Pediatrics Module Objectives

ORAL
ECC PREVENTION
WHY PRIMARY CARE PROVIDERS??
Most children have access to primary medical care. Primary care clinicians have regular, consistent contact through well-child visits.
Consider the following:
63.4 % of low-income children 19-35 months of age have completed all the primary vaccine series.
96% of children in the United States had a usual place of health care.
Clinicians see children for well and acute care a minimum of eight times by age two, & frequently thereafter.
In contrast, few preschool children from low-income families regularly receive dental care.

EFFECTS & SOURCES OF FLUORIDE
The use of fluoride, both through dietary and topical applications, has led to dramatic drops in caries rates.
How Does Fluoride Help Prevent Dental Caries?
Through topical mechanisms, the main effect, fluoride works by:
o Inhibiting tooth demineralization
o Enhancing remineralization
o Inhibiting bacterial metabolism
Through systemic mechanisms, the lesser effect, fluoride works by:
o Reducing enamel solubility through incorporation into its structure during tooth development
What Are the Primary Sources of Fluoride?
Systemic Fluoride is obtained through Water fluoridation; Dietary fluoride supplements
Topical Fluoride is the most beneficial and is obtained through Fluoride toothpastes; Gels, foams, mouthwashes; Fluoride
varnish

SYSTEMIC FLUORIDE
Guidelines
All children at high caries risk should receive fluoride through systemic water fluoridation or dietary supplements.
Children who drink optimally fluoridated water should NOT receive supplements.
Optimal water fluoridation is 0.7 ppm.
Steps to Take Before Considering Prescribing Supplements
Determine the source of your patient's water, which may be: Fluoridated city water; Nonfluoridated city water; Bottled water
(variable fluoride levels); Well water (variable fluoride levels)
Determine the fluoride content: Public water supply: Contact local health departments or water company for fluoride levels OR Well
water: Test the well water for fluoride level. Local health departments can provide resources for water testing.
Additional factors affecting fluoride content:
o Water filters: Most filters are charcoal based and do not remove fluoride. Only reverse osmosis water filters (very costly to
install) remove fluoride.
o Bottled water: If companies add fluoride, this must be listed on the bottle. The fluoride content of most bottled water is
unknown as natural water may or may not contain naturally occurring fluoride.
DIETARY FLUORIDE SUPPLEMENTATION
Dietary fluoride supplementation by
prescription for children at high caries risk
who do not have access to optimally
fluoridated water is recommended by the
American Academy of Pediatrics, the American
Academy of Pediatric Dentistry, and the
Centers for Disease Control and Prevention.
In May 2014, USPSTF recommended primary
care clinicians prescribe oral fluoride
supplementation starting at age 6 mths for
children whose water supply is deficient in
fluoride, not based on risk assessment.

Guidelines
If the fluoride content of the main water used for cooking and drinking cannot be determined, then supplemental fluoride should NOT
be prescribed.
In optimally fluoridated communities where children drink bottled water, supplements should NOT be prescribed due to halo effect.
Supplementation is not recommended for breast feeding infants or formula fed infants until age six months.
All prescriptions for fluoride should specify a sugar-free preparation.

FLUOROSIS
Fluorosis is a discoloration of the teeth due to chronic excessive exposure to fluoride during tooth development. It is a cosmetic issue
that does NOT affect systemic health.
Clinical Appearance Usually consists of white mottling
Prevalence & Risk Factors
Prevalence of fluorosis (mostly mild) in the United States is 0.2%27% and rising.
The risk of developing fluorosis is greatest at an intake of more than 0.06 milligram per kilogram of body weight per day.
Varnish is not a major risk factor for fluorosis as it is an irregular source of fluoride rather than a daily one.
Risk Reduction
Determine the fluoride content of the child's drinking water before prescribing supplements.
Avoid duplicate fluoride prescriptions.
Follow current dosage schedules for systemic fluoride supplementation.
Tell the child's caregiver to place only a smear (under two years) or pea size dab (children over age 3 or when the child can spit
effectively) of fluoridated toothpaste on the child's toothbrush.
Keep fluoride-containing products out of the reach of small children.


HYGIENE: TOOTH BRUSHING
Regular tooth brushing is important to remove plaque and food debris, and most importantly for distributing the fluoridated
toothpaste.
Brushing Guidelines
Brush 2x daily beginning as soon as teeth emerge Bedtime is most critical due to decreased salivary flow.
Caregiver should brush child's teeth until age 8 or 9, at least until they have developed the manual dexterity to write in cursive and
tie their own shoes.
Children will not reliably spit and may swallow flavored toothpaste.
Young children have difficulty adequately brushing all areas.
Parents should continue to intermittently supervise brushing after children assume independence.
Caregiver should stand or sit behind child.
Child should spit out, not rinse, after brushing to increase topical fluoride exposure.

HOW MUCH TOOTHPASTE??
Excessive ingestion of toothpaste can cause fluorosis which is a minor cosmetic problem, relative to losing teeth to caries. In rare
situations, such as consuming a large portion of a family sized tube, systemic toxicity including electrolyte abnormalities can result
in a medical emergency.
Guidelines
Use a small smear for children less than two years old (size of a grain of rice).
Apply a pea-sized amount of toothpaste for children three years and older regardless of caries risk status.
Most preschool children swallow much of the toothpaste placed on the brush. These guidelines take this into account and these
amounts are safe to swallow, but spitting out should always be encouraged.
Parents should keep toothpaste tubes out of reach of small children.

BRUSHING TECHNIQUES
Often families receive no formal instruction in correct brushing, and if the clinician does not provide it no one else will. Encourage
patients to follow these guidelines:
1. The caregiver should stand or sit behind the child and brush the exposed surfaces of each tooth.
2. Lift lip to allow proper visualization.
3. Brush along the gum line where caries commonly begins, both on the outside (buccal) and inside (lingual) of the tooth.
4. Brush the top or chewing surface (occlusal).
5. Use small backwards and forwards brushing movements or small circles.
6. Spit out toothpaste and don't rinse after brushing.
7. No food or drink after brushing.
8. Begin flossing daily once teeth touch.
9. Encourage use of electric toothbrush beginning at age 4 years.
Make Toothbrushing Fun
Sing a song that lasts two minutes and brush until done.
Sing the alphabet and brush each quadrant until done.
Brush in front of the mirror.
Use an electric toothbrush featuring timers, lights, or favorite characters.

CARIOGENICITY OF FOODS
In addition to avoiding the frequent use of juice and soda, caretakers must be mindful of seemingly "innocent" products, such as
"sport drinks" and processed fruit products. Potato chips and other refined, processed carbohydrate snacks can be broken down into
simple sugars which allow the bacteria to ferment the sugars into acids. Frequent consumption of these foods can lead to caries.
Encourage caregivers to offer sugar free, dentally appropriate snacks
Low Risk Snacks fruit, veggies, cheese, crackers, pretzels, popcorn, nuts, sugar free gum, plain milk, water
High Risk Snacks fruit-rollups; gummy bears; cookies; cupcakes; sugared cereals; granola bars; poptarts; soda; raisins

HIGH RISK EATING PATTERNS
Salivary pH remains low between meals which makes frequent snacking inadvisable. Maximizing the interval between food intake
allows time for teeth to remineralize after exposure to acids.
Follow these tips to lower caries risk:
Avoid frequent snacking (two or more times between meals) especially on foods like Juice or soft drinks; Candy, cookies, or
sweetened breakfast cereals
Refrain from eating sticky, retentive snacks and slow dissolving carbohydrates, such as: Raisins, dried fruit, fruit rolls, bananas,
caramels, jelly beans, or peanut butter and jelly sandwiches
Establish bedtime routines that include brushing after feedings. Do not eat or drink before bed after toothbrushing
No bottle use in bed

DIET & FEEDING ADVICE 0-12 MONTHS
Strongly encourage breast feeding.
Hold infant for bottle feeding.
Avoid giving bottles at bedtime or naptime.
Don't use sweetened pacifiers.
Introduce cup at six months.
Wean bottle by 12 months.
Avoid ad lib use of sippy cup unless it contains water.
Recommend no juice in the first year of life.
Snacks should contain no added sugar.

DIET & FEEDING ADVICE 1-5 y/o
Discontinue bottle by 12 months.
Limit juice to four ounces per day and serve with meals only.
Avoid carbonated beverages and juice drinks containing sweeteners.
Choose fresh fruits, vegetables, or sugar free whole grain snacks.
Only drink milk or water between meals.
Limit eating occasions to three meals a day with one snack in between.
Reserve soda, candy, and sweets for special occasions, preferably with meals.

ESTABLISH A DENTAL HOME
The American Academy of Pediatric Dentistry and the American Academy of Pediatrics both recommend establishment of a dental
home by the first birthday. Dentists will provide:
Enhanced preventative services
Comprehensive evaluation and diagnosis of oral disease
Evaluation of growth and development and provide counseling on oral habits and interceptive orthodontic treatment as needed
Fluoride varnish and cleanings
Dental x-rays when indicated
Sealants to permanent molars as child ages
Dental trauma management
Communities with Limited Dental Access
In many communities, those with no insurance or insured through Medicaid have limited or no access to dental care.
If limited dental access, the primary care clinician may need to:
Stratify the risk of the child.
Strive to assist children at moderate or high risk or with active disease in accessing the dental system in a timely manner.
Apply fluoride varnish to the teeth of children at moderate or high risk of caries in the medical office.
Follow low-risk children in the medical office:
o Ensure appropriate anticipatory guidance is given.
o Assess need for systemic fluoride supplementation and prescribe appropriately.
o Regularly assess oral health and provide dental referral when necessary and no later than age three years.
DEVELOPMENTAL ISSUES
Teething
Concerns Teething does not cause fever, upper respiratory infection, ear infection, or diarrhea.; Teething may cause fussiness;
Drooling is developmentally common at this age.
Anticipatory Guidance
Apply cold teething ring or cloth to gums.
Provide acetaminophen or ibuprofen if necessary.
Avoid teething gelsthey are not effective and contain high doses of topical anesthetics which can be dangerous in infants.
Remember tooth emergence may be preceded by a hematomano treatment is needed in primary dentition
Recommend never to dip pacifier in honey or other sweetened food.
Nonnutritive sucking- Nonnutritive sucking satisfies a psychological need and decreases as the child ages; most stop at two to
four years. It increases the risk of anterior open bite and delayed speech development if the habit persists.
Anticipatory Guidance
Intervene to stop habit by 36 months, especially if changes to occlusion are noted.
Offer positive reinforcement, such as a star chart or stickers.
Restrict to limited situations.
Cover hands at night with mittens.
Provide stuffed animal or other comfort object. In general, pacifier use is preferable to digit sucking as it is less likely to cause a
problem and the habit is easier to break (the pacifier can be removed).
Oral piercings- Oral piercings are increasingly popular, but there are significant risks.
Procedure-related risks: Swelling most common symptom post-piercing; Prolonged bleeding; Nerve damage
Jewelry-Related Complications: Injury to the gums and dental fractures, scarring; Interference with oral hygiene, speech, chewing and
swallowing; Allergic/hypersensitivity reaction to metal; Aspiration or ingestion if jewelry becomes loose
Grills on the teeth can increase the risk of developing caries and trigger allergic reactions to the metal.
Counsel grill-wearers to:Remove the grill to eat and sleep; Brush and floss regularly; Limit amount of time the grill is worn


THE NEWBORN INFANT CHP 2
ASSESSMENT & GROWTH- CHP 2 PG 9-30
Sucking reflex- newborn sucks in response to a nipple in
the mouth; observed by 14 wks gestation
Rooting reflex- head turns to the side of a facial stimulus,
present by 28 wks gestation
Traction reflex- infant is pulled by the arms to a sitting
position. Initially the head lags, then w/ active flexion,
comes to the midline briefly before falling forward.
Palmar grasp- evident w/ placement of examiners finer
in newborns palm; develops by 28 wks gestation &
disappears by 4 mths
Moro (startle) reflex- hold the infant supine while
supporting the head. Allow the top of the head to drop 1-2
cm suddenly. The arms will abduct at the shoulder &
extend at the elbow while spreading of the fingers.
Adduction w/ flexion will follow. This reflex develops by
28 wks gestation (incomplete) & disappears by 3 mths old
Newborn & Infant Growth
Newborns may lose up to 10% of their birth wt in the 1
st
wk of
life
Most regain birth weight in 7-10 days
First 6 months: gain 1 oz/day
At 6 months: approximately weigh 2x birth weight
At 12 months: approximately weigh 3x birth weight
Childhood Growth
After 2 years of age: 2-3 kg and 5-7 cm a year
Average 30 month old child weights 30lbs and is 30 inches tal
Average 4 year-old weighs 40 lbs and is 40 in. tall
Weight LOSS in a child is always suspicious


COMMON PROBLEMS IN THE TERM NEWBORN/INFANT
NEONATAL JAUNDICE
Transcutaneous bilirubin screening before 24 hours old
Scleral icterus & jaundiced oral mucosa hep distinguish this in dark pigmented babies
Physiologic Jaundice
Visible jaundice appearing after 24 hrs of age, peak at 3-5 days & resolves by 1 wk in full-term infant & by 2 wks in pre-term infant
Total bilirubin rises by < 5 mg/dl per day
Peak bilirubin occurs at 3-5 days of age, with a total bilirubin of no more than 15 mg/dl
Pathologic Unconjugated Hyperbilirubinemia
Multiple or unknown factors Racial differences; Prematurity
Breast Feeding and Jaundice
o Unconjugated hyperbilirubinemia lasting until 2-3 months of age is common in breast fed infants.
o Breast feeding associated jaundice: often referred to as lack of breast milk jaundice. Poor enteral intake and increased
enterohepatic circulation. Excess jaundice should be considered a possible sign of failure to establish adequate milk supply.
Decreased rate of Conjugation- reticulocyte counts remain normal
Crigler-Najjar
Gilbert syndrome
Increased bilirubin production
ABO blood group compatibility
o Tx- transfusion
RH-isoimmunizationTx- transfusion

HYPOGLYCEMIA
Blood glucose level of <40-45 mg/dL
MC found in infants born to diabetic moms & those who are intrauterine growth restricted
Presentation
Asymp or present w/ poor feeding, lethargy, jitteriness, tremulousness, irritability, apnea or seizures.
If associated w/ hyperinsulinemia, cardiac failure may develop
Diagnosis
Heel blood & bedside glucometer readings are adequate for screening. Abnorm results should be confirmed w/ whole-blood testing
Normal glucose level is 50-80 mg/dL at 3 hrs of age; an abnormal level is anything < 40-45
Treatment
Bolus of dextrose & water (D10W) & IV glucose PRN. Infant feeding is an option as well.
Resolution usually after 5
th
day of life.
Complications include diabetes & obesity development as children
RESPIRATORY DISTRESS
MC respiratory disorder in premature infants
o Immature lungs Pulmonary surfactant deficiency
o Incidence inversely proportional to gestational age at birth
25% at 34 weeks & 80% at 28 weeks
Surfactant deficiency
o Inflation of lungs without surfactant = Damage
o Respiratory epithelial injury & inflammation
o Advanced complications can involve edema & pulmonary hypertension
Presentation
Develops in first 2-6 hours of delivery
Worsens in first 24-48 hours
Tachypnea, retractions, grunting, cyanosis
Prevention
Delay delivery
Antenatal steroids Dexamethasone/Betamethasone. Promotes lung cell proliferation. Give to all mothers < 35 weeks
Treatment
Surfactants Synthetic & natural Expensive, unclear if differences exist with each product
Diuretics (Furosemide Lasix) Corrects acute edema
Nitric Oxide Pulmonary vasodilator, expensive, reduces pulmonary hypertension
No matter cause, respiratory distress treated with supplemental oxygen 60-70 mm Hg and oxygen saturation by pulse ox 92-96%
Supportive IV glucose and water

PRETERM INFANT P.39-47
APNEA
Defined as a respiratory pause lasting > 20 secs or any pause accompanied by cyanosis and bradycardia.
Apnea of prematurity is not associated with a predisposing factor, and is a diagnosis of exclusion. Most frequent cause of apnea.
Most common in infants born before 34 weeks gestation, onset before 2 weeks of age.
Apnea of prematurity = respiratory pause w/o airflow lasting >15-20 seconds or a respiratory pause of any duration if accompanied by
bradycardia/cyanosis or O2 desat
1) Central apnea: no chest wall movements or airflow
2) Apnea 2nd to obstruction
3) Mixed apnea (of 1 & 2): MC in premies
4) Idiopathic (increased risk w/decreasing gestational age)
Presentation:
Frequency of spells gradually increases with time
Pathologic apnea should be suspected if spells are sudden in onset, unusually frequency, or very severe
In full term or late preterm infant, presentation at birth suggests neuromuscular abnormalities of an acute or chronic nature
Treatment:
Underlying cause should be treated
Methylxanthines (eg, caffeine citrate) provide effective treatment
CPAP or high flow nasal cannula is effective in some infants

HYALINE MEMBRANE DISEASE
MC cause of respiratory distress in infants. Incidence increases from 5% of infants born at 35-36 weeks gestation to > 50% of infants
born at 26-28 weeks gestation.
Caused by a deficiency of surfactant production as well as surfactant inactivation by protein leak into airspaces.
Results in poor lung compliance and atelectasis
Infant must expend a great deal of effort to expand the lungs with each breath, and respiratory failure ensues
A result of surfactant deficiency alveolar collapse & diffuse atelectasis
Prevention
Antenatal GC treatment for women at risk for preterm delivery prior to 34 weeks of gestation
If gestation is >30 wks, the fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid by
amniocentesis
Presentation: Respiratory distress & cyanosis soon after birth; Tachypnea; Tachycardia; Chest wall retractions; Abdominal breathing
Diagnosis: CXR showing bilateral diffuse ground glass appearance with air bronchogram
Treatment
Supplemental oxygen, nasal CPAP, early intubation for surfactant administration & ventilation, & close physiologic monitoring
A ventilator gives synchronized with the infants respiratory effectors and deliver preset tidal volume (5-6 mL/kg)
Surfactant replacement is used both in the delivery room as prophylaxis for infants born before 27 weeks and with established
hyaline membrane disease as rescue (Survanta, Infasurf, and Curosurf)

PATENT DUCTUS ARTERIOSUS
Acyanotic
Closes spontaneously in normal term infants by 4 days. Common cardiac abnormality. Associated w./ maternal rubella infection
Presentation:
Harsh continuous machine murmur w/ bounding peripheral arterial pulses
Treatment
Refer to pediatric cardio for echo & for meds (indomethacin) to make ductal tissue regress or surgical repair

CARDIAC CHP 2 & 22
STILLS MURMUR
The MC innocent murmur of early childhood. Typically heard b/w 2-7 y/o
It is the loudest b/w the apex (midsternal border) & the lower left sternal border. Loudest when pt is SUPINE. Diminishes or
disappears w/ inspiration or when the pt is sitting/standing & Valsalva. Heard best at the tricuspid & mitral auscultation areas.
Musical (twangy, harmonic) or vibratory, short, high-pitched, grade I-III early systolic ejection murmur.
Louder in any pt w/ fever, anemia, or sinus tachycardia from any reason.

VENOUS HUM
Usually heard after 2 y/o (usually 3-6 y/o). Located in the infraclavicular area on the right (upper right & L sternal border) It is a
continuous musical hum of grade I-III intensity & may be accentuated in diastole & w/ inspiration. Best heard in the SITTING
position.
Turning the childs neck, placing the child supine, & compressing the jugular vein obliterates the venous hum.
Maneuvers distinguish it from the murmur or a PDA (which doesnt change w/ body position or head turn)
Venous hum is caused by the turbulence at the confluence of the subclacian & jugular veins.

ATRIAL SEPTAL DEFECT
Acyanotic (left- to-right)
Presentation:
May be asymptomatic unless there are other defects -R heart failure; Pulmonary edema; Increased pulmonary vasculature
Midsystolic pulmonary flow or ejection murmur accompanied by a fixed split S2
Treatment
Refer to pediatric cards for echo
Surgical repair at age 2-3 for most
Small defects in boys dont need closure if RV size is normal

VENTRICULAR SEPTAL DEFECT
VSD may be right-to-left or left-to-right. Acyanotic
MC diagnosed congenital heart defect
Presentation:
Holosystolic murmur
Loud, harsh, blowing holosystolic murmur-heard best over the lower left sternal border
May have thrill or diastolic rumble
Downs syndrome association
Treatment
Most will get smaller & disappear on their own
Surgical repair indicated for intractable CHF, failure to thrive

TETRALOGY OF FALLOT
The MC cyanotic heart defect. Cyanotic!!
Pulmonary stenosis, RV hypertrophy, overriding aorta, VSD
Presentation:
Progressive. May appear healthy & pink at birth
Cyanotic hypoxemic tet spells where child turns blue; dyspnea on exertion; Squats to Valsalva
Harsh, rough systolic ejection murmur in the 3
rd
intercostal space
May also have right aortic arch, Downs or DeGeorges syndrome
Diagnosis: boot-shaped heart
Treatment:
Surgical correction in early infancy
Complications: Brain abscess; CNS injury; stroke

PERSISTENT PULMONARY HYPERTENSION
Results when the normal decrease in pulmonary vascular resistance after birth dose not occur.
Most affected infants are full term or postterm, and many have experienced perinatal asphyxia.
Etiology:
Vasoconstriction due to perinatal hypoxia related to an acute even such as sepsis or asphyxia
Prenatal increase in pulmonary vascular smooth muscle development, often associated with meconium aspiration syndrome
Decreased cross-sectional area of the pulmonary vascular bed associated with lung hypoplasia (eg, diaphragmatic hernia)
Presentation:
Onset at first day of life, usually from birth
Respiratory distress is prominent
Pao2 is usually poorly responsive to high concentrations of inspired oxygen
Associated cardiology depression with systemic hypotension
Diagnosis:
Echo reveals right to left shunting at the level of the ductus arteriosus or foramen ovale, or both
CXR may show lung infiltrates related to associated pulmonary pathology
Treatment:
Treat other postasphyxia problems such as seizures, renal failure, hypoglycemia, and infection
Treatment aim is to decrease pulmonary arterial pressure to reverse the right-to-left shunt through fetal pathways
First line is oxygen and ventilation and crystalloid infusions
Second line is systemic pressors (dopamine, epinephrine, or both)

COARCTATION OF AORTA
Narrowing of the lumen in the thoracic portion of the descending aorta
SX: CHF in infancy, HTN in older children
o Disparity of pulses and BP between arms and legs; BP of upper extremity is > than lower extremity by 20 mm Hg
o X-ray: notching of ribs noted in late childhood

AORTIC STENOSIS
Most have no cardiovascular sx. Some mild exercise intolerance and easy fatigability
Systolic ejection murmur at upper sternal border
Dx: Echo

RHEUMATIC FEVER
Acquired heart dz
**Know the Jones Criteria ( 2 major or 1 major and 2 minor)
Major: carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules
Minor: fever, arthralgia, elevated ESR and/or c-reactive protein, prolonged PR interval on ECG

KAWASAKI DZ
Leading cause of acquired heart disease in US. 80% of pts are < 5 years old
Diagnostic Criteria: For more than 5 days and at least four of the following:
1) Bilateral, painless, nonexudative conjunctivitis
2) lip or oral cavity changes: lips cracking, strawberry tongue)
3) cervical lymphadenopathy
4) polymorphous exanthema
5) Extremity changes-redness and swelling of the hands and feet with subsequent desquamation

GI- CHP 21
ESOPHAGEAL ATRESIA & TRACHEOESOPHAGEAL FISTULA (P. 54)
Essentials of Dx:
Polyhydramnios; Excessive drooling & secretions; choking w/ attempted feeding. Unable to pass an orogastric tube to the stomach.
General
Esophageal atresia is characterized by a blind esophageal pouch w/ or w/o a fistulous connection b/w the proximal or distal
esophagus (or both) & the airway. In 85% of infants, the fistula is b/w the distal esophagus & the airway. Polyhydramnios is
common bc of high GI obstruction.
Presentation
Infants present in the 1
st
hours of life w/ copious secretions, chocking, cyanosis & respiratory distress.
Diagnosis
Confirm w/ CXR after careful placement of a NG tube to the point at which resistance is met. The tube will be seen radiographically
in the blind pouch. If a tracheoesophageal fistula is present to the distal esophagus, gas will be present in the bowel. In the
esophageal atresia w/o tracheoesophageal fistula, there is no gas in the bowel.
Treatment
The NG tube in the proximal pouch should be placed on low intermittent suction to drain secretions & prevent aspiration. The head
of bed should be elevated to prevent reflux of gastric contents thru the distal fistula into lungs. IV glucose & fluids should be
provided & oxygen administered PRN.
Definitive tx is surgical & the technique used depends on the distance b/w the segments of the esophagus. If the distance is not too
great, the fistula can be ligated & the ends of the esophagus anastomosed. If the ends of the esophagus cant be brought together, the
initial surgery if fistula ligation & a feeding gastrostomy. Echocardiography should be performed prior to surgery to R/O a R-sided
aortic arch (for which a L-sided thoracotomy would be preferred).
Prognosis
Determined primarily by the presence of absence of associated anomalies, particularly cardiac & low birth wt. Mortality is highest
when infant is < 2000 g & has a serious associated cardiac defect. Vertebral, anal, cardiac, renal & limb anomalies are the most likely
to be observed (VACTERL) association. Eval for associated anomalies should be initiated early.

ABDOMINAL WALL DEFECTS (P. 56)
OMPHALOCELE
A membrane covered herniation of abdominal contents into the base of the umbilical cord; occurs in 2 per 10,000 live births.
The sac may contain liver and spleen as well as intestine.
Over 50% of cases have either an abnormal karyotype or an associated syndrome.
Treatment
At delivery the omphalocele is covered with sterile dressing soaked with warm saline to prevent fluid loss.
NG decompression is performed, and IV fluids, glucose, and abx are given.
If sac contents can fit into abdomen and can be covered with muscle and skin primary surgery closer is done.
If not, staged closer is performed with placement of Fore-Tex patch over exposed contents.

GASTROSCHISIS
The uncovered intestine extrudes thru a small abdominal wall defect to the R of umbilical cord. No membrane or sac & no liver or
spleen outside the abdomen.
Associated with intestinal atresia in approximately 10-20% of infants, and with intrauterine growth resection (IUGR).
Etiology: Exact cause is unknown. Thought to be related with:
Methamphetamines and cocaine, and cyclooxygenase inhibitors such as ASA and IBU taken during pregnancy
Young maternal age
Related to abnormal involution of the right umbilical vein or a cascular accident involving the emphalomesenteric artery
Treatment:
Place bowel or lower half of infant into silastic bowel bag to decrease fluid and electrolyte losses and conserve heat
IV fluids, abx, and low intermittent gastric suction
Infant placed right side down to preserve bowel perfusion
Surgery to place bowel into abdomen

GASTROESOPHAGEAL REFLUX (P. 57)
Reflux of gastric contents into the esophagus occurs during spontaneous relaxations of the lower esophageal sphincter that are
unaccompanied by swallowing.
o Infants ~50% have reflux, but less than 10% have evidence of GERD.
o Usually benign and expected to resolve by 12-18 months of life
Promoting factors: Small stomach capacity, frequent large-volume feedings, short esophageal length, spine positioning, and slow
swallowing response to the flow to reflexed material up the esophagus
Presentation:
Recurrent postprandial spitting and vomiting in healthy infants, ranging from effortless to forceful; Failure to thrive; Food refusal;
Pain behavior; GI bleeding; Sandifer syndrome; Upper and lower airway associated respiratory symptoms; Older kids complain of
adult symptoms like regurg in the mouth, heartburn, and dysphagia
Diagnosis
History & PE sufficient in benign infants with GER
Determine if vomit contains bile intestinal obstruction
In older children, trial of acid suppressant therapy is both diagnostic and therapeutic
Esophagoscopy and mucosal biopsies are useful to evaluate for mucosal injury secondary to GERD
Warning signs that warrant further investigations in children: bilious emesis, GI bleeding, onset of vomiting after 6 months, failure to
thrive, diarrhea, fever, hepatosplenomegaly, abdominal tenderness or distension, or neurologic changes
Treatment:
Resolves spontaneously in 85% of affected infants by 12 months (erect posture and initiation of solid feedings)
Small feedings with frequent intervals and thicken feedings with rice cereal
H2 blockers and PPIs
Antireflex surgery (Nissen fundoplication) last line

PYLORIC STENOSIS
Typically in 2-4 wks, usually 1
st
born males. Rare at birth or over 6 months old
Presentation
Projectile post-prandial vomiting, ravenous hunger, palpable pyloric mass olive, poor wt gain, visible peristaltic waves
Diagnosis
KUB showing caterpillar sign of distended, hypertrophic stomach
US showing thickened stomach muscle (preferred imaging)
Treatment
Refer for surgical pyloromyotomy

INTUSSUSCEPTION
MC cause of intestinal obstruction in infants < 1 year
Most cases are between 3-12 months
Can occur multiple times
Etiologies
Idiopathic: most cases; Viral; Underlying condition: Meckel diverticulum
Presentation
Paroxysmal colicky abdominal pain w/ screaming & drawing u of the knees; Vomiting; Bloody currant jelly stools; Palpable mass
or sausage in RUQ; Lethargy
Differential Malignancy if child is over 3
Diagnosis
Plain films showing SBO
US showing pseudokidney sign or lasagna sign (test of choice)
Treatment
Barium air enema can be both diagnostic and therapeutic

VOLVULUS
Small bowel twists around the superior mesenteric artery, leads to kinking of the duodenum
>50 % present <1 month of age
Presentation
bilious vomiting and abdominal distention
Diagnosis
Double bubble sign on x-ray
Treatment
surgical repair

MECKELS DIVERTICULUM
MC congenital GI tract abnormality
Sx: bleeding (hematochezia), intestinal obstruction, intestinal volvulus
DX: technitium scan
Tx: surgical

PHENYLKETONURIA (PKU)
Autosomal recessive disorder
Screened for in newborn metabolic screening
From defective conversion of phenylalanine to tyrosine -Phenylalanine is found in breast milk & standard formulas
Presentation
Intellectual disability; Epilepsy; Abnormal gait, posture, or stance; Mousy urine or body odor; Eczematous rash; light complexion
Diagnosis
Elevated serum phenylalanine
Treatment
Dietary restriction- want low phenylalanie & strict control of protein intake is required for life
Frequent phenylalanine & tyrosine monitoring

EYE- CHP 16
STRABISMUS (TROPIA) p. 486-488
Marker for other disease: 20% of patients with retinoblastoma present with strabismus
Etiologies
Congenital: pseudostrabismus, prenatal drug exposure, nerve palsy, familial external ophthalmoplegia
Acquired: accommodative strabismus, intermittent exotropia, cataracts, tumors, increased ICP, orbital injury, head trauma, vascular
disorders, botulism, myasthenia gravis, nerve palsy, Guillain- Barre, ocular myopathy, multiple sclerosis, infection, drug or toxin, DM,
hypoglycemia, thyrotoxicosis
Differential Pseudostrabismus; Ocular instability of infancy (normal in first few months of life)
Diagnosis
Corneal light reflex/ Cover test- Affected eye will drift when covered, then moves quickly back if cover is removed
Differentiate congenital from acquired (may be vision-threatening or life-threatening)
Exotropia- (wall-eyed) eyes are divergent, can be intermittent or constant, bilateral or unilateral
Esoptropia-(crossed eye)deviation of the eyes towards the nose
Treatment
Refer to ophtho for consistent strabismus at any age, persistent strabismus after 4 months of age, altered light reflex, deviation with
cover test, deviation that changes depending on position of gaze, torticollis, parental concern
Sequelae If untreated may lead to amblyopia (vision reduction) or diplopia

AMBLYOPIA (p. 485-486)
Essentials of Dx
Amblyopia is a unilateral or bilateral reduction in vision due to strabismus, refractive errors, &/or visual deprivation.
Can only occur during the critical period of visual development in the first decade of life when the visual nervous system is plastic.
Approx 3% of the population is amblyopia.
Pathogenesis
Strabismic can occur in the nondominant eye of a stramismic child.
Refractive can occur in both eyes if significant refractive errors are untreated (ametropic or refractive).
Another type of refractive amblyopia can occur in eye w/worse refractive error when imbalance is present b/w eyes (anisometropic
amblyopia).
Deprivation amblyopia occurs when dense cataracts or complete ptosis prevents formation of a formed retinal image. This type
results in worst vision.
Presentation
Screening should be a component of WCC. The single best screening technique to discover amblyopia is obtaining visual acuity in
each eye. In preverbal kids unable to respond to visual acuity assessment, amblyogenic factors are sought, including strabismus,
media opacities, unequal Bruckner reflexes (papillary red reflexes), & a fam hx suggestive of strabismus, amblyopis or ocular dz
occurring in childhood
Treatment
Earlier the better the change of improving visual acuity. Tx usually D/C after 9 y/o.
Amblyogenic factors such as refractive errors are addressed. Bc of the extreme sensitivity of the visual nervous system in infants,
congenital cataracts & media opacities must be dx & tx w/n the first few wks of life. Visual rehab & amblyopia tx must then be
started to foster visual development.
After eradicating amblyogenic factors, the mainstay of tx is patching the sound eye, which causes the visual nervous system to
process input from the amblyopic eye & in that way permits the development of useful vision. Other tx modalities include fogging
the sound eye w/ cycloplegic drops (atropine), lenses & filters

DACRYOCYSTITIS
Blocked lacrimal glands
Etiologies- infection of the nasolacrimal sac
Viral: EBV; Bacterial: mumps, Staph, gonorrhea; Chronic: sarcoidosis, thyroid eye disease, orbital pseudotumor
Presentation
Swelling of upper lid; Lid redness & erythema; Lid pain; Excess tearing or purulent discharge; Swelling of preauricular nodes
Treatment
Warm compresses. Think malignancy if no improvement

DACROSTENOSIS
MC cause of persistent tearing and ocular disease in children
Cause: incomplete canalization of nasolacrimal duct
Sx: chronic or intermittent tearing
Tx: spontaneous resolution by 6 months
Massage and if needed optho consult for lacrimal duct probing

CHILD DEVELOPMENT & WELL-CHILD CHECKS- CHP 3

WCC Schedule (AAP)
Newborn: in hospital, 1 week, 2 week
o Birth hx: vaginal/C-S, APGARs, Birth wt, discharge wt, hearing screen, State metabolic screening (PKU), Vitamin K
administration
o Wt gained or lost since DC (BFing babies regain birth wt around 1.5-2 weeks, formula fed babies regain birth wt around 7-
10 days)
o Feeding patterns & schedules
o Stooling patterns (frequency, consistency)
o Sleeping patterns
o Parents status: sleep deprivation, support
o Sibling status: regression, acclimation
o Dont miss RED FLAGS
CHD- congenital hip dysplasia
Sacral dimple, pit, cleft, or hairy patch
Pupillary red reflex
GERD (spitty baby) vs pyloric stenosis
Congenital heart disease
Jaundice, Rh & ABO incompatibility
Testicles X 2
o cute little sack of potatoes cute, cuddly, warm, precious
1st two years: 2, 4, 6, 9 ,12, 15, 18 months old
o 2 months
Wt, Height, OFC; Feeding patterns; Stooling patterns; Sleep patterns; Social development (eye contact, follows)
RED FLAGS Papillary red reflex, hips (rechecking is important), hearing, objective, social development
Developmental highlights You smile at me WOW
Holds hands midline, prone push-up, follows side-to-side, social smile, recognizes parents & siblings
o 4 months
growth parameters, feeding patterns, stooling patterns, sleep patterns
RED FLAGS Papillary red reflex, eye conjugation, hips (last recheck), head shape (plageocephaly)
Highlights smiley bobble-head stage
Starting to roll over, push up on hands instead of arms, reaches & centralizes objects, social reciprocal
laugh, giggle, cooing, attempting to vocalize, directionally orients to noise & voice, loves being upright
o 6 month
growth, diet & starting solids (baby foods), stooling patterns, sleep patterns & sleep training
RED FLAGS Papillary red reflex & conjugation, head shape, abdominal exam (NB & Wilms), muscle tone
Highlights Im the life of the party
Eats their feet, unilateral reach, brings objects to midline, laughs, babbles constantly to hear themselves,
lateral orientation to non-voice sounds, may begin to experience stranger anxiety
o 9 months
growth parameters & the normal plateau, diet & starting soft table foods, NO eggs, PB, fish/seafood, stooling
patterns, sleeping patterns (consistency of schedule), baby-proofing the house, skeptical exam
RED FLAGS Social interaction, reciprocal, connected; gross motor progression, muscle tone; abdominal exam
Highlights I have my favorite people, thanks
Pulls to stand-starting to cruise, waves bye-bye, stairs become a reality, pincer grasp, transfers objects
from one hand to the other, throws objects, gesture games like so big & pat-a-cake
o 12 months
Growth parameters, expected uptick; Diet & transitioning to all table foods; Eggs & white fish if allowed; PB, if no
family history of peanut allergy; Sleep patterns; Safety of the home like gates, electric plugs; Using helmets in bike
carriers; Resistant exam
RED FLAGS Social interaction, emotional connection; Motor milestone progression from 9 months; Parent
connection: best & worst from year 1, relationship check, family & friend support
Highlights I can do that..
Walks alone; Uses two words other than mama & dad; Jargoning begins (self language); Imitates;
Comes when called by name; Mature pincer (eg. makes crayon marks)
o 15 months
Growth parameters, defining percentiles; Diet, a good variety; Sleep patterns, 2 naps 1 nap; Safety in public; A
will rears its ugly head start discipline; Power struggles around food & sleep; Combative exam
RED FLAGS Appropriate social connecting, M-CHAT; Behavioral counseling opportunit; Child Whisperer;
Because it works!; Timeout the right way- 2 minutes of silence for every year of age. Defiance & aggressiveness- no
warnings just do it.
Highlights Dont help me..
Masters stairs; Walks frontwards & backwards; Scribbles; Imitates block towers; 4-6 words consistently;
Desires to use eating utensil (like everyone else)
o 18 months
Food variety; Sleep schedule & consistency; Receptive language acquisition; Expressive language growth; Very
combative, sometimes explosive exam
RED FLAGS Behavior counseling opportunity; Establishing authority; Appropriate social development, M-CHAT
Highlights Dont fence me in
Start to understand the power of language; 7-10 word vocabulary; Knows five body parts; Copies parent
in chores; Plays by self, watching other kids, mine
o 24 months
Growth parameters; Expressive language explosion; Blossoming of social interaction; Gross motor & fine motor
progression
RED FLAGS Language; Social connectedness, M-CHAT; Motor
Highlights I think I know what youre thinking
Walks up & down steps by self; Removes clothing by self; Starts using pronouns; 50+ word vocabulary;
Follows two-step commands; Parallel play
Preschool: 3, 4, 5 years old
o Consistent growth patterns; Well-rounded diet; Sleep patterns; Progressive independence; Exponential language
acquisition; Power struggles over food, sleep & potty
o RED FLAGS Behavior counseling opportunities; Importance of calm & assertive parent as child meets adversity in the
real world for the first time; Relationship check of parents & monitoring family stress

School years: 6-18 yrs, yearly WCC
o Elementary years- 6-11 y/o
Growth parameters; Academic/cognitive progress; Technology use patterns; Sleep patterns; Age-appropriate
social-friendship connections; Activity & sports involvement
RED FLAGS Overloaded schedules; Technology addiction, overuse, abuse; Parenting needs to start changing
from nurture & protect to equip & free; Growth through responsibility, chores, expectations, rules, &
consequences
Highlights Im becoming my own person
Understanding social politics with peers; Loss of innocence; Realization the lifes not fair; Learning how
to constructively deal with adversities (bad teacher, bullying, failure)
o Tween- 12-14 y/o
Growth & diet (assessing for ED); Academics, sports, & overload; Technology patterns; Sleep patterns; Assessing
for depression; Social friendships; Drugs & alcohol
DONT MISS Opportunity to start talking about more sensitive issues like puberty, body changes, ED, body
image, relationships with parents, friendships, drugs/alcohol, sexual activity; Approach needs to be much more
mature & biologic, less fun & games
Highlights Whats my identity??
Tweens are either truly trying to figure out who they are & who they will become or they are beginning
to migrate toward escapes; Providers role is to plant the seeds about growing up into a functioning
young adult
o Teens- 15-18 y/o
Growth parameters; Academics; Involvement in sports, clubs, scouts; Sleep patterns (they need more than they
get); Assessing for mental illness (depression, anxiety, adjustment reactions); Drugs, alcohol, & sexual activity
DONT MISS Opportunity to start discussing future like what they might want to be, where they might want to
go to college; Ongoing discussion about the dangers of certain behaviors; Encouragement about the parts of their
lives that are going well & represent age-appropriate maturation
Highlights- who am I & why am I here?
Teens need someone in their lives assessing how life-ready they are; Teens needs someone to be
accountable to; Teens needs a safe person to confide in about sensitive issues

Parts of Every WCC
Vitals: Ht, Wt, OFC ( til age 2 yrs), BP 3 & up
Chronic problem list
Growth curves (percentiles)
Developmental Surveillance (validated)
School & academic status (grades, IEP, 504)

SUMMARY
Years 0-2: Growth & development
Years 3-5: Behavior & relationships
Years 6-11: Socialization into the world
Years 12-14: Beginning of identity
Years 15-18: Preparing for life-readiness

BEHAVIORAL & DEVELOPMENTAL VARIATIONS
ENCOPRESIS
Constipation is defined by 2 or more of the following for 2 months
(1) <3 bowel mvmts /week
(2) >1 episode of encopresis /week
(3) impaction of the rectum w/ stool
(4) passage of stool so large that is obstructs toilet
(5) retentive posturing & fecal withholding
(6) pain w/ defecation
Encopresis is the repeated passage of stool into inappropriate places (like pants) by a kid who is chronologically or developmentally
>4 y/o. Categorized as either Retentive encopresis; Continuous encopresis; Discontinuous encopresis
Etiology
Encopresis is triggered by voluntary holding then leakage around impaction. incontinence is MC in males & usually psychological,
such as not wanting to go to the bathroom at school & getting impacted then leakage around impaction.
>90% result from constipation. Highest prevelance is b/w 5-6 y/o
RFs metabolic d/o (hypothyroidism); neuro d/o (cerebral palsy or tethered cord & anatomical abnormalities of anus); stress or abuse
Diagnosis
abdominal xray to determine the degree of constipation, appearance of bowel, & whether or not there is an obstruction.
Treatment
Avoid punishing child, have child sit on toilet after meals to stimulate gastrocolic reflex, and getting bowel regimen
Oral medication or an enema for bowel cleanout followed by oral medications (fiber, laxatives, and mineral oil)

ENURESIS
Risk Factors
MC in M>F ; runs in family; higher threshold for arousal & dont wake to the sensation of a full bladder
Can be a result of overproduction of urine from decreased production of desmopressin or a resistance to antidiuretic hormone- in
this case the bladder has decreased functional capacity & empties before its filled.
Enuresis is defined as involuntary passage of urine into clothing during day & bed at night by a child who is chronologically &
developmentally >5 y/o; pattern must occur at least 2x/wk for 3 months.
Monosymptomatic uncomplicated noctural enuresis (NE; must never have been dry at night for > 6mths w/ no daytime
accidents); reflection of a maturational d/o & there is no underlying organic problem.
o Reflects a delay in achieving nighttime continence & reflects a delay in maturation of the urological & neuro system.
Nonmonosymptomatic (Daytime incontinence- usually achieved by 70% by 3 y/o & 90% by 6 y/o) consider cystitis, DI, DM,
seizure D/O, neurogenic bladder, urethral obstruction, constipation, stress, child maltreatment
most kids are continent at night w/n 2 yers of achieving daytime control. Primary enuresis is a child that has never been dry for a
significant portion of time. Secondary enuresis is the child that has been dry & now is having accidents; ask about home or school
issues (e.g. new sibling, parents getting divorce, bully at school)
Diagnosis
R/O any anatomical abnormalities; or the presence of constipation; urinalysis w/ specific gravity; urine culture esp for F (UTI);
Treatment
Reassurance, bed bell system (every time it goes off the kid goes to the bathroom)- use at least 3 months; child changes sheets after
wetting; waking the kid up at night to go to the bathroom (must have consistency & kid be fully awake) & possibly medications.
Recommend child does not drink fluids for 2 hours prior to going to bed.
Meds: DDVAP (decreases increases urine production); Imipramine (last resort); when meds stopped usually a high relapse rate

COMMON DEVELOPMENTAL CONCERNS
COLIC
Definition peaks at 2-3 months.
Presentation
an otherwise healthy infant aged 2-3 months seems to be in pain, cries for >3 hrs/day, for> 3 days/wk for > 3wks (rule of threes).
Severe and paroxysmal crying that occurs mainly in the late afternoon.
The infants knees are drawn up and its fists are clenched, flatus is expelled, and the facies has a pained appearance, and there is
minimal response to attempts at soothing.
Diagnosis: Before the dx of colic can be made the pediatrician must rule out diseases that might cause crying.
Treatment
Educate parents. Telling them that crying increases normally into the second month and abates by the third to fourth month.
Although these behaviors are stressful, they are normal variants and are usually self-limited.
One should encourage a quite environment without excessive handling. Rhythmic stimulation such as gentle swinging or rocking,
soft music, drives in the car or walks in the stroller may be helpful.
Change the feeding habits so that the infant is not rushed, has ample opportunity to burp & if necessary can be fed more frequently
Meds: Phenobarbital and dicyclomine are somewhat helpful, but not encouraged.

FEEDING-DISORDERS
Definition: Inadequate or disordered intake of food due to any of the following conditions: poor oral-motor coordination, fatigue
resulting from a chronic disease, lack of appetite, behavioral issues relating to parent-child interaction, pain associated with feeding.
Presentation: Child refuses to eat
Diagnosis:
PE should then be done with emphasis on oral motor behavior
The childs emotional state and developmental level must be determined.
The feeding interaction needs to be observed live.
Treatment: Parent and child behaviors need to be modified.

SLEEP DISORDERS
For most children, sleep problems are intermittent or temporary & often do not require treatment.
children younger than 12 years: difficulty initiating or maintaining sleep that is viewed as a problem by the child or caregiver.
May be characterized by its severity, chronicity, frequency and associated impairment in daytime function in the child or family
Adolescents- difficulty initiating or maintaining sleep or early morning awakening or nonrestoriative sleep, or a combination of
these problems.
Between 20 and 40% of children experience sleep disturbances at some point the first 4 years of life.
The most common disorder is insomnia which refers to problems with initiating and maintaining sleep.
New born sleep 10-19 hours per day in 2-5 hour blocks.
Most children stop napping between 3 and 5.
School aged children sleep 10-11 hours per night without a nap.
Parasonmias: include both NREM arousal disorders such as confusional arousals, night terrors, sleep talking and sleepwalking, and
REM associated sleep abnormalities.
Night terrors: w/in first two hours of falling asleep, often associated with sleep walking. Child will have no memory of the even the
next day. Parents should let the episode run its course. If the child sleep walks doors to the outside should be locked and objects
should be moved. Scheduled awakenings may also help with these problems.
Nightmares: frightening dreams that occur during REM sleep. incidence is between 25 and 50%. He or she can often describe the
frightening images, recall the dream, and talk about it during the day. Usually self-limited and need little treatment.
Insomnia: difficulty initiating sleep and nighttime awakenings. Occurs in 40-60% of children. Goal should be to establish clear
bedtime rituals, to put the child to bed while still awake and to create a quiet secure bedtime environment.
Sleep disordered breathing: characterized by obstructed breathing during sleep accompanied by loud snoring, chest retractions,
morning headaches and dry mouth and daytime sleepiness. Occurs in 1-3% of preschoolers. Lateral neck films may be helpful with
dx. Gold standard for dx is polysomnography.
Restless leg syndrome and periodic limb movement disorder: 2% in children. Associated w/ an uncomfortable sensation in the
lower extremities that occurs at night when trying to fall asleep, is relived by movement and is sometimes described as creepy-
crawly or itchy bones. PLMD is repetitive limb movements often associated w/ a partial arousal or awakening. Associated w/ iron
deficiency.
Normal sleep: Most children sleep for a stretch of at least 5 h by age 3 mo but then experience periods of night waking later in the
first years of life, often associated with illness. With maturation, the amount of rapid eye movement (REM) sleep increases, with
increasingly complex transitions between sleep stages. For most people, non-REM sleep predominates early in the night, with
increasing REM as the night progresses. Thus, non-REM phenomena cluster early in the night, & REM-related phenomena occur
later. Differentiating between true sleep (REM or non-REM)related phenomena & awake behaviors can help to direct treatment.
Night terrors & sleepwalking: Non-REM episodes of incomplete awakening with extreme anxiety shortly after falling asleep; they
are MC b/w the ages of 3 & 8. The child screams & appears frightened, with a rapid HR & rapid breathing. The child seems unaware
of the parents' presence, may thrash around violently, & does not respond to comforting. The child may talk but is unable to answer
questions. Usually, the child returns to sleep after a few minutes. Unlike with nightmares, the child cannot recall these episodes.
Night terrors are dramatic because the child screams & is inconsolable during the episodes. About one third of children with night
terrors also sleepwalk (the act of rising from bed & walking around while apparently asleep, also called somnambulism). About 15%
of children b/w 5-12 y/o have at least one episode of sleepwalking.
Night terrors & sleepwalking almost always stop on their own, although occasional episodes may occur for years. Usually, no
treatment is needed, but if a disorder persists into adolescence or adulthood & is severe, treatment may be necessary. In children
who need treatment, night terrors may sometimes respond to a sedative or certain antidepressants. There is some evidence that
disrupted sleep associated with periodic leg movements often responds to iron supplementation, even in the absence of anemia. If
children snore & thrash, evaluation for obstructive sleep apnea also should be considered.
Resistance to going to bed: Children, particularly b/w the ages of 1 & 2, often resist going to bed due to separation anxiety,
whereas older kids may be attempting to control more aspects of their environment. Young kids often cry when left alone in bed, or
they climb out & seek their parents. Another common cause of bedtime resistance is delayed sleep onset time. These situations arise
when kids are allowed to stay up later & sleep later than usual for enough nights to reset their internal clock to a later sleep onset
time. It can be difficult to move bedtime earlier, but brief tx w/ an OTC antihistamine or melatonin can help kids reset their clock.
Resistance to going to bed is not helped if parents stay in the room at length to provide comfort or let kids get out of bed. In fact,
these responses reinforce night waking, in which kids attempt to reproduce the conditions under which they fell asleep. To avoid
these problems, a parent may have to sit quietly in the hallway in sight of the child & make sure the child stays in bed. The child then
establishes a sleep-onset routine of falling asleep alone & learns that getting out of bed is discouraged. The child also learns that the
parents are available but will not provide more stories or play. Eventually, the child settles down & goes to sleep. Providing the child
with an attachment object (like a teddy bear) often is helpful. A small night-light, white noise, or both also can be comforting.
If the child is accustomed to falling asleep while in physical contact with a parent, the first step in establishing a different bedtime
routine is to gradually lessen the contact from full body to a hand touching the child to a parent sitting next to the child's bed. Once
the child is regularly falling asleep with a parent next to the bed, the parent can leave the room for increasing durations.
Awakening during the night: Everyone awakens multiple times each night. Most people, however, usually fall back to sleep with no
intervention. kids often experience repeated night awakening after a move, an illness, or another stressful event. Sleeping problems
may be worsened when kids take long naps late in the afternoon or are overstimulated by playing before bedtime.
Allowing the child to sleep with the parents because of the night awakening reinforces the behavior. Also counterproductive are
playing with or feeding the child during the night, spanking, & scolding. Returning the child to bed with simple reassurance is usually
more effective. A bedtime routine that includes reading a brief story, offering a favorite doll or blanket, & using a small night-light
(for kids > 3) is often helpful. To prevent arousal, it is important that the conditions under which the child awakens during the night
are the same as those under which the child falls asleep. Parents & other caregivers should try to keep to a routine each night, so that
the child learns what is expected. If kids are physically healthy, allowing them to cry for a few minutes often allows them to settle
down by themselves, which diminishes the night awakening. Extended crying is counterproductive, however, because parents then
may feel the need to revert to a routine of close contact. Gentle reassurance while keeping the child in bed is usually effective.

TEMPER TANTRUMS
A temper tantrum is a violent emotional outburst, usually in response to frustration.
Temper tantrums usually appear toward the end of the first year, are MC at age 2 (terrible twos) to 4, & are infrequent after age 5. If
tantrums are frequent after age 5, they may persist throughout childhood.
Causes include frustration, tiredness, & hunger. kids also may have temper tantrums to seek attention, obtain something, or avoid
doing something. Parents often blame themselves (because of imagined poor parenting) when the actual cause is often a
combination of the child's personality, immediate circumstances, & developmentally normal behavior. An underlying mental,
physical, or social problem rarely may be the cause but is likely only if tantrums last > 15 min or occur multiple times each day.
May involve shouting, screaming, crying, thrashing, rolling on floor, stomping, throwing things.
The child may become red in the face & hit or kick. Some kids may voluntarily hold their breath for a few seconds & then resume
normal breathing (unlike breath-holding spells, which also can follow crying bouts caused by frustration).
Although providing a safe setting for kids to compose themselves is often effective, many kids have difficulty stopping tantrums on
their own. In most cases, addressing the source of the tantrum only prolongs it. It is therefore preferable to redirect the child by
providing an alternative activity on which to focus. The child may benefit from being removed physically from the situation.

BREATH HOLDING
A breath-holding spell is an episode in which the child stops breathing involuntarily & loses consciousness for a short period
immediately after a frightening or emotionally upsetting event or after a painful experience.
Breath-holding spells occur in 5% of otherwise healthy children. They usually begin in the first year of life & peak at age 2. They
disappear by age 4 in 50% of kids & by age 8 in ab 83% of children. The remainder may continue to have spells into adulthood.
Breath-holding spells do not appear to be risk factors for true epilepsy but may be associated w/ an increased risk of fainting spells
in adulthood. There are 2 forms of breath-holding spells:
Cyanotic form: MC form & often occurs as part of a temper tantrum or in response to a scolding or other upsetting event.
o During a cyanotic breath-holding spell, kids hold their breath (without necessarily being aware they are doing so) until
they lose consciousness. Typically, the child cries out, exhales, & stops breathing. Shortly afterward, the child begins to
turn blue & unconsciousness ensues. A brief seizure may occur. After a few seconds, breathing resumes & normal skin
color & consciousness return. It may be possible to interrupt a spell by placing a cold rag on the child's face at onset.
Despite the spell's frightening nature, parents must try to avoid reinforcing the initiating behavior. As the child
recovers, parents should continue to enforce household rules. Distracting the child & avoiding situations that lead to
tantrums are good strategies. Cyanotic breath-holding has been found to respond to iron therapy, even in the absence
of anemia, & to treatment for obstructive sleep apnea (when present).
Pallid form: Typically follows a painful experience (falling & banging head) but can follow frightening or startling events.
o During a pallid breath-holding spell, vagal stimulation severely slows the heart rate. The child stops breathing, rapidly
loses consciousness, & becomes pale & limp. If the spell lasts more than a few seconds, muscle tone increases, & a
seizure & incontinence may occur. After the spell, the heart speeds up again, breathing restarts, & consciousness
returns without any treatment. Because this form is rare, further diagnostic evaluation & treatment may be needed if
the spells occur often. Simultaneous ECG & EEG can help to differentiate cardiac & neurologic
Both forms are involuntary & readily distinguished from uncommon brief periods of voluntary breath-holding by stubborn kid, who
invariably resume norm breathing after getting what they want or when they fail to get what they want.

DEVELOPMENTAL DELAY
FRAGILE X SYNDROME
Fragile X syndrome is a genetic abnormality in an X chromosome that leads to intellectual disability & behavioral disorders.
MC inherited cause of moderate ID, M>F.
The sxs are caused by an abnormality of FMR1 gene on X chromosome. The abnormality is an unstable triplet repeat expansion;
normally have < 60 CGG repeats & people w/ Fragile X syndrome have > 200. People w/ 60-200 CGG repeats are considered to have
a premutation bc increased # of repeats increases likelihood that further mutation will result in > 200 in a subsequent generation.
The premutation is MC. Fs are typically less impaired than Ms. Fragile X is inherited in an X-linked pattern & does not always cause
clinical sxs. Fragile X syndrome is now considered a single-gene disorder & not a chromosomal abnormality.
Presentation
Physical large, protuberant ears; a prominent chin & forehead; a high arched palate; and, in postpubertal Ms, macroorchidism. The
joints may be hyperextensible, & heart disease (mitral valve prolapse) may occur.
Cognitive abnormalities may include mild to moderate ID. Features of autism may develop, including perseverative speech &
behavior, poor eye contact, & social anxiety.
F w/ the premutation may have premature ovarian failure; sometimes menopause occurs in the mid-30s.
Diagnosis
DNA testing
Frequently not suspected until school age or adolescence, depending on the severity of the sxs. Boys w/ autism & ID should be tested
for Fragile X syndrome. Molecular DNA analysis is done to detect the increased # of CGG repeats.
Treatment
Supportive measures
Early intervention, including speech & language therapy & OT, can help kids maximize their abilities. Stimulants, antidepressants, &
antianxiety drugs may be beneficial for some children.

FETAL ALCOHOL SPECTRUM DISORDERS
Alcohol is MC teratogen to which the fetus will be exposed.
The amount of alcohol needed to get teratogenic effects is unknown.
Fetal alcohol syndrome associated with pre- & post-natal growth deficiency, mental retardation, average IQ of 63 particularly in full
syndrome, irritability, hyperactive as children, fine motor dysfunction.
Physical findings include microcephaly, short palpebral fissures, maxillary hypoplasia, short nose, smooth philtrum, thin upper lip,
micrognathia.
FAS associated with cardiac anomalies, usually septal defects. May have ptosis, cleft lip, tetrology of Fallot.
Appear as failure to thrive because they have thin adipose tissue.
FAS with 2 drinks/day results in a smaller birth size; 4-6 results in subtle physical findings; 8-10 results in severe FAS.
There is no treatment for FAS
Fetal alcohol syndrome: refers to the full syndrome associated with prenatal alcohol exposure. Dx requires the presence of a
characteristic pattern of facial abnormalities (short palpebral fissures, thin upper lip, and indistinct or smooth philtrum, for which
there are standard measurements), growth deficiency, and evidence of CNS damage and neurodevelopment abnormalities. The dx
can be made w/ or w/out confirmed maternal prenatal use of alcohol.
Partial fetal alcohol syndrome: presence of at least two of the facial anomalies as well as at least one of the following: growth
retardation, CNS neurodevelopmental abnormalities, or behavioral or cognitive abnormalities that are inconsistent with the childs
developmental level and cannot be explained by familial background or environment. Does not require the confirmation of prenatal
alcohol exposure.
Alcohol-related neurodevelopmental disorder: does not require the presence of dysmorphic facial feature, but does require the
presence of neurodevelopmental abnormalities or evidence of a pattern of behavioral or cognitive abnormalities. This diagnosis
requires confirmation of prenatal alcohol exposure.
Alcohol-related birth defects: requires a history of prenatal alcohol exposure, at least two characteristic facial features, and the
presence of one or > congenital anomalies, including malformations and dysplasias in cardiac, skeletal, renal, ocular or auditor areas.
The physician should always ask about alcohol and other drug intake during pregnancy.
The exact amount of alcohol consumption that leads to teratogenesis remains unclear.

ADOLESCENT GROWTH & DEVELOPMENT CHP 4 (PG 113-124)
PUBERTY
Result of activation of the hypothalamic-pituitary-gonadal axis in late childhood. Before puberty, pituitary & gonadal hormone levels
are low. At onset of puberty, the inhibition of gonadotropin-releasing hormone in the hypothalamus is removed, allowing pulsatile
production & release of the gonadotropins, LH & FSH. In early to middle adolescence, pulse frequency & amplitude of LH & FSH
increase, stimulating the gonads to produce estrogen or testosterone. In F, FSH stimulates ovarian maturation, granulosa cell fxn &
estradiol secretion. LH is important in ovulation & also is involved in corpus luteum formation & progesterone secretion. Initially,
estradiol inhibits the release of LH & FSH. Eventually, estradiol becomes stimulatory & the secretion of LH & FSH cyclic. Estradiol
levels progressively increase, resulting in maturation of the F genital tract & breast development.
In M, LH stimulates interstitial cells of testes to produce testosterone. FSH stimulates production of spermatocytes in presence of
testosterone. Testes also produce inhibin, a Sertoli cell protein that inhibits secretion of FSH. During puberty, circulating
testosterone levels increase >20-fold. Levels of the testosterone correlate w/ physical stages of puberty & degree of skeletal
maturity.

PHYSICAL GROWTH/ SEXUAL MATURATION
FEMALE TANNER STAGES
I. Stage: Tanner 1 (Prepubertal)
Height increases at basal rate: 5-6 cm/year
Breast Papilla elevation only
Pubic Hair Villus hair only; No coarse, pigmented hair

II. Stage: Tanner 2
Height increases at accelerated rate: 7-8 cm/year
Breast Breast buds palpable and areolae enlarge
Age 10.9 years (8.9-12.9 years)
Pubic Hair Minimal coarse, pigmented hair mainly on labia
Age 11.2 years (9.0-13.4 years)
Modifications based on increasingly earlier
Puberty
White: Stage 2 changes may appear 1 year earlier
Black: Stage 2 changes may appear 2 years earlier

III. Stage: Tanner 3
Height increases at peak rate: 8 cm/year (age 12.5)
Breast Elevation of Breast contour; areolae enlarge
Age 11.9 years (9.9-13.9 years)
Pubic Hair Dark, coarse, curly hair spreads over mons pubis
Age 11.9 years (9.6-14.1 years)
Other changes Axillary hair develops (13.1 years); Acne
Vulgaris develops (13.2 years)

IV. Stage: Tanner 4
Height increases at 7 cm/year
Breast Areolae forms secondary mound on the Breast
Age: 12.9 years (10.5-15.3 years)
Pubic Hair Hair of adult quality

V. Stage: Tanner 5
No further height increases after age 16 years
Breast Adult Breast contour; Areola recesses to general
contour of Breast
Pubic hair Adult distribution of hair; Pubic hair spreads to
medial thigh; Pubic hair does not extend up linea alba


MALES
I. Stage: Tanner 1 (Prepubertal)
Height increases at basal rate: 5-6 cm/year
Testes Smaller than 4 ml or long axis <2.5 cm
Pubic Hair No coarse, pigmented hair
Penis Stage No growth

II. Stage: Tanner 2
Height increases at basal rate: 5-6 cm/year
Testes Size 4 ml or long axis 2.5 to 3.2 cm; Age 11.5 years
(age 9.5 to 13.5 years)
Pubic Hair Minimal coarse, pigmented hair at base of penis
Age 12.0 years (age 9.9 to 14.0 years)
Penis Stage Earliest increased length & width. Age 11.5 years
(age 10.5-14.5 years)
III. Stage: Tanner 3
Height increases at accelerated rate: 7-8 cm/year
Testes Size 12 ml or long axis 3.6 cm; Age 14.0 years (11.5-
16.5 years)
Pubic Hair Coarse, dark curly hair spread over the pubis
Age 13.1 years (11.2-15.0 years)
Penis Stage Increased length and width
Age 12.4 years (10.1-14.6 years)
Other Changes Gynecomastia may occur (age 13.2 years);
Voice breaks (age 13.5 years); Muscle mass increases

IV. Stage: Tanner 4
Height increases at peak rate: 10 cm/year (age 13.8)
Pubic Hair Hair of adult quality. Not spread to junction of
medial thigh with perineum. Age 13.9 years (12.0-15.8 years)
Penis Continued growth in length and width
Age 13.2 years (11.2-15.3 years)
Testes Length 4.1 to 4.5 cm
Other Changes Axillary hair (age 14.0 years); Voice changes
(age 14.1 years); Acne Vulgaris (age 14.3 years)

V. Stage: Tanner 5
No further height increases after age 17 years
Pubic Hair Adult pubic hair distribution (15.3 years); Pubic
hair spreads to medial thigh; No hair spread to linea alba
Penis Mature genital size by 16.5 years
Testes Length >4.5 cm
Secondary sexual characteristics
Facial hair present on sides
Mature male physique
Gynecomastia disappears


PSYCHOSOCIAL DEVELOPMENT

IMMUNIZATION SCHEDULE- CHP 10

INFECTIOUS DISEASE- CHP 40 & 42
PERTUSIS
Etiology: Bordetella pertussis gram-negative bacteria
Epidemiology: MC in adolescents and adults; Most severe in infants
RFs: < 18 mos old; Exposure including intrauterine >34 wks, teacher, health care worker; No immunization elective or age related
Prevention: Dtap vaccine series for kids & Tdap vaccine for adults to protect kids
Presentation
Initial/Catarrhal: cold-like; rhinorrhea, lacrimation, dry w/ episodes of severe cough, LG fever; post-tussive emesis; apnea
Paroxysmal stage: coughing becomes more severe & may persist up to 10 wks at this stage; paroxysmal whooping may be heard
Convalescent stage: coughing diminishes as pt recovers & disappears over 2-3 wks but may recur with subsequent URIs
Diagnosis
Inspiratory whooping noise
Bordetella culture or PCR from nasopharyngeal swab & CBC: increased WBC
Treatment
Macrolides are DOC -Septra is an alternative; Azithromycin. MUST REPORT TO CDC.
Prognosis May be infectious for several weeks if untreated. Can be fetal: PNA, seizures, rib fractures, apneic episodes

MEASLES RUBEOLA or 1
st
DZ
Etiology: Genus: Morbillivirus Family: Paramyxoviridae. Spread Droplets epithelial cells nose and conjunctivae
Epidemiology: Ages 5-9. Not endemic in US (except imports, unvaccinated) . Leading cause of vaccine-preventable deaths in kids <5
Presentation
Day 7-11 after infection Prodrome- Cough; Coryza; Conjunctivitis; Kopliks spots; fever
Day 14 Maculopapular rash starting at hairline & spreading down to confluence
Diagnosis
Measles IgM antibody- 3-14 days after onset of rash
Treatment
Self-resolution in 7-10 days
Supportive care- antipyretics, rest, avoid respiratory illness. Developing countries Vit A. Antivirals in immunosuppressed pts.
Complication: subacute sclerosing panencephalitis, a rare fatal infection years after initial infection; OM; encephalitis; PNA

GROUP B STREP- NEWBORN
Etiology: MC cause of early severe infection in newborns. Streptococcus agalactiae
Epidemiology
Spread vertically from mother to child Higher rates of transmission in black infant
50% of infants with mothers with GBS become colonized 1-2% develop invasive disease
Diagnosis
Early onset 0-6 days after delivery; usu w/in 12 hours Maternal transmission: meconium aspiration, L&D
Late onset 7-89 days after deliver; usu w/in 4 weeks Usually unrelated to delivery nosocomial
Maternal Symptoms Fever, bacteriuria, PROM, pre-term delivery
Physical
o Early Onset grunting, pallor, hypotonia, temp instability
Meningitis bulging fontanels, seizures, stiff neck, Kernig/Brudzinski signs (often absent, do LP)
Pneumonia resp distress, cyanosis, nasal flaring, accessory muscles, crackles, pleural rub, decreased BS
UTI suprapubic or CVA tenderness
Sepsis tachycardic, tachypneic, hypotension, poor cap refill
o Late Onset Meningitis MC
Labs
o CBC, BUN, Lytes, Glucose, Coag profile, LFTs, CRP
o Definitive is isolating GBS from sterile fluid CSF, blood, urine, sputum
o If + sepsis, MUST do LP
Treatment
Same medicine no matter where the source
o Pen G AND Gentamicin Penicillin G 250-450K units/kg/d IM/IV div q8h; Gent dose dependent on gest age and days old
Length of treatment variable Meningitis 14-21 days & All other 10 days
Follow-up and Complications
Shock, seizures, empyema, endocarditis, osteomyelitis, necrotizing fasciitis. Prevention via screening pregnant women

ROSEOLA (6
th
DZ)
Etiology: Agent is HHV-6 or HHV-7
Epidemiology: Affects young children, 6 mo to 3 years rarely <3 months or >4 years
Presentation
High fevers to 104 for 3-7 days with no rash (15% febrile seizures)
Rash after fever goes away (defervescence) usually day 3-5 rash starts. Fades in hours-days
o Discrete macules & papules; trunk & upper extremities; Occ. Diarrhea, URI ssxs. Nagayama spots (red papules on soft
palate & uvula)
Treatment
Antipyretics & hydration . Antivirals- for immunocompromised Comps- immune compromised (reactivation of virus, worsening of
HIV)

ERYTHEMA INFECTIOSUM (5
th
DZ)
Etiology: Agent is human parvovirus B19
Epidemiology: school-aged kids. >50% of adolescents have antibodies
Presentation
Mild flulike illness. Possible prodrome (fever, flu or URI ssx)
Rash at days 10-17: initially appears as flushed (slapped) cheeks, then encompasses whole body as a maculopapular rash, becoming
lacy in the arms & legs- easiest to see on forearms
Migratory arthritis in older patients that can last 6-8 weeks
Papular purpuric glove & sock syndrome in older adolescents, lasts 1-2 weeks
Diagnosis
clinical unless immunocompromised or hx of RBC deficiency- then do a CB C & Retic to screen for anemia if dec Hgb & absent retic;
refer to hematology for aplastic crisis
Treatment
Supportive with antipyretics & NSAIDs for arthralgias & fever.
F/U & Complications: can be spread from mom to fetus results in hdrops fetalis (fetal demise). Aplastic crisis

CROUP/ LARYNGOTRACHEOBRONCHITIS
Etiology
Usually parainfluenza virus; RSV; Human metapneumovirus; upper airway infection 2/2 edema & inflammation.
Presentation
Average child is 18 months of age (6 months -3 years). May have a hx of URI
Stridor (whistling noise) or chest wall moving, hoarseness, sudden onset of a barking seal cough, low-grade fever
Rales, rhonchi, wheezing, retractions, lethargy/agitation
Symptoms worse at night
Diagnosis
RSV, influenxa A/B cultures
CXR showing steeple sign narrowed trachea. DO NOT do if concern epiglottis
Treatment
Mild moderate croup::: Supportive; Inhaled corticosteroid Dexamethasone 0.15mg/kg orally or nebulized
Severe::: +/- parenteral corticosteroids Dexamethasone 0.6 mg/kg IM one time dose; Oxygen; Nebulized epinephrine

ACUTE BRONCHIOLITIS
Research definition = first episode of wheezing in a child younger than 12 to 24 months who has physical findings of a viral
respiratory infection & has no other explanation for the wheezing, such as pneumonia or atopy
Broader definition = an illness in kids <2 years of age characterized by wheezing & airway obstruction due to primary infection or
reinfection with a viral or bacterial pathogen, resulting in inflammation of the small airways/bronchioles
Mostly in infants < 2 months
Prophylaxis with Synagis given to high risk infants during first RSV season
Etiology: Usually RSV, rhinovirus, human metapneumovirus, influenza, parainfluenza, adenovirus
Epidemiology: worse in December-May (Jan/Feb is the peak). By 3 y/o most kids have been exposed.
Presentation:
Cough, rhinitis, fever < 104 (UPPER respiratory symptoms) Cough can sound wet or croupy
Then LOWER respiratory symptoms start Retractions, audible wheezing, labored breathing
conjunctivitis or OM, wheezing, tachypnea, retractions, crackles
Differential asthma, FB
Diagnosis
Diagnosis is usually clinical. CBC & CXR is suspicious of bacterial infection
CXR showing hyperinflation, interstitial pneumonitis, infiltrates
ELISA for RSV available
Treatment
No prior history of wheezing
o Albuterol 0.15 0.3 mg/kg nebulized q 4 hr
o Keep O2 > 92% - Supplemental O2 prn
Prior history of wheezing
o As above, plus oral steroid Prednisone 2 mg/kg/day div bid
Add antiviral if immunocompromised
F/U & Complications: recurrent wheezing ab 6 months s/p infection. Ped asthma

CHILD & ADOLESCENT PSYCHOLOGY CHP 3 P. 103 & CHP 7 P. 202
AUTISM SPECTRUM DISORDERS
Neurodevelopmental disorders characterized by qualitative abnormalities in social/emotional behavior/interactions &
communication as well as restricted, stereotyped & repetitive interests or activities
Autism has all 3
Asperger has impairment in social interaction and restricted interest/repetitive behavior
Prevelance 1%... 4x more likely in M
Causes Multifactorial. No known etiology in 80-90%
Genetic (primarily) (up to 90% have genetic component)
Fragile X Syndrome or Chromosome 15q duplication 10-20%
Environmental factors (lesser extent)
Parental age (Mothers 10y increase 38% increase & Fathers 10y increase 22% increase)
Low birth weight/gestational age
Intrapartum hypoxia
Maternal smoking
Toxins Mercury in vaccines (thimerosal)- no association
Diagnostic Criteria Must meet criteria 1, 2, & 3:
1) Clinically significant, persistent deficits in social communication & interactions, as manifest by at least 2 of the following:
Marked deficits in nonverbal (eye contact) & verbal communication used for social interaction:
Lack of social or emotional reciprocity;
Failure to develop & maintain peer relationships appropriate to developmental level
Lack of social or emotional reciprocity
2) Restricted, repetitive patterns of behavior, interests, & activities, as manifested by at least 1 of the following:
Stereotyped motor or verbal behaviors, or unusual sensory behaviors (hand flapping)
Preoccupation with restricted interest
Inflexible adherence to nonfunctional routines or rituals
Persistent preoccupation with parts of objects
3) Qualitative impairment in communication (at least one)
Delay in or lack of spoken language
If speech is present, lack of ability to initiate or sustain conversation
Stereotyped and repetitive/idiosyncratic language
Partied speech after 18 month. Able to answer factual ?s but struggle when needing to understand concepts.
Lack of pretend/social imitative play
Severity 3 levels
LEVEL 3
Social communication
Severe deficits in verbal & nonverbal social communication skills cause severe impairments in functioning, very limited
initiation of social interactions, & minimal response to social overtures from others.
For example, a person with few words of intelligible speech who rarely initiates interaction and, when he or she does,
makes unusual approaches to meet needs only & responds to only very direct social approaches
Restricted, repetitive behaviors
Inflexibility of behavior, extreme difficulty coping with change, or other restricted/repetitive behaviors markedly
interfere with functioning in all spheres. Great distress/difficulty changing focus or action.
LEVEL 2
Social communication
Marked deficits in verbal & nonverbal social communication skills; social impairments apparent even with supports in
place; limited initiation of social interactions; & reduced or abnormal responses to social overtures from others.
For example, a person who speaks simple sentences, whose interaction is limited to narrow special interests, & how has
markedly odd nonverbal communication.
Restricted, repetitive behaviors
Inflexibility of behavior, difficulty coping with change, or other restricted/repetitive behaviors appear frequently enough
to be obvious to the casual observer & interfere with functioning in a variety of contexts. Distress and/or difficulty
changing focus or action.
LEVEL 1
Social communication
Without supports in place, deficits in social communication cause noticeable impairments. Difficulty initiating
social interactions, & clear examples of atypical or unsuccessful response to social overtures of others. May appear to have
decreased interest in social interactions.
For example, a person who is able to speak in full sentences & engages in communication but whose to- and-fro
conversation with others fails, & whose attempts to make friends are odd & typically unsuccessful.
Restricted, repetitive behaviors
Inflexibility of behavior causes significant interference with functioning in one or more contexts. Difficulty switching
between activities. Problems of organization & planning hamper independence.
Screening MCHAT
Typically diagnosed at age 3-4 because disturbances in reciprocal social interaction and communication become more apparent.
Because early intervention is so important evidence that diagnosis can be made by age 2 y.o.
Screen at 18 months
Joint attention shared focus of two individuals on an object: shifting eye gaze, pointing, saying look. Point to get
needs met or show (Look at that)
Follow a point, imitate others and engage in functional play (using toys in the way they are intended)
Second Screening at 24-30 months
2-level Screening Approach:
If fail specific autism screening, referral for a formal evaluation by an experienced clinician (pediatric specialist) is
recommended: Autism Diagnostic Observation Schedule-Generic (ADOS) (Gold Standard)
Other Screening Points - Referral is recommended immediately if:
Child does not babble or point/use gestures by 12 months; Child does not use single words by 16 months; Child does not
use spontaneous 2-word phrases by 24 months; Child experiences any loss of language or social skills at any age
Possible Lab Tests
High-resolution chromosome analysis and fluorescence in situ hybridization for 15q duplication; Array Comparative Genomic
Hybridization; DNA for Fragile X; Lead level; Thyroid studies (TSH); Wood lamp test for tuberous sclerosis; Neuroimaging ONLY
if microcephaly or focal neuro deficits
Treatment 2 prong approach
Educational interventions - fostering acquisition of skills & knowledge for developing independence & personal responsibility
early intensive intervention may result in substantially better outcomes
Ex// Early Start Denver Model -
Occupational Therapy - promote development of self-care skills teach them to fxn in their environment
Sensory Integration Therapy - remediate deficits in neurologic processing & sensory info integration to allow the child to
interact w/ environment in a more adaptive fashion
Medical management to address medical problems associated with ASD
Seizures ~30% patients with ASD
GI problems upwards of 70% of patients
Sleep problems 44-83% of patients
Maladaptive behaviors 45% of children/adolescents & 75% adults are treated w/ psychotropic medication
Risperidone is the 1st (and only) FDA approved tx of irritability in children/adolescents with ASDs
Final notes
30% of children may plateau or lose skills (usually language and social skills only) between 12 an 24 months of age.
Usually occurs before child develops a vocabulary of 10 words.
If regression is seen refer to neurology
Will need overnight EEG to rule out epileptiform discharges during sleep. Will also need MRI to rule out other pathology
Early, intensive behavioral intervention is essential (25 hours per week)
Role of PCP Manage medical concerns: Sleep disorders, seizures and GI symptoms. Worsening behavior may be secondary to
medical DX. Help coordinate care

ANXIETY-BASED SCHOOL REFUSAL
A persistent pattern of school avoidance related to symptoms of anxiety
Somatic symptoms on school mornings, with symptoms resolving if the child is allowed to remain at home
No organic medical disorder that accounts for the symptoms
High levels of parental anxiety are commonly observed.
Consider when Absence for more than 2 weeks that is medically unexplained
Contributing factors Dread of leaving home (separation anxiety); Fear of some aspect of school; Fear of feeling exposed or
embarrassed (Social Phobia)
A realistic cause of the fear needs to be ruled out Bully; Intimidating teacher
3 peaks of incidence 6-7 y/o; 10-11 y/o; early adolescence
Presentation
Usually occurs after a precipitating stress in the family
Somatic sxs or anxiety is displaced onto some aspect of school
Somatic Manifestations Dizziness; Nausea; Stomach upset/distress
Complaints increase as school approaches and decrease when allowed to stay home.
Look for social withdrawal and depression
Treatment
Identify issue is this psychological or medical
Help facilitate returning to school
Help parents understand there is nothing medically wrong with child and help them teach child how to face anxiety and cope.
Involvement with therapist if needed
Treatment with SSRIs with persistent symptoms that do not improve with behavioral interventions.
Prognosis worsens the longer the child is out of school

EMERGENCIES & INJURIES CHP 12
ASSESSMENT & MANAGEMENT OF ACUTELY ILL INFANT/ CHILD
2 levels: Rapid cardiopulmonary assessment, w/ indicated stabilizing measures, venous access is gained & cardiopulmonary
monitoring initiated
Gather the team & Assign team responsibilities
Gather age-appropriate equipment Laryngoscope blade, ET tubes, NG or OG tubes, IV lines, urinary catheters, Cardiorespiratory
monitor, pulse oximeter, blood pressure cuff
STEPS
ABCs 100% O2 Cardiorespiratory monitoring, pulse ox and end tidal CO2 (if intubated) Vascular access 2 lines preferred
Blood draw and sent. Bedside blood glucose? Full vital signs Clothes removed Foley catheter and NG/OG tube inserted
Complete hx Notification of needed consultants Family support Law enforcement or security activation if needed ?Immobilize
Neck ?Obtain CXR Insert Central Venous Pressure and Arterial Line
FEVER
Many ED/Urgent Care visits (?20%)
Definition Rectal temperature 38C or 100.4F
Concern in fever without source Occult bacteremia
Most fevers will be viral in origin
Inflammatory disease Appendicitis; Kawasakis disease; Rheumatologic disease
Non-serious bacterial infection Otitis media; Streptococcal pharyngitis
Neonatal Principles
Serious bacterial infection
Susceptible to generally harmless organisms (GBS, Listeria)
Tend to disseminate infection
Do not reliably show localizing signs
Meningismus (HA, stiff neck, etc) not reliable until 12 months of age
As many as 15% of kids < 2 months of age may have a serious bacterial infection
0-30 days old
Full workup for all CBC/diff & blood culture; UA & urine culture; LP & CSF culture
Admit all
Treat all Ampicillin for all; Gentamicin (no evidence of meningitis); Cefotaxime (evidence of meningitis/traumatic tap)
30-60 days old
Philadelphia Protocol (modified)
o WBC > 5000 & < 15,000
o Band:Neutrophil ratio < 1:4
o Spun UA < 10 WBC/hpf, no bacteria
o CSF < 8 WBC/mm3
o Negative CXR
Follow cultures
No antibiotics
Reassessment in 24 hours
Negative predictive value = 100%
60-90 days old
No consensus on workup or management
Late onset Group B Strep still possible
3-36 months
General approach for healthy kids
o Bacterial infections identified by exam Otitis media; Cellulitis/Abscess/Lymphangitis; Lymphadenitis; Septic arthritis;
Some cases of meningitis
o Bacterial infections identified by history Acute sinusitis
Other bacterial infections endocarditis, pyomyositis; brain abscess; osteomyelitis; deep tissue abscess
Special cases immunodeficiencies; receiving chemotherapy; Neurologically impaired; sickle-cell disease; w/ central-lines
Inflammatory conditions to worry ab Appendicitis; Kawasaki Disease; Rheumatic fever; Juvenile idiopathic arthritis
Viral infections Make up the majority of causes of fever
Occult Bacteremia
o Historically (H.Flu B)
o Post-immunization era (Strep Pneumoniae)
Occult UTI
o Most common serious bacterial infection in young children Risk for renal scarring
o Strongly consider UTI in kids with fever without source > 39C (102.2F)
All girls less than 2 years
Uncircumcised boys less than 1 year
Circumcised boys less than 6 months
Lower threshold for prolonged fever or if accompanied by vomiting
o TX: 1st line agent PO cephalexin
Occult Pneumonia
o Physical Exam is not reliable for diagnosing pneumonia in young kids
Thin chest walls
Acute reactive airway disease (RAD)/bronchiolitis can sound like pneumonia
o When to get a CXR Fever AND Tachypnea; Hypoxemia; No clinical bronchiolitis or RAD; Prolonged sxs; Fever > 38C;
Tachypnea (0-6 months RR 59 ; 6-12 months RR 52 ; 12-24 months RR 42)
Dont forget Flu
o Clinical diagnosis is challenging in this age range
o White count typically normal to low
o Specific lab test recommended Direct fluorescent antibody staining of nasopharyngeal epithelial cells show influenza
virus; Optic immunoassay; ELISA; PCR

RECOGNITION OF ABUSE
Potential Child Abuse Medical Emergencies
Any infant w/ bruises (esp. head, facial or abdominal), burns, or fractures
Any infant or kid <2 y/o w/ a hx of suspected shaken baby head trauma or inflicted head injury
Any kid who has sustained suspicious or known inflicted abdominal trauma
Any kid w/ burns in a stocking or glove distribution or in other unusual pattern, burns to genitalia & any unexplained burn injury
Any kid w/ disclosure or sign of sexual assault w/n 48-72 hrs after the alleged even if the possibility of acute injury is present or if
forensic evidence exists
Presentations of sexual abuse
General or direct statements ab sexual abuse
Sexualized knowledge, play or behavior in developmentally immature kids
Sexual abuse of other kids by the victim
Behavorial changes Sleep disturbances (nightmares/terrors); appetite disturbances (anorexia/bulimia); depression, social
withdrawal, anxiety, aggression, temper tantrums, impulsiveness, neurotic or conduct disorders, phobias, or avoidant behaviors,
guilt, low self-esteem, mistrust, feelings of helplessness, hysterical or conversion reactions, suicidal, runaway threats or behavior,
excessive masturbation
Medical conditions Recurrent abdominal pain or frequent somatic complaints; genital, anal or urethral trauma; recurrent
complaints of genital or anal pain, discharge, bleeding; enuresis or encopresis; STIs; pregnancy
Promiscuity or prostitution, sexual dysfunction, fear of intimacy
School problems or truancy
Substance abuse
Presentation
Bruising in neonate or young infant or extensive bruising at any age
Railroad track signs from switching
Fractures
Sexual abuse: sexual acting out, excessive masturbation, self-injurious behavior, eating or sleeping changes, promiscuity, substance
abuse, fears, depression, aggression, anxiety, school issues, suicide attempt, chronic medical complaints, stomachaches, anal pain,
constipation, encopresis, bleeding, anal discharge, dysuria, hematuria, frequency, enuresis

HEAD INURY
Traumatic brain injury is the most common injury in children
Can result from direct trauma and rapid acceleration-deceleration forces (shaken baby)
History Distance of fall; What did they land on? Level of consciousness at event did they cry instantly? Subsequent mental status
and activity; Amnesia; Vomiting
Physical Exam Detailed neuro exam; Look at area of injury; Keep cervical spine injury in your mind; CNS fluid from ears or nose;
Raccoon eyes or Battle Sign; CT before LP risk of herniation
Always correlate history with physical think child abuse
Complications Infection
o Open head injuries fractures with overlying lacerations
o Basal skull fractures that involve cribriform plate or middle ear cavity Strep Pneumoiae
o Major complications come from intracranial injury not fracture
o Acute Intracranial hypertension Headache; Vision changes; Vomiting; Gait difficulties; Progressively decreasing level of
consciousness; Papilledema**; Stiff neck; Cranial nerve palsies; Progressive hemiparesis; Cushings Triad is a late and
ominous finding (Bradycardia, hypertension and irregular respirations)
Treatment
Mannitol
Hypertonic saline
Elevate head of bed to 30 degrees
Surgical intervention Evacuation of hematoma; Decompressive craniectomy; CSF drainage by placing external ventricular drain in
lateral ventricles

THERMAL BURNS
Major cause of accidental death and disfigurement in children
Causes Hot water or food; Appliances; Flames; Grills; Vehicle-related burns Curling irons
Occur commonly in toddles Male>Female
Prevention: Place hot containers away from counter edge; Hot H20 heaters set <120 degrees; Cords kept out of reach; Sunscreen SPF
30+; Minimize sun exposure
Presentation
Classified according to nature, extent and thickness. Electrical burns can be deceptive in their destruction.
Superficial Painful, dry, red and hypersensitive (Sunburn)
Partial Thickness
o Superficial partial-thickness Red, blister
o Deep partial-thickness white, dry, blanch with pressure, decreased pain
Full Thickness Affect all epidermal & dermal elements, leaving devascularized skin. Wound is white or black, dry, depressed,
leathery & not painful.
Deep full-thickness go all the way into underlying facia, muscle and even bone.


Complications
Superficial and superficial partial-thickness heal well
Deep partial-thickness and full thickness Scar; Infection; Loss of function; Contractures; Compartment syndrome; Renal failure
myoglobinuria or microangiopathic hemolysis; Hyperkalemia from rhabdomyolysis
Scald burns are 85% seen in kids < 4yo, typically story is child pulling something off the table or stove. Alsocan be seen in abuse,
when child is dipped into very hot bath water.
Rule of 9s is diff in kids, more surface on head in infant. Rule of palm used for <10% where kids palm is ab 1% of burn surface area.
Treatment
Superficial and partial-thickness
o Outpatient; Analgesia; Cool compresses
o Antiseptic cleansing, topical antimicrobial coverage and observation for infection if partial-thickness with blisters
o If debrided cleanse with dilute povidine-iodine solution, normal saline and covered with topical antibiotic
o Cover with bulky dressing and examine every 24 hours
o Refer: potential for disfigurement or functional impairment face, hands, digits or perineum.
Full-Thickness, deep or extensive partial-thickness and subdermal burns
o ABCs and Trauma management
o Establish airway ASAP for oral or nasal burns
o Fluid resuscitation 4 mL/kg/%body surface area burned for first 24 hrs w/ administered in the first 8 hrs
o Debridement of the wound
o Placement of temporary wound coverage
o Skin graft

SUBMERSION INJURIES
Drowning is a submersion that results in asphyxia & death while submerged or within one day of the episode.
Survival after 24h of submersion is near-drowning, whether patient dies or not. Child may appear well at presentation, but late CNS
and pulmonary changes can occur hours later
Near drowning is 2
nd
MC cause of accidental death in children. About 40% of victims are under the age of 4yo.
At risk population are Ms/adolescents, unsupervised toddlers, kids w/ seizure d/o, & concomitant use of drugs & alcohol Home is
MC site of drowning in freshwater
Wet drowning is w/ aspiration of fluid. Most drowning start at dry drowning due to laryngospasm to prevent aspiration, eventually
you gasp for air & aspirate.
Freshwater drowning may cause more lung damage secondary to hypotonic fluid that flushes out the surfactant. Salt water
drowning tend to have more pulmonary edema. Treat hypothermia.
Obtain CXR, blood gases, consider cervical injuries (e.g. diving).
Treatment is supportive, prevention is key. Minimum observation period is 8-12 hrs.
Lungs can be eventually fixed, main problem that cannot be fixed is hypoxia & ischemia to the brain.
CNS and pulmonary injuries account for major morbidity
Water has to be very cold to get neuro-protective effect. WARM before pronouncing dead.

ANIMAL & HUMAN BITES
DOG:
MC bite, least likely to get infected. M >F. dog is usually known by victim. Younger kids have a higher incidence of head & neck
wounds, whereas school-age kids are bitten most often on the upper extremities. Kids should be taught not to taunt dogs or
approach them when they are eating, sleeping or are unknown to them.
Presentation:
Abrasions, lacerations & puncture wounds. Larger dogs may tear skin, subcutaneous tissue & muscle or even cause fractures.
Diagnosis
Bites caused by large dogs associated w/ significant crush injury may be associated w/ fractures. Dislodged teeth may also be
present in the wound.
Treatment
Provide appropriate analgesia or anesthesia before starting wound care. Debride any devitalized tissue & remove any foreign
matter. Irrigate using normal saline w/ high pressure & volume. Consider tetanus ppx depending on immunication status. Rabies
risk is low in developed countries, ppx rarely indicated.
Suture wounds only necessary for cosmesis as closure increases the risk of infxn. DO NOT USE TISSUE ADHESIVES. Ppx abx do not
decrease infection rates in low-risk dog bites, except those involving the hands & feet.
Bites involving a joint, periosteum, or associated w/ fracture require prompt ortho surgery consult.
Pasteurella canis & Pasteurella multocida, streptococci, staphylococci & anaerobes may infect dog bites. BS coverage w/
amoxicillin & clavulanic acid is 1
st
line tx.
Complications scarring, CNS infections, septic arthritis, osteomyelitis, endocarditis, sepsis & PTS.
CAT:
F>M. Principal complication is infection & the risk is > than w/ dog bites bc cats produce a puncture wound.
Presentation
Typically result in abrasion & puncture wounds. w/n 12 hrs, untxed bites may result in cellulitis or when involving the hand,
tenosynovitis & septic arthritis.
Cat Scratch Dz (CSD) can occur after bites or scratches esp from kittens. Local findings include a papule, vesicle, or pustule at the site
of inoculation. HALLMARK: regional lymphadenitis
Diagnosis
Serologic tests for Bartonella henselae are available when CSD is suspected.
C-reactive protein & sedimentation rate may be helpful to monitor tx response in infected bites.
Complications cellulitis, tenosynovitis, & septic arthritis are important potential complications of cat bites. Systemic illness is rare.
Treatment:
Provide appropriate analgesia or anesthesia before starting wound care. Debride any devitalized tissue & remove any foreign
matter. With isolated puncture wounds, high-pressure irrigation is CI- as it may force bacteria deeper into tissue. Alternatively, the
wound may be soaked in dilute povidone-iodine solution for 15 minutes. Consider tetanus ppx in the under or unimmunized. Rabies
risk is low in developed countries & ppx is rarely indicated.
Cat bites should NOT be closed except when absolutely necessary for cosmesis.
P multocida is MC pathogen. Ppx abx are recommended. 1
st
line tx is amoxicillin & clavulanic acid. The dosage of the amoxicillin
component should be 80mg/kg/24 hrs in 3 divided doses. The max dosage is 2g/24hrs.
Strongly consider admission & parenteral abx for infected wounds on the hands & feet.
HUMAN
Most infected human bites occur during fights when a clenched fist strikes bared teeth. Pathogens MC include streptococci,
staphylococci, anaerobes, & Eikenella corrodens.
Hand wounds & deep wounds should be tx w/ ppx abx against e. corrodens & gram + pathogens w/ a PCN-resistant abx (amoxicillin
w/ clavulanic acid).
Only severe lacerations involving face should be sutured. Other wounds can be managed by delayed primary closure or healing by
secondary intention.
A major complication of human bites is infection of the metacarpophalengeal joints. A hand surgeon should evaluate clenched-fist
injuries from human bites if extensor tendon injury is identified or joint involvement is suspected.

FOREIGN BODY ASPIRATIONS- P. 518
Most common site is the right lung, followed by left lung, trachea/carina, & larynx
MC objects peanuts, popcorn, small coins, hard candy, hot dogs & small toys
Highest risk 6 mths to 4 years
Presentation
Sudden onset of coughing, choking, wheezing or respiratory distress
Difficulty vocalizing or cough & cyanosis (complete obstruction)
Often sudden onset child running with food in mouth or playing with seeds, small coins or toys.
Drooling, stridor, able to vocalize (partial obstruction)
Foreign body can lodge anywhere but often is trapped in the supraglottic airway resulting in laryngospasm.
o Sometimes foreign bodies can lodge in the esophagus and compress the airway
Diagnosis
CXR is problematic because most swallowed objects are radiolucent
Rigid bronchoscopy is the GS for dx
Treatment
<1 y/o place infant face down over arm w/ head lower than trunk 5 back blows followed by 5 chest compressions until
obstruction relieved.
>1 y/o Abdominal Thrusts using care not to damage abdominal organs
NO blind finger sweep can push object farther down


PEDIATRIC ORTHOPEDICS- CHP 26
ANKLE SPRAINS
Hx indicates either forceful inversion or eversion. Reinjury is common.
Inversion injury (MC) results in tearing or injury to the lateral ligaments & Eversion injury- medial ligaments injured of the ankle
Diagnosis
Palpate for point tenderness around ankle.
Treatment
Airsplint produces joint rest & protect the extremity by using crutches. The joint should be supported/immobilized in the functional
position (right angle).
Functional rehab to include edema control, ROM, strengthening, & restoration of proprioceptive sensation can prevent LT disability.

KNEE SPRAINS
Sprains of the collateral & cruciate ligaments are uncommon b/c they are so strong. MC to injure the growth plates, which are the
weakest structures in knees of kids.
In adolescence, as physes start to close, rupture of the ACL can result from a rotational injury.
If the injury produces avulsion of the tibial spine, anatomic reduction & fixation are often required. Effusion of the knee after trauma
deserves referral to an ortho specialist.
Nontraumatic effusion should be evaluated for inflamm conditions (JRA) or patellar malalignment
Treatment: RICE

NURSEMAIDS ELBOW (SUBLUXATION OF THE RADIAL HEAD)
MOI: being pulled up too hard by hand or wrist radial head slipping out of annular ligament
Presentation:
Crying, screaming, holding arm flexed against belly (fully protonated), refusal to use arm
Diagnosis:
Point tenderness over the radial head; no swelling or deformity; X-ray (normal); Assess neurovascular involvement
Treatment
Reduce with flexion & supination of the arm (usually occurs during x-ray positioning) may feel a click at the level of the radial head

GREENSTICK FRACTURE
Frank disruption of the cortex on 1 side of the bone but no discernable cleavage plane (disruption) on the opposite side. Bone ends
are not separated, making these fractures angulated but not displaced.
Treatment
Reduction is achieved by straightening the arm into normal alignment & maintaining alignment w/ a snugly fitting cast
Obtain Xrays again in 7-10 days to make sure that the reduction has been maintained in the cast.
A slight angular deformity can be corrected by remodeling of the bone. The farther the fracture is from the growing end of the bone,
the longer the time required for remodeling.
Fracture is healed when no tenderness is present & a bony callus is seen on Xray kids heal 2x as fast as adults.

TORUS FRACTURE
Etiology: buckling of the cortex due to compression of the bone.
Presentation: MC in the distal radius or ulna
Diagnosis:
IMPT:: do NOT misdx as green stick fracture at initial presentation. Kids w/ torus who are misdx w/ greenstick report having MORE
pain after application of a soft bandage or cast.
Treatment
Alignment is usually satisfactory & simply immobilization for 3 wks
Soft bandage therapy & cast therapy are effective in preventing further angulation

CONGENITAL DYSPLASIA OF THE HIP
A spectrum of developmental hip abnormalities (present at birth) ranging from joint laxity to dislocating hips. The diagnosis is
related to development and is present from birth. You dont want to miss this!
Risk factors: First born; F; Frank Breech; Fam hx
Presentation: Laxity is common in the perinatal period, shallow acetabulum, subluxatable hips, dislocatable hips, or fixed
dislocatable hips (most severe)
Diagnosis: Observe gait, spine (dimpes or hairy patches), and skin (skin folds should be symmetric, cutaneous markings,
birthmarks). Examine only a relaxed baby. Galeazzi sign (right), Barlow (dislocates), Ortolani (reduces)
o Barlow- hips flexed, thigh adducted while pushing posteriorly, dislocates hip, clunk
o Ortolani-Hips flexed, aduct one at a time; reduces dislocation; clunk
o Imaging: If there is concern get US of infants hips btwn 4-6 wks of age. Once bony development begins, Xray becomes
more accurate at 5-7 mths.
Treatment: Refer. Pavlik harness at 90-100 degrees of flexion. If no improvement with pavlik, then abduction orthosis (stiffer
brace) or open vs closed reduction + spica casting

OSGOOD-SCHLATTER
Micro-fracture at the insertion of the patellar tendon into the tibial tubercle. Most common adolescent male athletes
Sx: activity related pain that lasts 12-24 hours, swelling, tenderness and increased prominence of the tibia tubercle
Tx: rest/restriction of activities

OSTEOSARCOMA
60% of malignant bone tumors in childhood Mostly adolescents and young adults
Sx: bone or joint pain not responding to conservative therapy within a reasonable amount of time should be investigated thoroughly
Dx: X-ray: lytic lesions with sunburst pattern

Growth Plate Fractures-Salter Harris Classification
I- S Separation
II- A- Above
III- L Lower
IV- T Through
V- ER- Everything is ruined

POISIONING- CHP 13
PREVENTION
Include as part of the well-child starting at 6 months.
SAFETY TIPS: If you or your child comes in contact with poison, call the poison center (1800-222-1222). Nurses and pharmacists
(that are poison experts) will answer your call. In most cases, they can help you take care of the problem right at home. When you
need to get to the hospital, they will call ahead with detailed information to help doctors treat you or your child quickly & correctly.
How people get poisioned People can breathe poison, eat or drink it, or get it on the skin or in the eyes. You probably know that
antifreeze, bleach and bug spray are poisonous. But did you know that vitamins, perfume, and makeup can be dangerous? Eating
some plants can be toxic. Some spider bites can be dangerous. Taking medicine that is too old or not prescribed for you can make
you sick. Also, mixing different kinds of medicines can be dangerous.
GENERAL TREATMENT OF POISIONING
Call Poison Control 1800-222-1222
Proper telephone management can reduce morbidity and prevent unwarranted or excessive treatment.
Basic information is obtained patients name, age, weight, address and telephone number; the agent and amount of agent ingested;
the patients present condition; and the time elapsed since ingestion or other exposure.
High risk agents Caustic solutions, hydrogen fluoride, drugs of abuse, meds such as CCBs, opoids, hypoglycemic agents or
antidepressants
Self induced (Suicide?). Emergency situation
If the child requires transport to a health facility, instruct parent that everything in the vicinity of the child that may be a cause of
poisoning should be brought to the health care facility.
95% of cases of ingestion does not require trip to hospital. Follow up at 1 hour and 4 hours and assess any changes in symptoms.
An additional follow up call should be made at 24 hours
Prevention of absorption
Emesis and Levage rarely used in peds. Only used in potential lethal exposures w/ poor tx options, like large tricyclic
antidepressant overdose & only done in consult w/ the poison center.
Charcoal
1-2 g/kg (max 100g) per dose. Repeat Q2-6hrs until charcoal is passed thru rectum.
can be considered in pts who are awake, alert & able to drink it voluntarily. NEVER give to pts w/ altered sensorium who are
unable to protect their airway due to risk of aspiration. NOT useful in ingestions of heavy metals, & may be harmful in
hydrocarbons, caustics & solvent ingestions
Catharsis Despite their widespread use, they do not improve outcomes and should be avoided. Stimulate bowel movements
Castor Oil, Magnesium Sulfate, Milk of Magnesium, Lactulose, etc.)
Whole Gut Levage
Oral administration, nonabsorbable hypertonic solution such as GoLytely.
Use is controversial. Underlying bowel pathology & intestinal obstruction are relative CIs to its use. Consult w/ poison center
May be helpful with sustained-release meds, mechanical movement of items through bowels (ie cocaine packets, iron tablets)
and poisoning with substances that are poorly absorbed by charcoal (ie lithium, iron)
Enhancement of Excretion
Enhancement of certain substances can be hastened by urinary alkalinization or dialysis & is reserved for special cases. Make sure
the pt isnt volume depleted. Volume-depleted pts should receive a normal saline bolus of 10-20mL/kg, followed by sufficient IV fluid
administration to maintain urine output of 2-3mL/kg/h
Urinary Alkalinization
Alkaline Diuresis Reserved for substances with pKa (measures strength of acid in solution) < 7.5. Alkanlinization is achieved
with sodium bicarb. Observe for hypokalemia, caused by the shift of potassium intracellularly- watch the serum K+ & ECG for
those changes. MC used for tx of salicylate toxicity & to prevent methotrexate toxicity.
Hemodialysis typically not useful except in critically ill patients and as part of supportive care if patient meets the following
criteria
o Potentially life-threatening toxicity that is caused by a dialyzable drug and cannot be treated by conservative means
o Hypotension threatening renal or hepatic function that cannot be corrected by adjusting volume
o Marked hyperosmolality or severe acid-base or electrolyte disturbances not responding to therapy
o Marked hypothermia or hyperthermia not responding to therapy.
o Immediate dialysis should be considered in ethylene glycol and methanol poisoning only if acidosis is refractory, the
patient does not respond to fomepixole treatment, or blood levels of ethanol of 100mg/dL are consistently maintained.
Refractory salicylate intoxication may benefit from dialysis.