
the infection, cost of drugs, and risk for emergence of resistant organisms, there is a persuasive logic in favor
of empirical treatment of all children in whom shigellosis is strongly suspected. Even if not fatal, the untreated
illness may cause a child to be quite ill for weeks with chronic or recurrent diarrhea. Malnutrition may develop
or worsen during prolonged illness, particularly in children in developing countries. The risk for continued
excretion and subsequent infection of family contacts further argues against the strategy of withholding
Ceftriaxone (50 mg/kg/day as a single daily dose IV or IM) can be used for empirical therapy. Oral 1st and 2nd
generation cephalosporins are inadequate as alternative drugs despite in vitro susceptibility. Nalidixic acid (55
mg/kg/day divided qid PO), where available, is also an acceptable alternative drug. Azithromycin (12
mg/kg/day PO for the 1st day followed by 6 mg/kg/day for the next 4 days) has proven to be an effective
alternative drug for shigellosis. Quinolones such as ciprofloxacin, norfloxacin, or ofloxacin, which have been
recommended for use in persons 18 yr of age, are not routinely used for children because of the putative risk
for arthropathy. Use of these agents is reserved for seriously ill children with bacillary dysentery due to an
organism that is suspected or known to be resistant to other agents. Treatment is typically for a 5 day course.
Zinc (20 mg/day for 14 days) improves immune response to Shigella infection, at least in settings where
malnutrition is common. It should probably be included in therapy of dysenteric patients in such settings.
Treatment of patients suspected on clinical grounds of having Shigella infection should be initiated when they
are first evaluated. Stool culture is obtained to exclude other pathogens and to assist in antibiotic changes
should a child fail to respond to empirical therapy. A child who has typical dysentery and who responds to
initial empirical antibiotic treatment should be continued on that drug for a full 5 day course, even if the stool
culture is negative. The logic of this recommendation is based on the difficulty of culturing Shigella from
stools. In a child who fails to respond to therapy of a dysenteric syndrome in the presence of initially negative
stool culture results, cultures should be retaken and the child re-evaluated for other possible diagnoses.
o Prevention
Education about handwashing and proper food preparation
E. coli
o Types
ETEC: watery diarrhea, self-limited, traveler's diarrhea
EIEC: watery diarrhea or dysentery with fever, colonic lesions with ulcerations
EPEC: major cause of infant acute and persistent diarrhea
STEC/EHEC: mild diarrhea to severe hemorrhagic colitis, children 6 mos-10 years, person to person /
food and water transmission, low number of organisms sufficient to cause disease, affects colon most
severely, HUS (ARF, thrombocytopenia, hemolytic anemia)
Fever is an uncommon manifestation (vs in shigellosis or EIEC)
Antibiotics should not be given (increases risk for HUS)
EAEC: acute and persistent diarrhea in children > 12 mos
V. cholera
o Types
O1 El Tor and O139
Large inoculum required to cause disease; antacids increase risk of disease
o Clinical manifestations
Cholera is characterized by an acute onset of copious watery diarrhea and vomiting without abdominal
cramps or fever. The stools are colorless with small flecks of mucus (rice-water) and are sometimes
described as having a fishy odor. At first, children may be restless or extremely thirsty, but if fluid and
electrolyte losses are not replaced, they may become lethargic or unconscious. Other signs of
dehydration may rapidly manifest, including poor skin turgor, sunken eyes, dry mouth and tongue, no
urine output, delayed capillary refill, rapid or weak pulse, and low blood pressure ( Fig. 198-1 ). Severe
dehydration, metabolic acidosis, and hypokalemia can occur in 412 hr. The fluid losses may be so rapid
that the child quickly develops hypovolemic shock, hypoglycemia, coma, and seizures and is at risk of
dying within a few hours of onset.

TABLE 337-5 -- Extraintestinal Manifestations of Enteric Infections
Focal infections due to systemic spread All major pathogens Onset usually during the acute
of bacterial pathogens, including can cause such direct infection, but may present subsequently.
vulvovaginitis, urinary tract infection, extraintestinal Prognosis depends on infection site.
endocarditis, osteomyelitis, meningitis, infections, including
pneumonia, hepatitis, peritonitis, Salmonella,
chorioamnionitis, soft tissue infection,
and septic thrombophlebitis
Shigella, Yersinia,
Clostridium difficile
Reactive arthritis Salmonella, Shigella, Typically occurs about 13 wk after
Yersinia, infection. Relapses after reinfection
Campylobacter, may develop in 1550% of people but
Cryptosporidium, most children recover fully within 26
Clostridium difficile mo after the 1st symptoms appear.
Guillain-Barr syndrome Campylobacter Usually occurs a few weeks after the
original infection. Prognosis good
although 1520% may have sequelae.
Glomerulonephritis Shigella, Can be of sudden onset in acute,
Campylobacter, referring to a sudden attack of
Yersinia inflammation, or chronic, which comes
on gradually. In most cases, the kidneys
heal with time.
IgA nephropathy Campylobacter Characterized by recurrent episodes of
blood in the urine, this condition results
from deposits of the protein
immunoglobulin A (IgA) in the
glomeruli. IgA nephropathy can
progress for years with no noticeable
symptoms. Men seem more likely to
develop this disorder than are women.
Erythema nodosum Yersinia, Although painful, is usually benign and
Campylobacter, more commonly seen in adolescents.
Salmonella Resolves with 46 weeks.
Hemolytic uremia syndrome Shigella dysenteriae 1, Sudden onset, short-term renal failure.
Escherichia coli 0157: In severe cases, renal failure requires
H7, others several sessions of dialysis to take over
the kidney function, but most children
recover without permanent damage to
their health.
Hemolytic anemia Campylobacter, Relatively rare complication and may
Yersinia have a chronic course.

TABLE 337-6 -- Symptoms Associated with Dehydration
Mental status Well;alert Normal, fatigued or restless, Apathetic, lethargic,
irritable unconscious
Thirst Drinks normally; might Thirsty;eager to drink Drinks poorly; unable to drink
refuse liquids
Heart rate Normal Normal to increased Tachycardia, with bradycardia
in most severe cases
Quality of Normal Normal to decreased Weak, thready, or impalpable
Breathing Normal Normal;fast Deep
Eyes Normal Slightly sunken Deeply sunken
Tears Present Decreased Absent
Mouth and Moist Dry Parched
Skinfold Instant recoil Recoil in <2 sec Recoil in >2 sec
Capillary Normal Prolonged Prolonged;minimal
Extremities Warm Cool Cold;mottled;cyanotic
Urine output Normal to decreased Decreased Minimal

TABLE 337-7 -- Summary of Treatment Based on Degree of Dehydration

Minimal or no Not applicable <10 kg body weight: 60120 Continue breast-
dehydration mL oral rehydration solution feeding, or resume
(ORS) for each diarrheal age-appropriate
stool or vomiting episode; normal diet after
>10 kg body weight: 120 initial hydration,
240 mL ORS for each including adequate
diarrheal stool or vomiting caloric intake for
episode maintenance[*]
Mild to moderate ORS, 50100 mL/kg body Same Same
dehydration weight over 34 hr
Severe dehydration Lactated Ringer solution or Same;if unable to drink, Same
normal saline in 20 mL/kg body administer through
weight intravenous amounts until nasogastric tube or
perfusion and mental status administer 5% dextrose
improve; then administer 100 normal saline with 20 mEq/L
mL/kg body weight ORS over 4 potassium chloride
hr or 5% dextrose normal intravenously
saline intravenously at twice

maintenance fluid rates


TABLE 329-1 -- Distinguishing Features of Hirschsprung Disease and Functional Constipation
Onset of constipation After 2 yr of age At birth
Encopresis Common Very rare
Failure to thrive Uncommon Possible
Enterocolitis None Possible
Forced bowel Usual None
Abdominal Uncommon Common
Poor weight gain Rare Common
Anal tone Normal Normal
Rectal examination Stool in ampulla Ampulla empty
Malnutrition None Possible
Anorectal Distention of the rectum causes relaxation of the internal No sphincter relaxation or paradoxical increase in

manometry sphincter pressure
Rectal biopsy Normal No ganglion cells, increased acetylcholinesterase
Barium enema Massive amounts of stool, no transition zone Transition zone, delayed evacuation (>24 hr)

Respiratory Disorders
Cough (and other respiratory symptoms)
TABLE 381-1 -- Indicators of Serious Chronic Lower Respiratory Tract Disease in Children
Persistent fever
Ongoing limitation of activity
Failure to grow
Failure to gain weight appropriately
Clubbing of the digits
Persistent tachypnea and labored ventilation
Chronic purulent sputum
Persistent hyperinflation
Substantial and sustained hypoxemia
Refractory infiltrates on chest x-ray
Persistent pulmonary function abnormalities
Family history of heritable lung disease
Cyanosis and hypercarbia
TABLE 381-3 -- Characteristics of a Chronic Cough and Their Etiologic Significance
Loose (discontinuous), productive Bronchitis, asthmatic bronchitis, cystic fibrosis, bronchiectasis
Brassy Tracheitis, habit cough
With stridor Laryngeal obstruction, pertussis
Paroxysmal (with or without gagging) Cystic fibrosis, pertussis syndrome, and foreign body
Staccato Chlamydial pneumonitis
Nocturnal Upper or lower respiratory tract allergic reaction, or both, sinusitis
Most severe on awaking in morning Cystic fibrosis, bronchiectasis, chronic bronchitis
With vigorous exercise Exercise-induced asthma, cystic fibrosis, bronchiectasis
Disappears with sleep Habit cough, mild hypersecretory states such as in cystic fibrosis and asthma
Tight (wheezy) Reactive airways

TABLE 381-4 -- Clinical Clues About Cough

Staccato, paroxysmal Pertussis, cystic fibrosis, foreign body, Chlamydia spp., Mycoplasma spp.
Followed by whoop Pertussis
All day, never during sleep Psychogenic, habit
Barking, brassy Croup, psychogenic, tracheomalacia, tracheitis, epiglottitis
Hoarseness Laryngeal involvement (croup, recurrent laryngeal nerve involvement)

Abrupt onset Foreign body, pulmonary embolism
Follows exercise Reactive airways disease
Accompanies eating, drinking Aspiration, gastroesophageal reflux, tracheoesophageal fistula
Throat clearing Postnasal drip
Productive (sputum) Infection
Night cough Sinusitis, reactive airways disease
Seasonal Allergic rhinitis, reactive airways disease
Immunosuppressed patient Bacterial pneumonia, Pneumocystis carinii, Mycobacterium tuberculosis, Mycobacterium avium
intracellulare, cytomegalovirus
Dyspnea Hypoxia, hypercarbia
Animal exposure Chlamydia psittaci (birds), Yersinia pestis (rodents), Francisella tularensis (rabbits), Q fever
(sheep, cattle), hantavirus (rodents), histoplasmosis (pigeons)
Geographic Histoplasmosis (Mississippi, Missouri, Ohio River Valley), coccidioidomycosis (southwest),
blastomycosis (north and midwest)
Workdays with clearing on Occupational exposure
days off
TABLE 418-1 -- Respiratory Signs and Symptoms Originating from Outside the Respiratory Tract
Chest pain Cardiac disease Inflammation (pericarditis), ischemia Precordial pain, friction rub on
(anomalous coronary artery, vascular examination; exertional pain, radiation
disease) to arm or neck
Chest pain Gastroesophageal reflux Esophageal inflammation and/or spasm Heartburn, abdominal pain
Cyanosis Congenital heart disease Right-to-left shunt Neonatal onset, lack of response to
Cyanosis Methemoglobinemia Increased levels of metHgb interfere Drug or toxin exposure, lack of
with delivery of oxygen to tissues response to oxygen
Dyspnea Toxin exposure, drug side Variable, but often metabolic acidosis Drug or toxin exposure confirmed by
effect, or overdose history or toxicology screen, normal
Dyspnea Anxiety, panic disorder Increased respiratory drive and Occurs during stressful situation, other
increased perception of respiratory symptoms of anxiety or depression
Exercise Anemia Inadequate oxygen deliver to tissues Pallor, tachycardia, history of bleeding,
intolerance history of inadequate diet
Exercise Deconditioning Self-explanatory History of inactivity, obesity
Hemoptysis Nasal bleeding Posterior flow of bleeding causes History and physical examination
appearance of pulmonary origin suggest nasal source, normal chest
examination, and chest radiography
Hemoptysis Upper gastrointestinal tract Hematemesis mimics hemoptysis History and physical examination
bleeding suggest gastrointestinal source, normal
chest examination and chest
Wheezing, Congenital or acquired Pulmonary overcirculation (ASD, Murmur
cough, dyspnea cardiac disease VSD, PDA), left ventricular
Refractory to bronchodilators
Radiographic changes (prominent
pulmonary vasculature, pulmonary

Wheezing, Gastroesophagel reflux Laryngeal and bronchial response to Emesis, pain, heartburn
cough disease stomach contents
?Vagally mediated bronchoconstriction Refractory to bronchodilators


Pleural Effusion
TABLE 397-5 -- Differentiation of Pleural Fluid
Appearance Clear Cloudy Purulent
Cell count <1000 >1000 >5000
Cell type Lymphocytes, monocytes PMNs PMNs
LDH <200 U/L >200 U/L >1000 U/L
Pleural/serum LDH ration <0.6 >0.6 >0.6
Protein >3 g Unusual Common Common
Pleural/serum protein ratio <0.5 >0.5 >0.5
Glucose Normal Low Very low[*](<40 mg/dL)
pH[*] Normal (7.407.60) 7.207.40 <7.20, chest tube placement required
Gram stain Negative Usually positive >85% positive unless patient received prior antibiotics

Rheumatic Fever
TABLE 182-2 -- Guidelines for the Diagnosis of Initial Attack of Rheumatic Fever (Jones Criteria, Updated 1992)

Carditis Clinical features:

Polyarthritis Arthralgia


Erythema marginatum Laboratory features:

Subcutaneous nodules Elevated acute phase reactants:

Erythrocyte sedimentation rate

C-reactive protein

Prolonged PR interval

From Jones criteria, updated 1992. JAMA 1992;268:20692073. Copyright American Medical Association.
* The presence of 2 major or of 1 major and 2 minor manifestations indicates a high probability of acute rheumatic fever
if supported by evidence of preceding group A streptococcal infection.
Diagnosis can be made without fulfilling the Jones criteria in 3 instances.
o Chorea may occur as the only manifestation of acute rheumatic fever.
o Indolent carditis may be the only manifestation in patients who 1st come to medical attention months after the onset of acute
rheumatic fever.
o Although most patients with recurrences of acute rheumatic fever fulfill the Jones criteria, some may not.
Clinical maneuvers to elicit features of chorea
o (1) demonstration of milkmaid's grip (irregular contractions of the muscles of the hands while squeezing the examiner's fingers)
o (2) spooning and pronation of the hands when the patient's arms are extended
o (3) wormian darting movements of the tongue upon protrusion
o (4) examination of handwriting to evaluate fine motor movements.

TABLE 182-5 -- Duration of Prophylaxis for People Who Have Had Acute Rheumatic Fever: Recommendations of the
American Heart Association

Rheumatic fever without carditis 5 yr or until 21 yr of age, whichever is longer

Rheumatic fever with carditis but without residual heart 10 yr or well into adulthood, whichever is longer
disease (no valvular disease[*])

Rheumatic fever with carditis and residual heart disease At least 10 yr since last episode and at least until 40 yr of age;
(persistent valvular disease[*]) sometimes lifelong prophylaxis
From the American Academy of Pediatrics: Red Book: 2006 Report of the Committee on Infectious Diseases,27th ed. Elk Grove Village,
IL, American Academy of Pediatrics, 2006, p 619.
* Clinical or echocardiographic

Hematology and Oncology

Iron Deficiency Anemia
TABLE 455-2 -- Responses to Iron Therapy in Iron-Deficiency Anemia
1224 hr Replacement of intracellular iron enzymes; subjective improvement;
decreased irritability; increased appetite
3648 hr Initial bone marrow response; erythroid hyperplasia
4872 hr Reticulocytosis, peaking at 57 days
430 days Increase in hemoglobin level
13 mo Repletion of stores

Blood Component Transfusions

TABLE 470-1 -- Guidelines for Pediatric Red Blood Cell Transfusions [*]

Acute loss of >25% at circulating blood volume

Hemoglobin of <8.0 g/dL[] in the perioperative period
Hemoglobin of <13.0 g/dL and severe cardiopulmonary disease
Hemoglobin of <8.0 g/dL and symptomatic chronic anemia
Hemoglobin of <8.0 g/dL and marrow failure


Hemoglobin of <13.0 g/dL and severe pulmonary disease

Hemoglobin of <10.0 g/dL and moderate pulmonary disease
Hemoglobin of <13.0 g/dL and severe cardiac disease
Hemoglobin of <10.0 g/dL and major surgery
Hemoglobin of <8.0 g/dL and symptomatic anemia
TABLE 103-2 -- Transfusion Protocol (Neonates)
Hct Infants requiring moderate or significant mechanical ventilation (MAP > 8 cm H 2O and 15 mL/kg PRBCs[*] over period of 24
35/Hgb FIO2 > 0.4) hr

Hct Infants requiring minimal respiratory support (any mechanical ventilation or 15 mL/kg PRBCs over period of 24 hr
30/Hgb endotracheal/nasal CPAP > 6 cm H2O and FIO2 0.4)
Hct Infants not requiring mechanical ventilation but who are receiving supplemental O 2 or 20 mL/kg PRBCs over period of 24 hr
25/Hgb 8 CPAP with an FIO2 0.4 and in whom 1 or more of the following is present: (divide into 210 mL/kg volumes if
fluid sensitive)

24 hr of tachycardia (HR > 180) or tachypnea (RR > 80)

An increased oxygen requirement from the previous 48 hr, defined as a 4-
fold increase in nasal canula flow (i.e., 0.25 to 1 L/min) or an increase in nasal
CPAP 20% from the previous 48 hr (i.e., 5 to 6 cm H2O)
Weight gain <10 g/kg/day over the previous 4 days while receiving 100
An increase in episodes of apnea and bradycardia (>9 episodes in a 24-hr
period or 2 episodes in 24 hr requiring bag and mask ventilation) while
receiving therapeutic doses of methylxanthines
Undergoing surgery

Hct Asymptomatic and an absolute reticulocyte count <100,000 cells/L 20 mL/kg PRBCs over period of 24 hr
20/Hgb 7 (210 mL/kg volumes)

TABLE 471-1 -- Guidelines for Pediatric Platelet Transfusions [*]


PLTs < 50 109/L and bleeding

PLTs < 50 109/L and an invasive procedure
PLTs < 20 109/L and marrow failure with hemorrhagic risk factors
PLTs < 10 109/L and marrow failure without hemorrhagic risk factors
PLTs at any count, but with PLT dysfunction plus bleeding or an invasive procedure


PLTs < 100 109/L and bleeding

PLTs < 50 109/L and an invasive procedure
PLTs < 20 109/L and clinically stable
PLTs < 100 109/L and clinically unstable
PLTs at any count, but with PLT dysfunction plus bleeding or an invasive procedure

TABLE 473-1 -- Guidelines for Pediatric Fresh Frozen Plasma Transfusions [*]

Severe clotting factor deficiency and bleeding

Severe clotting factor deficiency and an invasive procedure
Emergency reversal of warfarin effects
Dilutional coagulopathy and bleeding
Anticoagulant protein (antithrombin III, proteins C and S) replacement
Plasma exchange replacement fluid for thrombotic thrombocytopenic purpura

Solid Tumors
TABLE 499-3 -- Differential Diagnosis of Abdominal and Pelvic Tumors in Infants and Children
Wilms Preschool Unilateral flank mass, aniridia, Hematuria;bone scintigraphy (clear cell
hemihypertrophy sarcoma)
Neuroblastoma Preschool GI/GU obstruction, raccoon eyes, myoclonus- Increased VMA;increased HVA;increased
opsoclonus, diarrhea, skin nodules (infants) ferritin; stippled calcification in mass.
Bone marrow positive
Non-Hodgkin >1 yr Intussusception in >2-yr-old Increased urate; bone marrow positive
Rhabdomyosarcoma All GI/GU obstruction, sarcoma botryoides,
vaginal bleeding, paratesticular mass
Germ cell/teratoma Preschool, Girls:abdominal pain, vaginal bleeding Increased hCG;Increased AFP
Boys:testicular mass, new-onset hydrocele
Sacrococcygeal mass/dimple
Hepatoblastoma Birth3 yr Large, firm liver Increased AFP
Hepatoma School age, Large, firm liver; hepatitis B, cirrhosis Increased AFP
TABLE 501-1 -- Comparison of Features of Osteosarcoma and the Ewing Family of Tumors
Age Second decade Second decade
Race All races Primarily whites
Sex (M : F) 1.5 : 1 1.5 : 1
Cell Spindle cellproducing osteoid Undifferentiated small round cell, probably of neural
Predisposition Retinoblastoma, Li-Fraumeni syndrome, Paget None known
disease, radiotherapy
Site Metaphyses of long bones Diaphyses of long bones, flat bones
Presentation Local pain and swelling; often, history of injury Local pain and swelling; fever
Radiographic Sclerotic destruction (less commonly lytic); Primarily lytic, multilaminar periosteal reaction (onion
findings sunburst pattern skinning)
Differential Ewing sarcoma, osteomyelitis Osteomyelitis, eosinophilic granuloma, lymphoma,
diagnosis neuroblastoma, rhabdomyosarcoma
Metastasis Lungs, bones Lung, bones
Treatment Chemotherapy Chemotherapy
Ablative surgery of primary tumor Radiotherapy and/or surgery of primary tumor
Outcome Without metastases: 70% cured; with metastases at Without metastases: 60% cured; with metastases at
diagnosis, 20% survival diagnosis, 2030% survival

Urologic Disorders
TABLE 545-1 -- Differential Diagnosis of Scrotal Masses in Boys and Adolescents
Testicular torsion Hydrocele
Torsion of appendix testis Inguinal hernia[*]
Epididymitis Varicocele[*]
Trauma:ruptured testis, hematocele Spermatocele[*]
Inguinal hernia (incarcerated) Testicular tumor [*]
Mumps orchitis Henoch-Schnlein purpura[*]
Idiopathic scrotal edema
May be associated with discomfort.

TABLE 545-2 -- Differential Diagnosis of Scrotal Swelling in Newborns

Inguinal hernia (reducible)
Inguinal hernia (incarcerated)[*]
Testicular torsion [*]
Scrotal hematoma
Testicular tumor
Meconium peritonitis

Neurologic Disorders
TABLE 595-2 -- Indications for Neuroimaging in a Child with Headaches
Abnormal neurologic signs
Recent school failure, behavioral change, fall-off in linear growth rate
Headache awakens child during sleep; early morning headache, with increase in frequency and
Periodic headaches and seizures coincide, especially if seizure has a focal onset
Migraine and seizure occur in the same episode, and vascular symptoms precede the seizure (20
50% risk of tumor or arteriovenous malformation)
Cluster headaches in child; any child <56 yr whose principal complaint is a headache
Focal neurologic symptoms or signs developing during a headache (i.e., complicated migraine)
Focal neurologic symptoms or signs (except classic visual symptoms of migraine) develop during
the aura, with fixed laterality; focal signs of the aura persisting or recurring in the headache phase
Visual graying-out occurring at the peak of a headache instead of the aura
Brief cough headache in a child or adolescent

CNS Infections
TABLE 602-1 -- Cerebrospinal Fluid Findings in Central Nervous System Disorders
Normal 5080 <5, 75% lymphocytes 2045 >50 (or 75% serum glucose)
Acute bacterial meningitis Usually elevated 10010,000 or more; usually 3002,000; PMNs Usually 100500 Decreased, usually <40 (or Organisms usually seen on Gram stain and recovered
(100300) predominate <50% serum glucose) by culture.
Partially treated bacterial Normal or 510,000; PMNs usual but mononuclear cells may Usually 100500 Normal or decreased Organisms may be seen on Gram stain. Pretreatment
meningitis elevated predominate if pretreated for extended period of time may render CSF sterile. Antigen may be detected by
agglutination test
Viral meningitis or Normal or Rarely >1,000 cells. Eastern equine encephalitis and Usually 50200 Generally normal; may be HSV encephalitis is suggested by focal seizures or by
meningoencephalitis slightly elevated lymphocytic choriomeningitis (LCM) may have cell decreased to <40 in some viral focal findings on CT or MRI scans or EEG.
(80150) counts of several thousand. PMNs early but diseases, particularly mumps Enteroviruses and HSV infrequently recovered from
mononuclear cells predominate through most of the (1520% of cases) CSF. HSV and enteroviruses may be detected by PCR
course of CSF
Tuberculous meningitis Usually elevated 10500; PMNs early, but lymphocytes predominate 1003,000;may <50 in most cases; decreases Acid-fast organisms almost never seen on smear.
through most of the course be higher in with time if treatment is not Organisms may be recovered in culture of large
presence of block provided volumes of CSF. Mycobacterium tuberculosis may be
detected by PCR of CSF
Fungal meningitis Usually elevated 5500; PMNs early but mononuclear cells 25500 <50;decreases with time if Budding yeast may be seen. Organisms may be
predominate through most of the course. Cryptococcal treatment is not provided recovered in culture. Cryptococcal antigen (CSF and
meningitis may have no cellular inflammatory serum) may be positive in cryptococcal infection
Syphilis (acute) and Usually elevated 50500;lymphocytes predominate 50200 Usually normal Positive CSF serology. Spirochetes not demonstrable
leptospirosis by usual techniques of smear or culture; darkfield
examination may be positive
Amebic (Naegleria) Elevated 1,00010,000 or more; PMNs predominate 50500 Normal or slightly decreased Mobile amebae may be seen by hanging-drop
examination of CSF at room temperature
Brain abscess Usually elevated 5200; CSF rarely acellular; lymphocytes 75500 Normal unless abscess ruptures No organisms on smear or culture unless abscess
(100300) predominate; if abscess ruptures into ventricle, PMNs into ventricular system ruptures into ventricular system
predominate and cell count may reach >100,000
Subdural empyema Usually elevated 1005,000; PMNs predominate 100500 Normal No organisms on smear or culture of CSF unless
(100300) meningitis also present; organisms found on tap of
subdural fluid
Cerebral epidural abscess Normal to 10500;lymphocytes predominate 50200 Normal No organisms on smear or culture of CSF

slightly elevated
Spinal epidural abscess Usually low, 10100;lymphocytes predominate 50400 Normal No organisms on smear or culture of CSF
with spinal block
Chemical (drugs, dermoid Usually elevated 1001,000 or more; PMNs predominate 50100 Normal or slightly decreased Epithelial cells may be seen within CSF by use of
systs, myelography dye) polarized light in some children with dermoids
Sarcoidosis Normal or 0100;mononuclear 40100 Normal No specific findings
elevated slightly
Systemic lupus Slightly elevated 0500; PMNs usually predominate; lymphocytes may 100 Normal or slightly decreased No organisms on smear or culture. Positive neuronal
erythematosus with CNS be present and ribosomal P protein antibodies in CSF
Tumor, leukemia Slightly elevated 0100 or more; mononuclear or blast cells 501,000 Normal to decreased (2040) Cytology may be positive
to very high

Bone and Joint Disorders

TABLE 698-1 -- Juvenile Osteochondroses
Legg-Calv-Perthes disease Capital femoral epiphysis 312 yr
Osgood-Schlatter disease Tibial tubercle 1016 yr
Sever disease Os calcaneus 610 yr
Freiberg disease Head of second metatarsal 1014 yr
Scheuermann disease Vertebral bodies Adolescence
Blount disease Medial aspect of proximal tibial epiphysis Infancy or adolescence
Osteochondritis dissecans Subchondral regions of knee, hip, elbow, and ankle Adolescence

Effects of In Utero Positioning
o Normal full term newborns can have 20-30 degree hip and knee flexion contractures
Resolve at 4-6 months
o Changes due to positioning
Hip externally rotates 80-90 degrees
Limited internal rotation 0-10 degrees
Lower leg has inward rotation and feet are supinated
Top leg shows more changes than bottom leg
Face may be distorted
Spine and upper ex less affected
o Effects completely resolve by 3-4 years

Developmental Dysplasia of the Hip

o Risk factors
More common in females and in the left hip
Large birth weight
First pregnancy
Caesarian section
Infants cared for in special units after birth
o Maneuvers
Barlow Ortolani

Potential for dislocating a nondisplaced hip Reduce a dislocated hip

Start with knees and hips flexed Start with knees and hips flexed

Adduct thigh and direct force posteriorly Lift greater trochanter and abduct the hip
o Most reliable sign of a dislocated hip: limitation of abduction
o Shortening of the thigh, the Galeazzi sign, is best appreciated by placing both hips in 90 degrees of flexion and comparing the height of the knees, looking for asymmetry ( Fig. 677-5 ). Asymmetry
of thigh and gluteal skin folds may be present in 10% of normal infants but is suggestive of DDH. Another helpful test is the Klisic test, in which the examiner places the 3rd finger over the greater
trochanter and the index finger of the same hand on the anterior superior iliac spine. In a normal hip, an imaginary line drawn between the two fingers points to the umbilicus. In the dislocated hip,
the trochanter is elevated, and the line projects halfway between the umbilicus and the pubis ( Fig. 677-6 ).

o Most important complication: avascular necrosis of the capital femoral epiphysis

Other Disorders of the Hip

Legg-Calve-Perthes - femoral head is deformed
o Impaired epiphyseal growth and femoral head deformity (because of temporary interruption of blood supply to the proximal femoral epiphysis)
o 4-10 years (3-8 or 3-10 years) old, usually painless limp (pain may be referred to the thigh or knee)
o Self-limited; avascular necrosis of the hip
o Usually small for age with retarded bone age
o PE: atrophy of the affected thigh, limited hip motion
o Tx: activity limitation, PT, orthosis, surgery

Slipped capital femoral epiphysis
o Displacement of the CFE from the metaphysis; displacement of the femoral head from the femoral neck
o May be acute or chronic
o Older children and adolescents (10-17 years) - epiphysis of the femoral head slips away from the femoral neck because of weakened epiphyseal plate; painful limp; pain may be referred to the knee;
obese limping adolescent complaining of knee pain
o Possible causes: increased shearing stress, endocrine factors
o Tx: immobilization, osteotomies

Osgood Schlatter disease

10-15 years, more common in males
Point tenderness over the tibial tubercle
Tx: rest, restriction of activities, exercise program
Complete resolution in 12-24 mos

Fingertip amputation
When referring, all amputated parts should be saved, wrapped in saline-soaked gauze, placed into a watertight bag, and then placed in ice water. Ice should never directly contact the part, as it can cause
severe osmotic and thermal injury.

The differences in the pediatric skeletal system predispose children to injuries different from those of adults. The important differences are the presence of periosseous cartilage, physes, and a thicker,
stronger, more osteogenic periosteum that produces new bone called callus more rapidly and in greater amounts. The other factors are a disproportionately large head, pliable rib cage, unprotected large and
small bowel, and open epiphyseal plates in children. The pediatric bone has low density and more porosity. The low density is due to lower mineral content and the increased porosity due to increased
number of haversian canals and vascular channels. These differences result in a comparatively lower modulus of elasticity and lower bending strength. The bone in children may fail either in tension or in
compression; the fracture lines do not propagate as in adults, and hence there is less chance of comminuted fractures.

Characteristics of pediatric fractures

Remodeling: younger have greater remodeling potential
Overgrowth: present for 6 mos-1 yr after injury
Progressive deformity: most common is complete or partial closure of the growth plate
Rapid healing: children's fractures heal more quickly

Suspect child abuse if

Femoral fracture in a nonambulatory child
Fractures of: distal femoral metaphysis, proximal humerus
Fractures of: posterior rib, scapular spinous process
Transcondylar fracture in neonates

The Spine
o Thoracic curves < 30 deg rarely progress
o Lumbar curves more likely to progress
Congenital scoliosis
o GU abnormalities in 20-40%; renal UTZ should be done