Pediatrics

Every age-specific diagnosis, milestone, vaccination, weight-based dosing, neonatal condition, and management strategy from birth through adolescence in one place.

01 Pediatric Anatomy & Physiology

Children are not small adults. Virtually every organ system differs from adult physiology in ways that have direct clinical consequences — from airway anatomy that predisposes to obstruction, to immature renal function that alters drug clearance, to a higher metabolic rate that demands proportionally greater caloric and fluid intake. Understanding these age-specific differences is the foundation of all pediatric care.

Airway & Respiratory Differences

The pediatric airway is narrower, more anterior, and more cephalad than the adult airway. The infant larynx sits at C3–C4 (versus C4–C5 in adults). The epiglottis is omega-shaped and floppy. The narrowest point is the cricoid ring (subglottic region) in children <8 years, unlike adults where the glottis is narrowest. Infants are obligate nasal breathers until approximately 4–6 months of age — nasal obstruction (e.g., choanal atresia, mucus from URI) can cause significant respiratory distress. The chest wall is highly compliant in neonates, leading to paradoxical breathing with subcostal and intercostal retractions as early signs of respiratory distress.

A 1 mm reduction in airway radius in an infant (4 mm trachea) reduces cross-sectional area by 44% and increases resistance 16-fold (Poiseuille's law). The same 1 mm edema in an adult (16 mm trachea) reduces area by only 12%. This is why croup and subglottic edema are disproportionately dangerous in young children.

Cardiovascular Differences

The neonatal myocardium has fewer contractile elements and is less compliant than the adult heart. Cardiac output in infants is heart-rate dependent because stroke volume is relatively fixed — bradycardia is poorly tolerated and is the most common preterminal rhythm in children (unlike adults, where VF/VT predominates). Normal heart rates are much higher in infants (120–160 bpm in neonates) and decrease with age. Blood pressure is lower in young children; hypotension is a late sign of shock in pediatrics because children compensate with tachycardia and increased SVR until they decompensate precipitously.

Fluid & Caloric Requirements

Children have a higher body surface area-to-mass ratio and higher metabolic rate per kilogram than adults. Maintenance fluid is calculated using the Holliday-Segar formula:

WeightFluid RateCaloric Need
First 10 kg100 mL/kg/day (4 mL/kg/hr)100 kcal/kg/day
Next 10 kg (11–20 kg)50 mL/kg/day (2 mL/kg/hr)50 kcal/kg/day
Each kg >20 kg20 mL/kg/day (1 mL/kg/hr)20 kcal/kg/day
Example: A 25 kg child needs (10×100) + (10×50) + (5×20) = 1,600 mL/day maintenance fluid, or ~67 mL/hr.

Thermoregulation

Neonates, especially preterm infants, are highly susceptible to hypothermia due to large surface area-to-volume ratio, thin subcutaneous fat, and inability to shiver (neonates generate heat via non-shivering thermogenesis using brown fat). Hypothermia increases oxygen consumption, causes metabolic acidosis, and worsens respiratory distress. Maintaining a neutral thermal environment (36.5–37.5°C axillary) is critical in neonatal care.

Renal & Hepatic Maturation

The GFR at birth is ~20 mL/min/1.73 m² in term neonates and even lower in preterm infants; it does not reach adult values (~120 mL/min/1.73 m²) until 1–2 years of age. This affects drug clearance for renally eliminated medications (aminoglycosides, vancomycin). Hepatic enzyme systems (particularly glucuronidation via UGT) are immature at birth — this explains physiologic jaundice and the risk of gray baby syndrome with chloramphenicol.

Comparison of infant and adult airway anatomy showing differences in epiglottis shape, laryngeal position, and subglottic narrowing
Figure 1 — Pediatric vs. Adult Airway. The infant airway is more anterior and cephalad, with an omega-shaped epiglottis and subglottic narrowing at the cricoid ring (the narrowest point in children <8 years). Source: Wikimedia Commons. Public domain.

Age-Specific Vital Signs

AgeHeart Rate (bpm)Respiratory RateSystolic BP (mmHg)
Newborn120–16030–6060–76
Infant (1–12 mo)100–15025–5072–104
Toddler (1–3 yr)90–14020–3086–106
Preschool (4–5 yr)80–12020–2589–112
School age (6–12 yr)70–11018–2297–120
Adolescent (13–18 yr)60–10012–20110–131
A quick estimate for minimum acceptable systolic BP in children ≥1 year: 70 + (2 × age in years). Below this threshold, the child is hypotensive and likely in decompensated shock.

02 The Pediatric Assessment

The pediatric assessment begins the moment you enter the room. The Pediatric Assessment Triangle (PAT) provides a rapid (<30 second) visual assessment of severity before any hands-on examination. It evaluates three components: Appearance (TICLS: Tone, Interactiveness, Consolability, Look/Gaze, Speech/Cry), Work of Breathing (retractions, nasal flaring, grunting, positioning), and Circulation to Skin (pallor, mottling, cyanosis).

ABCDE Approach

ComponentPediatric-Specific Considerations
A — AirwayHead in sniffing position (not hyperextended); large occiput in infants may require shoulder roll; suction secretions; consider jaw thrust in trauma
B — BreathingCount respiratory rate before disturbing child; look for retractions, nasal flaring, grunting, head bobbing; auscultate all fields
C — CirculationAssess cap refill (<2 sec normal), pulses (brachial in infants, radial/femoral in older children), skin temperature/mottling; HR is the primary compensatory mechanism
D — DisabilityAVPU scale (Alert, Voice, Pain, Unresponsive) or GCS; pupil reactivity; glucose check (neonates/infants prone to hypoglycemia)
E — ExposureFull undressing with temperature; look for rashes, bruising patterns (NAT); keep warm — rapid heat loss in small children

Growth Charts & Percentiles

Growth monitoring is the cornerstone of well-child care. The WHO growth standards are used for children 0–2 years (based on breastfed children), and CDC growth charts for children 2–20 years. Parameters tracked include weight-for-age, length/height-for-age, head circumference (until age 2–3), and BMI-for-age (starting at age 2). A child consistently tracking along a percentile is reassuring; crossing two or more major percentile lines (either up or down) warrants investigation.

Developmental Screening Tools

ToolAgesWhat It Screens
ASQ-3 (Ages & Stages Questionnaire)1–66 monthsCommunication, gross motor, fine motor, problem solving, personal-social
M-CHAT-R/F16–30 monthsAutism spectrum disorder
PEDS (Parents’ Evaluation of Developmental Status)0–8 yearsGeneral developmental concerns
Edinburgh Postnatal Depression ScalePostpartumMaternal depression (screened at well-child visits)
PHQ-A / PHQ-9 Modified for Adolescents≥12 yearsAdolescent depression
The AAP recommends standardized developmental screening at 9, 18, and 30 months, and autism-specific screening at 18 and 24 months. Surveillance (informal assessment) should occur at every well-child visit.

03 Key Terminology & Abbreviations

Pediatrics uses age-specific terminology and abbreviations that differ from adult medicine in important ways. Mastering this vocabulary is essential for interpreting growth data, immunization records, neonatal documentation, and pediatric emergency protocols.

AbbreviationMeaning
AGA / SGA / LGAAppropriate / Small / Large for gestational age
APGARAppearance, Pulse, Grimace, Activity, Respiration (newborn scoring)
NECNecrotizing enterocolitis
RDSRespiratory distress syndrome (surfactant deficiency)
TTNTransient tachypnea of the newborn
GBSGroup B Streptococcus
NICUNeonatal intensive care unit
VLBW / ELBWVery low birth weight (<1,500 g) / Extremely low (<1,000 g)
GAGestational age
PMAPostmenstrual age
BPDBronchopulmonary dysplasia
IVHIntraventricular hemorrhage
PDAPatent ductus arteriosus
VSD / ASDVentricular / Atrial septal defect
TOFTetralogy of Fallot
TGATransposition of the great arteries
RSVRespiratory syncytial virus
PALSPediatric Advanced Life Support
IOIntraosseous (vascular access)
FTTFailure to thrive
NATNon-accidental trauma
VCUGVoiding cystourethrogram
VURVesicoureteral reflux
DKADiabetic ketoacidosis
ADHDAttention-deficit/hyperactivity disorder
ASD (neuro)Autism spectrum disorder

04 Developmental Milestones

Developmental milestones represent the expected acquisition of skills across four domains: gross motor, fine motor, language, and social-emotional. While there is normal variation, consistent delay in reaching milestones may indicate developmental disability, neurologic disease, or environmental deprivation. The CDC/AAP updated milestone checklists in 2022 to reflect when most children (75th percentile) achieve a skill, rather than the 50th percentile used previously.

Milestones by Age

AgeGross MotorFine MotorLanguageSocial
2 monthsLifts head proneHands unfisted 50%Coos, vowel soundsSocial smile
4 monthsHolds head steady upright; pushes up on elbowsReaches for objectsLaughs, squealsSmiles spontaneously
6 monthsRolls both ways; sits with supportTransfers objects hand to hand; raking graspBabbles (consonant sounds)Stranger anxiety begins
9 monthsSits unsupported; pulls to standPincer grasp (immature)"Mama/dada" nonspecificObject permanence; separation anxiety
12 monthsWalks with one hand held; cruisesMature pincer grasp; releases objects1–3 words with meaningWaves bye-bye; plays pat-a-cake
15 monthsWalks independentlyStacks 2 blocks; scribbles4–6 wordsPoints to desires; imitates activities
18 monthsRuns; kicks ballStacks 3–4 blocks; feeds self with spoon10–25 words; points to body partsParallel play; temper tantrums
2 yearsWalks up/down stairs (2 feet per step); jumpsStacks 6 blocks; turns pages one at a time2-word phrases; 50+ words; 50% intelligibleParallel play; follows 2-step commands
3 yearsPedals tricycle; climbs stairs alternating feetCopies circle; uses scissors3-word sentences; 75% intelligible; knows name/age/sexGroup play; shares; knows gender
4 yearsHops on one foot; throws overhandCopies cross (+); draws person with 4 partsTells stories; 100% intelligible; counts to 4Cooperative play; imaginary friends
5 yearsSkips; balances on one foot 10 secCopies triangle; ties shoesSpeaks in full sentences; names colorsUnderstands rules; plays organized games
Red flags for referral: no social smile by 2 months, no babbling by 9 months, no words by 16 months, no 2-word phrases by 24 months, and any loss of previously acquired skills at any age. Loss of milestones suggests a neurodegenerative process or autism spectrum disorder.

Primitive Reflexes

ReflexHow to ElicitPresent AtDisappears By
Moro (startle)Sudden head drop or loud noiseBirth4–6 months
RootingStroke cheek → turns toward stimulusBirth3–4 months
Palmar graspPlace finger in palmBirth4–6 months
BabinskiStroke lateral sole → toe dorsiflexion & fanningBirth12–24 months
Tonic neck (fencing)Turn head to side → ipsilateral arm extendsBirth4–6 months
SteppingHold upright, feet touch surfaceBirth2 months
ParachuteSuspend prone, lower toward surface → arms extend8–9 monthsPersists for life
Persistence of primitive reflexes beyond their expected age of disappearance suggests upper motor neuron pathology (e.g., cerebral palsy). An asymmetric Moro reflex suggests brachial plexus injury (Erb palsy) or clavicle fracture.

05 Immunization Schedule

Vaccination is the single most effective preventive intervention in pediatrics. The CDC immunization schedule is updated annually and published by the Advisory Committee on Immunization Practices (ACIP). Understanding the schedule, minimum intervals, contraindications, and the distinction between live and inactivated vaccines is essential for every pediatric provider.

Routine Childhood Immunization Schedule (Birth–18 Years)

VaccineTypeScheduleKey Notes
Hepatitis B (HepB)InactivatedBirth, 1 mo, 6 moFirst dose within 24 hours of birth; monovalent only at birth
Rotavirus (RV)Live oral2, 4 mo (RV1) or 2, 4, 6 mo (RV5)Must start by 15 weeks; cannot give after 8 months 0 days
DTaPInactivated2, 4, 6, 15–18 mo, 4–6 yr5-dose series; Tdap booster at age 11–12
HibInactivated2, 4, (6), 12–15 moNumber of doses depends on product; PRP-OMP (PedvaxHIB) needs no 6-month dose
IPV (Polio)Inactivated2, 4, 6–18 mo, 4–6 yr4-dose series; OPV no longer used in U.S.
PCV15 or PCV20Inactivated2, 4, 6, 12–15 moPCV15 followed by PPSV23 at high risk; PCV20 alone is alternative
MMRLive12–15 mo, 4–6 yrCI in severe immunodeficiency and pregnancy
VaricellaLive12–15 mo, 4–6 yrCI in immunocompromised; avoid aspirin for 6 weeks after
Hepatitis AInactivated12–23 mo (2 doses, 6 mo apart)2-dose series starting at age 1
HPVInactivated11–12 yr (2 or 3 doses)2 doses if started before age 15; 3 doses if ≥15 yr
Meningococcal ACWYInactivated11–12 yr, booster 16 yrHigh-risk groups start earlier
Meningococcal BInactivated16–23 yr (shared decision)Recommended for asplenia, complement deficiency
InfluenzaInactivated or Live (LAIV)Annually starting 6 mo2 doses first year if <9 years and first-time; LAIV not for <2 yr or immunocompromised

Live vs. Inactivated Vaccines

Live Attenuated Vaccines

MMR, Varicella, Rotavirus, LAIV (intranasal flu), BCG, Oral Polio (OPV), Yellow Fever. Live vaccines are contraindicated in severe immunodeficiency (e.g., SCID, high-dose steroids ≥2 mg/kg/day for ≥14 days, chemotherapy). If two live vaccines are not given on the same day, they must be separated by ≥28 days. Live vaccines can cause mild illness (vaccine-strain disease) and can rarely revert to virulence.

Egg allergy is no longer a contraindication to influenza or MMR vaccination. Severe allergic reaction (anaphylaxis) to a vaccine component is the only true contraindication applicable to all vaccines.

06 Growth & Nutrition

Expected Growth Patterns

AgeWeight GainLength/Height GainHead Circumference
0–3 months30 g/day (1 oz/day)3.5 cm/month2 cm/month
3–6 months20 g/day2 cm/month1 cm/month
6–12 months10 g/day1.5 cm/month0.5 cm/month
1–2 years~2.5 kg/year12 cm/year
2–puberty~2 kg/year5–7 cm/year
Birth weight doubles by 4–5 months, triples by 12 months, and quadruples by 24 months. Birth length increases by 50% at 12 months and doubles by 4 years.

Breastfeeding

Breast milk is the recommended sole source of nutrition for the first 6 months. It provides optimal nutrition, immunoglobulins (especially secretory IgA), and growth factors. The AAP recommends continued breastfeeding with complementary foods through at least 12 months. Breast milk is deficient in vitamin D (supplement 400 IU/day from birth) and iron after 4–6 months (supplement 1 mg/kg/day or introduce iron-rich foods).

Formula Feeding

Standard cow’s milk-based formula (20 kcal/oz) is the alternative when breastfeeding is not possible. Soy-based formula is for galactosemia or cow’s milk protein intolerance (but 10–14% cross-react). Extensively hydrolyzed (e.g., Alimentum, Nutramigen) or amino acid-based (EleCare) formulas are for true cow’s milk protein allergy. Whole cow’s milk should not be introduced before 12 months (low iron, excess protein/sodium, risk of GI blood loss).

Introduction of Solid Foods

Begin complementary foods at approximately 4–6 months when the infant shows developmental readiness (sits with support, good head control, loss of tongue thrust reflex). Introduce one new food every 3–5 days. Early introduction of allergenic foods (peanut, egg, milk) between 4–6 months is now recommended by the AAP and LEAP study data to reduce allergy risk, especially in high-risk infants (eczema, egg allergy).

Failure to Thrive (FTT)

Defined as weight <3rd percentile for age, weight-for-length <5th percentile, or crossing down 2 or more major percentile lines. Causes are classified as inadequate intake (most common — poverty, neglect, feeding difficulties, cleft palate), inadequate absorption (celiac, CF, cow’s milk protein allergy), or increased metabolic demand (CHD, chronic infection, hyperthyroidism). Workup includes a detailed feeding history, calorie count, CBC, CMP, urinalysis, and celiac screening. In FTT, weight is affected first, then length, then head circumference (this pattern distinguishes nutritional FTT from genetic/endocrine short stature).

Childhood Obesity

CategoryBMI Percentile (age 2–20)
Underweight<5th percentile
Normal weight5th–84th percentile
Overweight85th–94th percentile
Obese≥95th percentile
Severe obesity≥120% of 95th percentile or BMI ≥35

07 Anticipatory Guidance & Screening

Preventive care in pediatrics involves both surveillance for disease and anticipatory guidance for safety, nutrition, and development at each well-child visit.

AAP Recommended Screening Schedule

ScreeningAgesMethod
Newborn metabolic screen24–48 hours of lifeHeel-stick blood spot (PKU, hypothyroidism, sickle cell, CAH, CF, galactosemia, and ~30 others)
HearingBefore hospital discharge; repeat 1, 3, 5 yr (risk-based)OAE or ABR
VisionNewborn (red reflex); 3–5 yr (visual acuity); annually school-ageRed reflex, Snellen chart, instrument-based screening
Lead12 and 24 months (universal in high-risk areas)Venous lead level; action level ≥3.5 µg/dL (CDC 2021)
Iron deficiency12 monthsCBC or hemoglobin; risk-based at other ages
Autism (M-CHAT-R/F)18 and 24 monthsParent questionnaire; follow-up interview if positive
Dyslipidemia9–11 years (universal); 2+ yr if family historyFasting lipid panel or non-fasting non-HDL cholesterol
Depression (PHQ-A)≥12 years annuallyPatient Health Questionnaire for Adolescents
STI screeningSexually active adolescentsChlamydia, gonorrhea, HIV; per USPSTF

Anticipatory Guidance Highlights by Age

AgeKey Topics
NewbornSafe sleep (back to sleep, no co-sleeping, firm surface), skin-to-skin, breastfeeding support, car seat safety
2–6 monthsTummy time, fall prevention, choking hazards, no honey before 1 year (botulism)
6–12 monthsChildproofing, poison control number, introduction of solids, dental care (first tooth/first birthday)
1–4 yearsWater safety/drowning prevention, car seat transitions (rear-facing until age 2+), limit screen time
5–12 yearsBicycle helmets, seatbelt use, stranger safety, screen time limits, bullying
AdolescentSubstance use, safe sex, mental health, driving safety, sleep hygiene, social media
Unintentional injury is the leading cause of death in children ages 1–18 in the United States. Drowning is the #1 cause of injury death in ages 1–4; motor vehicle accidents are #1 in ages 5–18. Anticipatory guidance about prevention saves lives.

08 Newborn Assessment

APGAR Score

Assessed at 1 and 5 minutes after birth (and every 5 minutes thereafter if score <7). It is a rapid assessment of the newborn’s transition to extrauterine life, not a predictor of long-term neurologic outcome.

Sign0 Points1 Point2 Points
Appearance (color)Blue/pale all overPink body, blue extremities (acrocyanosis)Completely pink
Pulse (heart rate)Absent<100 bpm≥100 bpm
Grimace (reflex irritability)No responseGrimace/weak cryCough, sneeze, vigorous cry
Activity (muscle tone)LimpSome flexionActive motion, well-flexed
RespirationAbsentSlow/irregular, weak cryGood effort, strong cry
Score interpretation: 7–10 = reassuring; 4–6 = moderately depressed (stimulation, possible PPV); 0–3 = severely depressed (immediate resuscitation). Note: Resuscitation should NOT be delayed to calculate APGAR scores.

Gestational Age Assessment

The New Ballard Score uses neuromuscular maturity (6 items: posture, square window, arm recoil, popliteal angle, scarf sign, heel-to-ear) and physical maturity (6 items: skin, lanugo, plantar surface, breast, eye/ear, genitals) to estimate GA from 20–44 weeks. Each item is scored −1 to +5; the sum maps to GA.

Common Birth Injuries

InjuryDescriptionPrognosis
Caput succedaneumDiffuse scalp edema crossing suture linesResolves spontaneously in days
CephalohematomaSubperiosteal hemorrhage; does NOT cross suture linesResolves in weeks–months; risk of jaundice
Subgaleal hemorrhageBleeding between periosteum and galea aponeurotica; can cross suture lines and expand rapidlyLife-threatening; can hold entire blood volume; emergent management
Erb palsy (C5–C6)Upper trunk brachial plexus; "waiter’s tip" position80–90% recover by 3–6 months
Klumpke palsy (C8–T1)Lower trunk brachial plexus; "claw hand"Poorer prognosis than Erb
Clavicle fractureMost common fracture during birth; asymmetric MoroHeals spontaneously; palpable callus at 7–10 days
Subgaleal Hemorrhage — Emergency

A rapidly expanding, fluctuant scalp mass that crosses suture lines in a newborn (often after vacuum-assisted delivery) is a subgaleal hemorrhage until proven otherwise. The subgaleal space can hold 260 mL of blood — nearly the entire blood volume of a neonate. Manage with immediate volume resuscitation, serial hemoglobin/hematocrit, and blood product transfusion as needed.

09 Neonatal Jaundice

Jaundice (hyperbilirubinemia) affects ~60% of term and ~80% of preterm newborns. Most is benign physiologic jaundice, but severe unconjugated hyperbilirubinemia can cause kernicterus (bilirubin encephalopathy) — irreversible brain damage to the basal ganglia, hippocampus, and cranial nerve nuclei, presenting as choreoathetoid cerebral palsy, sensorineural hearing loss, and upward gaze palsy.

Physiologic vs. Pathologic Jaundice

FeaturePhysiologicPathologic
OnsetAfter 24 hours of lifeWithin first 24 hours
PeakDay 3–5 (term); Day 5–7 (preterm)Rises rapidly (>5 mg/dL/day)
DurationResolves by 1–2 weeksPersists >2 weeks (term) or >3 weeks (preterm)
LevelUsually <12–15 mg/dL>17–20 mg/dL (or threshold for age/risk on Bhutani nomogram)
TypeUnconjugated (indirect)Unconjugated or conjugated (>2 mg/dL or >20% of total = always pathologic)
Jaundice within the first 24 hours is ALWAYS pathologic. Think hemolysis: ABO incompatibility (most common), Rh incompatibility, G6PD deficiency, hereditary spherocytosis. Check direct Coombs, CBC with smear, reticulocyte count, blood type.

Breastfeeding vs. Breast Milk Jaundice

FeatureBreastfeeding JaundiceBreast Milk Jaundice
TimingFirst week (days 2–5)After first week (peaks 2–3 weeks)
CauseInadequate intake → decreased stooling → increased enterohepatic circulationSubstance in breast milk (beta-glucuronidase) that increases bilirubin reabsorption
ManagementIncrease breastfeeding frequency (8–12 times/day); lactation supportContinue breastfeeding; resolves by 12 weeks; rarely exceeds phototherapy threshold

Management

Use the Bhutani nomogram (hour-specific total serum bilirubin plotted against age in hours) to determine risk zone and guide management. Treatment includes phototherapy (blue-green light, 430–490 nm, converts unconjugated bilirubin to water-soluble photoisomers excreted without conjugation) and, in severe cases, exchange transfusion (double-volume exchange, ~160 mL/kg, to rapidly lower bilirubin and remove antibodies in hemolytic disease).

Exchange Transfusion Indications

Consider exchange transfusion when total serum bilirubin rises to exchange level on AAP nomogram (typically >25 mg/dL in term healthy newborns, lower thresholds with risk factors), when intensive phototherapy fails to reduce bilirubin by 1–2 mg/dL within 4–6 hours, or when signs of acute bilirubin encephalopathy are present (hypertonia, retrocollis, opisthotonos, fever, high-pitched cry).

10 Neonatal Respiratory Distress

Respiratory distress is the most common reason for NICU admission. The differential is guided by gestational age, mode of delivery, and timing of symptom onset.

Causes of Neonatal Respiratory Distress

ConditionPathophysiologyRisk FactorsCXR FindingsTreatment
RDS (HMD)Surfactant deficiency → alveolar collapsePrematurity (<34 wk), maternal diabetes, C-section without laborDiffuse bilateral ground-glass opacities, air bronchograms, low lung volumesSurfactant replacement (via ETT or LISA); CPAP; supportive
TTNDelayed resorption of fetal lung fluidC-section without labor (no catecholamine surge), term/near-termPerihilar streaky opacities, fluid in fissures, hyperinflationSupportive (O2, CPAP); resolves 24–72 hours
MASMeconium aspiration → chemical pneumonitis, airway obstruction, surfactant inactivationPost-term, fetal distress, meconium-stained amniotic fluidPatchy bilateral infiltrates, hyperinflation, possible pneumothoraxSuction if not vigorous; surfactant; mechanical ventilation; iNO if PPHN
PneumothoraxAir leak into pleural spaceMAS, RDS, positive pressure ventilation, spontaneousHyperlucent hemithorax, mediastinal shift (tension)Needle decompression (tension); chest tube; observation if small
PPHNFailure of normal fall in pulmonary vascular resistance → right-to-left shunting via PDA/foramen ovaleMAS, RDS, sepsis, CDH, idiopathicMay be clear or show underlying cause; differential cyanosis (pre- vs post-ductal SpO2 >5% difference)iNO (first-line pulmonary vasodilator); ECMO if refractory; treat underlying cause
Neonatal Respiratory Distress — Emergency Signs

Grunting (auto-PEEP to maintain FRC), nasal flaring, intercostal/subcostal retractions, tachypnea (>60/min), and cyanosis are the cardinal signs. Grunting in a premature neonate suggests RDS until proven otherwise. A term baby with respiratory distress immediately after C-section is TTN until proven otherwise. Progressive respiratory failure with differential cyanosis suggests PPHN.

Antenatal corticosteroids (betamethasone 12 mg IM ×2 doses, 24 hours apart) given to mothers at 24–34 weeks gestation accelerate fetal lung maturation and reduce RDS incidence by ~50%. This is one of the most impactful interventions in neonatal medicine.

11 Neonatal Sepsis

Neonatal sepsis is a clinical syndrome of systemic infection in the first 28 days of life. It is the leading infectious cause of neonatal mortality. The immature neonatal immune system (poor opsonization, low complement, deficient neutrophil function) makes neonates uniquely susceptible to overwhelming bacterial infection.

Early-Onset vs. Late-Onset Sepsis

FeatureEarly-Onset (≤72 hours)Late-Onset (>72 hours–28 days)
TimingBirth to 72 hours (most within 24 hr)3–28 days
SourceVertical transmission (maternal genital tract)Horizontal/nosocomial or community
Common organismsGroup B Strep (GBS), E. coli (most common in VLBW), ListeriaCoagulase-negative Staphylococci (CoNS), S. aureus, GBS, gram-negatives, Candida (in VLBW)
Risk factorsMaternal GBS colonization, PROM >18 hr, chorioamnionitis, prematurityPrematurity, central lines, prolonged hospitalization, TPN
Empiric antibioticsAmpicillin + GentamicinVancomycin + Gentamicin (or cefepime based on local resistance)
Neonatal Sepsis — Emergency

Neonates with sepsis may present with nonspecific signs: temperature instability (hypothermia more common than fever in neonates), lethargy, poor feeding, apnea, respiratory distress, tachycardia or bradycardia, jaundice, abdominal distension. A "well-appearing" neonate can deteriorate within hours. When sepsis is suspected: obtain blood culture, CBC with differential, CRP/procalcitonin, urinalysis and urine culture (late-onset), and LP if clinically indicated. Start empiric antibiotics within 1 hour of suspicion — do not delay for LP.

GBS Prevention

Universal screening with vaginal-rectal culture at 36–37 weeks gestation. Intrapartum antibiotic prophylaxis (IAP) is indicated for: GBS-positive culture, GBS bacteriuria during current pregnancy, previous infant with GBS disease, or unknown GBS status with risk factors (preterm <37 wk, ROM ≥18 hr, intrapartum fever ≥38.0°C). First-line IAP: Penicillin G 5 million units IV then 2.5–3 million units q4h until delivery. Penicillin allergy: cefazolin if low risk; clindamycin or vancomycin if high-risk allergy.

The Kaiser Permanente Neonatal Early-Onset Sepsis Calculator integrates maternal and neonatal factors to provide an individualized risk estimate, allowing selective observation rather than universal empiric antibiotics for all at-risk neonates. It has reduced unnecessary NICU admissions and antibiotic use by 40–50%.

12 Congenital Anomalies

TORCH Infections

InfectionKey Congenital FindingsDiagnosis
ToxoplasmosisIntracranial calcifications (diffuse/scattered), hydrocephalus, chorioretinitis, hepatosplenomegalyToxoplasma IgM/IgA; PCR
Other (Syphilis)Snuffles (rhinitis), rash, osteochondritis, Hutchinson teeth (late), saddle nose, saber shinsRPR/VDRL, FTA-ABS
RubellaCataracts, sensorineural deafness, PDA (most common cardiac lesion), "blueberry muffin" rash (extramedullary hematopoiesis)Rubella IgM; viral culture
CMVPeriventricular calcifications, microcephaly, sensorineural hearing loss, petechiae/purpura, hepatosplenomegaly — most common congenital infectionUrine CMV PCR or culture within first 3 weeks of life
HSVSkin vesicles, encephalitis, disseminated disease with liver failure, seizures; typically acquired during deliveryHSV PCR of vesicle/CSF; viral culture
CMV is the most common congenital infection worldwide, affecting ~0.5–1% of all live births. It is also the leading non-genetic cause of sensorineural hearing loss in children. Only 10–15% of congenitally infected infants are symptomatic at birth, but 10–15% of initially asymptomatic infants develop late sequelae (especially hearing loss).

Newborn Metabolic Screening

All U.S. states screen for a core panel of conditions via heel-stick blood spot at 24–48 hours of life (and often a second screen at 1–2 weeks). The Recommended Uniform Screening Panel (RUSP) includes >35 core conditions:

CategoryKey Conditions
Amino acid disordersPKU, maple syrup urine disease, homocystinuria, tyrosinemia
Fatty acid oxidation disordersMCAD, VLCAD, LCHAD
Organic acid disordersMethylmalonic acidemia, propionic acidemia, isovaleric acidemia
EndocrineCongenital hypothyroidism, congenital adrenal hyperplasia (21-hydroxylase deficiency)
HemoglobinopathiesSickle cell disease (SS, SC, S-beta thal), other hemoglobinopathies
OtherCystic fibrosis (IRT → sweat chloride), galactosemia, biotinidase deficiency, SCID (TREC assay)

Congenital Heart Disease Screening

Pulse oximetry screening is performed on all newborns after 24 hours of life (or before discharge if earlier). SpO2 is measured on the right hand (preductal) and either foot (postductal). The screen fails if any reading is <90%, if both readings are <95% on three measurements separated by 1 hour, or if there is >3% difference between right hand and foot. A failed screen requires echocardiography.

13 Asthma in Children

Asthma is the most common chronic disease of childhood, affecting ~8% of U.S. children. It is characterized by reversible airway obstruction, bronchial hyperresponsiveness, and chronic airway inflammation. The NAEPP EPR-4 (2020) guidelines provide stepwise therapy recommendations.

Classification of Asthma Severity (Ages ≥12, similar for younger with modifications)

SeveritySymptomsNighttime AwakeningsSABA UseFEV1
Intermittent≤2 days/week≤2×/month≤2 days/week>80%
Mild Persistent>2 days/week (not daily)3–4×/month>2 days/week (not daily)≥80%
Moderate PersistentDaily>1×/weekDaily60–80%
Severe PersistentThroughout the dayOften nightlySeveral times/day<60%

Stepwise Therapy (Children 5–11 Years)

StepPreferred ControllerAlternative
Step 1SABA PRN (no daily controller)
Step 2Low-dose ICS dailyLTRA (montelukast) or cromolyn
Step 3Low-dose ICS + LABA, or medium-dose ICSLow-dose ICS + LTRA
Step 4Medium-dose ICS + LABAMedium-dose ICS + LTRA
Step 5High-dose ICS + LABAConsider biologics (omalizumab, mepolizumab, dupilumab)
Step 6High-dose ICS + LABA + oral corticosteroidsBiologics; refer to specialist

Acute Asthma Exacerbation Management

SeverityTreatment
Mild-ModerateAlbuterol MDI 4–8 puffs (or nebulizer 2.5–5 mg) q20min ×3; oral prednisolone 1–2 mg/kg (max 60 mg)
SevereContinuous albuterol nebulization; ipratropium 0.5 mg q20min ×3; IV/IM methylprednisolone 2 mg/kg; magnesium sulfate 25–75 mg/kg IV (max 2 g)
Impending respiratory failureIV terbutaline; consider ketamine for intubation (bronchodilator properties); avoid histamine-releasing agents
Children <5 years cannot reliably perform spirometry, so asthma classification is based on symptom frequency alone. In this age group, intermittent wheezing with viral URIs may represent viral-induced wheeze rather than true asthma. The "Asthma Predictive Index" (API) helps predict which wheezy preschoolers will develop persistent asthma.

14 Croup & Epiglottitis

Croup (Laryngotracheobronchitis)

Croup is the most common cause of acute upper airway obstruction in children ages 6 months to 3 years (peak 1–2 years). It is caused by parainfluenza virus (types 1 and 3 most common) and produces subglottic edema with a characteristic "barking" or "seal-like" cough, inspiratory stridor, and hoarse voice. Symptoms are typically worse at night.

SeverityFindingsTreatment
MildOccasional barky cough; no stridor at rest; no retractionsSingle dose dexamethasone 0.6 mg/kg PO/IM (max 10 mg); cool mist; reassurance
ModerateFrequent barky cough; stridor at rest; mild retractions; no agitationDexamethasone 0.6 mg/kg + racemic epinephrine 0.5 mL of 2.25% solution nebulized; observe ≥2–4 hours after epinephrine
SevereStridor at rest; significant retractions; agitation or lethargy; cyanosisDexamethasone + racemic epinephrine (may repeat); minimize agitation; prepare for airway management
CXR (if obtained) shows the classic "steeple sign" — subglottic narrowing of the tracheal air column on AP view. CXR is not required for typical presentations but helps differentiate from other causes of stridor.

Epiglottitis

Epiglottitis — Airway Emergency

Epiglottitis is a life-threatening infection of the epiglottis and supraglottic structures, now rare due to Hib vaccination but still seen (now more often caused by Streptococcus spp. and Staphylococcus spp.). Classic presentation: acute onset of high fever, toxic-appearing, "tripod" or sniffing position, drooling, muffled "hot potato" voice, dysphagia, and minimal cough. Do NOT examine the throat, do NOT lay the child supine, do NOT agitate the child — any of these can precipitate complete airway obstruction. Lateral neck X-ray shows the "thumbprint sign" (enlarged epiglottis). Management: controlled intubation in the OR with a surgeon ready for tracheostomy; IV antibiotics (ceftriaxone or cefotaxime + vancomycin).

Differentiating Croup from Epiglottitis

FeatureCroupEpiglottitis
Age6 months–3 years2–7 years (now any age)
OnsetGradual (1–2 days URI prodrome)Rapid (hours)
FeverLow-gradeHigh (>39°C)
CoughBarking/seal-likeAbsent or minimal
VoiceHoarseMuffled/"hot potato"
DroolingAbsentPresent
PositionAnyTripod/sniffing
X-raySteeple signThumbprint sign
EtiologyParainfluenzaH. influenzae type b (historically); Strep/Staph now

15 Bronchiolitis

Bronchiolitis is the most common lower respiratory tract infection in infants <12 months (peak 2–6 months). RSV causes ~70% of cases (other causes: rhinovirus, human metapneumovirus, parainfluenza, adenovirus). It produces inflammation, edema, and mucus plugging of the small airways (bronchioles), causing wheezing, crackles, and respiratory distress.

AAP Clinical Practice Guideline (2014, reaffirmed 2023)

RecommendationDetails
DiagnosisClinical diagnosis based on history and physical exam; routine CXR and viral testing are NOT recommended
TreatmentSupportive care only: nasal suctioning, supplemental O2 if SpO2 persistently <90%, adequate hydration (oral or IV/NG)
BronchodilatorsAlbuterol and epinephrine should NOT be routinely used; one trial of bronchodilator is acceptable but should be discontinued if no improvement
CorticosteroidsNOT recommended for bronchiolitis
AntibioticsNOT indicated unless bacterial co-infection documented
Hypertonic saline (3%)May be considered for hospitalized patients (not in ED); modest benefit in reducing length of stay
High-flow nasal cannula (HFNC)Increasingly used for moderate-severe bronchiolitis; provides CPAP-like effect, heated humidification, and washout of dead space

RSV Prevention

Nirsevimab (Beyfortus) — a long-acting monoclonal antibody — is now recommended for all infants <8 months entering their first RSV season and for high-risk infants 8–19 months entering their second season. It replaced palivizumab (Synagis), which required monthly injections and was limited to high-risk groups. Palivizumab is still available for eligible infants when nirsevimab is not available.

Bronchiolitis is a clinical diagnosis. Obtaining CXRs in bronchiolitis often leads to false-positive reads for "pneumonia" and unnecessary antibiotics. The AAP explicitly recommends against routine imaging. An exception is the infant who fails to improve or has focal findings on exam.

16 Pneumonia in Children

The most likely causative organisms vary significantly by age group, which determines empiric therapy.

Etiology by Age

AgeMost Common OrganismsEmpiric Therapy
Neonates (<28 days)GBS, E. coli, Listeria, HSVAmpicillin + gentamicin (± acyclovir if HSV suspected)
1–3 monthsChlamydia trachomatis (afebrile pneumonitis), RSV, S. pneumoniae, B. pertussisMacrolide (azithromycin) if afebrile; cephalosporin if febrile/toxic
3 months–5 yearsViral (most common overall), S. pneumoniae (most common bacterial)High-dose amoxicillin 90 mg/kg/day (outpatient); ampicillin IV (inpatient)
5–18 yearsMycoplasma pneumoniae (most common), S. pneumoniae, Chlamydophila pneumoniaeMacrolide (azithromycin 10 mg/kg day 1, then 5 mg/kg days 2–5) for atypical; amoxicillin or ampicillin if typical bacterial
The "staccato cough" with bilateral diffuse infiltrates in an afebrile 4–8 week-old infant with conjunctivitis is classic for Chlamydia trachomatis pneumonia (acquired from the birth canal). CBC often shows eosinophilia. Treat with oral azithromycin (not topical erythromycin, which only treats the eye).

Parapneumonic Effusion & Empyema

Complicated parapneumonic effusions occur in ~5% of pediatric pneumonias. Ultrasound is the initial imaging modality. Pleural fluid pH <7.2, glucose <40 mg/dL, or positive Gram stain/culture indicates empyema requiring drainage (chest tube or VATS). S. pneumoniae and S. aureus (including MRSA) are the most common organisms.

17 Fever in Children

Fever is the most common presenting complaint in pediatric emergency departments. The approach to fever varies dramatically by age because the risk of serious bacterial infection (SBI) — UTI, bacteremia, meningitis — is highest in the youngest infants who may appear well despite serious illness.

Age-Based Approach to Fever Without a Source

AgeRisk LevelWorkupManagement
<28 daysHighest risk; neonatal immune immaturityFull sepsis workup: blood culture, UA/urine culture (cath), LP, CBC, CRP/procalcitonin; CXR if respiratory symptoms; stool culture if diarrheaAdmit and empiric IV antibiotics (ampicillin + gentamicin or cefotaxime) pending cultures; consider HSV coverage (acyclovir) if risk factors
29–60 daysHigh risk; may use validated criteria to risk-stratifyBlood culture, UA/urine culture, CBC, CRP/procalcitonin; LP if ill-appearing or high inflammatory markersLow-risk by validated criteria (Rochester, Step-by-Step, PECARN): may observe closely without antibiotics. High-risk: admit and empiric antibiotics
61–90 daysModerate riskUA/urine culture; blood culture and CBC if ill-appearing; LP if warrantedWell-appearing with negative UA: consider close outpatient follow-up. Ill-appearing: admit
3–36 monthsLower risk (post-PCV era)UA/urine culture if female <24 mo or uncircumcised male <12 mo; blood work if T ≥39°C and ill-appearingUTI is most common SBI; occult bacteremia rare (<1%) in post-PCV/Hib era; treat identified source
Febrile Neonate <28 Days — Emergency

Any fever (rectal temperature ≥38.0°C / 100.4°F) in an infant <28 days old requires a full sepsis workup and empiric IV antibiotics regardless of appearance. This is non-negotiable. These infants can harbor bacteremia, meningitis, or UTI while appearing well. HSV should also be considered in neonates with fever, vesicles, seizures, or elevated LFTs — add acyclovir 60 mg/kg/day IV divided q8h.

18 Otitis Media & Pharyngitis

Acute Otitis Media (AOM)

AOM is the most common reason for antibiotic prescriptions in children. Peak incidence is 6–24 months. Diagnosis requires: (1) acute onset of symptoms, (2) middle ear effusion (bulging TM, impaired mobility on pneumatic otoscopy, air-fluid level), and (3) signs of middle ear inflammation (erythematous TM, otalgia). Most common organisms: S. pneumoniae, nontypeable H. influenzae, and Moraxella catarrhalis.

ScenarioManagement
Age ≥6 months, unilateral, non-severeWatchful waiting for 48–72 hours with follow-up (per AAP 2013); pain management with ibuprofen/acetaminophen
Age ≥6 months, bilateral or severe (T ≥39°C, severe otalgia, >48 hr symptoms)Amoxicillin 80–90 mg/kg/day divided BID ×10 days (<2 yr) or 5–7 days (≥2 yr)
Treatment failure (no improvement at 48–72 hr)High-dose amoxicillin-clavulanate (90 mg/kg/day of amoxicillin component); or ceftriaxone IM ×3 days
Penicillin allergyCefdinir, cefuroxime, or azithromycin (less effective)
Recurrent AOM (≥3 episodes in 6 mo or ≥4 in 12 mo)Refer for tympanostomy tubes

Pharyngitis — Group A Streptococcus (GAS)

GAS pharyngitis accounts for ~15–30% of pharyngitis in children ages 5–15 (rare <3 years). Treatment prevents rheumatic fever (ARF) but primarily targets symptom relief and reduced transmission.

FeatureGAS PharyngitisViral Pharyngitis
Age5–15 yearsAny age
SymptomsSudden onset sore throat, fever, headache, abdominal pain, tonsillar exudates, palatal petechiae, tender anterior cervical lymphadenopathyCough, rhinorrhea, conjunctivitis, hoarseness, diarrhea, oral ulcers
DiagnosisRapid strep test (high specificity); if negative, confirm with throat culture (gold standard) in childrenClinical; viral features suggest non-GAS etiology
TreatmentPenicillin V 250 mg BID or 500 mg BID ×10 days; OR amoxicillin 50 mg/kg once daily (max 1 g) ×10 days; pen-allergy: cephalexin, azithromycinSupportive care only
The modified Centor (McIsaac) score predicts GAS probability: fever, tonsillar exudates, anterior cervical lymphadenopathy, absence of cough, age 3–14 (+1) or 15–44 (0) or ≥45 (−1). The IDSA recommends testing (RADT ± culture) rather than using clinical scores alone in children, because untreated GAS can cause ARF.

19 Common Childhood Exanthems

DiseaseAgentRash DescriptionKey Features
Measles (Rubeola)ParamyxovirusErythematous maculopapular rash starting at face/hairline → spreads cephalocaudal; confluent3 C’s: Cough, Coryza, Conjunctivitis; Koplik spots (white spots on buccal mucosa) before rash; high fever; highly contagious
Rubella (German measles)RubivirusPink maculopapular rash starting on face → spreads downward; clears in 3 daysPostauricular and suboccipital lymphadenopathy; mild illness in children; teratogenic in first trimester
Roseola (Exanthem subitum)HHV-6Rose-pink macular/maculopapular rash on trunk → spreads peripherallyHigh fever for 3–5 days, then rash appears as fever breaks; age 6–24 months; febrile seizures common
Erythema infectiosum (Fifth disease)Parvovirus B19"Slapped cheek" facial erythema → reticular (lace-like) rash on trunk/extremitiesChild is no longer contagious when rash appears; aplastic crisis in sickle cell; hydrops fetalis if maternal infection
Varicella (Chickenpox)VZVPruritic vesicles on erythematous base ("dewdrop on rose petal"); lesions in different stages (crops)Centripetal distribution (trunk > extremities); highly contagious until all vesicles crusted
Hand-Foot-Mouth DiseaseCoxsackievirus A16 (or Enterovirus 71)Vesicles/ulcers on oral mucosa; maculopapular or vesicular lesions on palms and solesPeak 1–4 years; summer/fall; usually self-limited; EV71 can cause severe neurologic disease
Scarlet FeverGAS (erythrogenic toxin)Diffuse erythematous "sandpaper" rash; spares face (circumoral pallor); Pastia lines (petechiae in skin folds)Strawberry tongue; follows GAS pharyngitis; treat with penicillin/amoxicillin
Example of a childhood maculopapular exanthem showing pink-red spots distributed across the skin
Figure 2 — Childhood Exanthem. Maculopapular rash characteristic of rubella, showing fine pink spots distributed across the trunk. Source: Wikimedia Commons, CDC. Public domain.
The classic teaching that roseola rash appears AFTER the fever resolves is the key distinguishing feature. If a parent brings in a well-appearing child with a new rash and says "the fever just broke yesterday," think roseola (HHV-6). No treatment needed; it is self-limited.

20 Meningitis in Children

Bacterial meningitis is a medical emergency in pediatrics. Prompt recognition and treatment reduce mortality and long-term neurologic sequelae (hearing loss, intellectual disability, seizures).

Age-Based Empiric Therapy

AgeCommon OrganismsEmpiric Antibiotics
<1 monthGBS, E. coli, ListeriaAmpicillin + cefotaxime (or gentamicin)
1–3 monthsGBS, E. coli, Listeria, S. pneumoniae, N. meningitidisAmpicillin + cefotaxime (or ceftriaxone if >28 days) + vancomycin
3 months–18 yearsS. pneumoniae, N. meningitidisCeftriaxone + vancomycin; add dexamethasone 0.15 mg/kg IV q6h ×4 days (give before or with first antibiotic dose for Hib and S. pneumoniae)
Ceftriaxone is avoided in neonates <28 days because it displaces bilirubin from albumin (risk of kernicterus) and can precipitate with calcium in IV solutions. Use cefotaxime instead in this age group. Ampicillin covers Listeria, which is resistant to cephalosporins.

CSF Interpretation

ParameterNormalBacterialViral (Aseptic)TB/Fungal
Opening pressure<20 cm H2OElevatedNormal/mildly elevatedElevated
WBC<5 cells/µL>1,000 (neutrophil predominant)10–500 (lymphocyte predominant)10–500 (lymphocyte predominant)
Protein<45 mg/dLVery elevated (>100)Normal/mildly elevatedVery elevated
Glucose>40 mg/dL (or CSF:serum >0.6)Low (<40)NormalLow
Gram stainNegativePositive in 60–90%NegativeAFB/India ink

Chemoprophylaxis

OrganismWho Needs ProphylaxisRegimen
N. meningitidisClose contacts (household, daycare, direct exposure to secretions)Rifampin 10 mg/kg (max 600 mg) q12h ×2 days; OR ciprofloxacin 500 mg ×1 (adults); OR ceftriaxone 250 mg IM ×1
H. influenzae type bHousehold contacts if any unvaccinated child <4 years in householdRifampin 20 mg/kg (max 600 mg) daily ×4 days

21 UTI in Children

UTI is the most common serious bacterial infection in febrile infants. Presentation varies dramatically with age: neonates present with nonspecific signs (fever, irritability, poor feeding, jaundice), while older children present with classic dysuria, frequency, and suprapubic/flank pain. E. coli causes 80–90% of first UTIs in children.

AAP Guidelines (2011, reaffirmed 2016) — Children 2–24 Months

StepDetails
DiagnosisRequires BOTH positive urinalysis (pyuria and/or bacteriuria) AND ≥50,000 CFU/mL on culture from catheterized or suprapubic specimen; bag specimens are for screening only (high false-positive rate)
TreatmentOral antibiotics for non-toxic children: cephalexin 50–100 mg/kg/day, cefixime, or TMP-SMX; IV antibiotics if toxic-appearing, unable to tolerate PO, or <2 months old; 7–14 day course
ImagingRenal/bladder ultrasound (RBUS) after first febrile UTI; VCUG indicated if RBUS is abnormal, atypical UTI, or recurrent febrile UTI

Vesicoureteral Reflux (VUR) Grading

GradeDescription
IReflux into non-dilated ureter only
IIReflux into renal pelvis without dilation
IIIMild-moderate dilation of ureter, pelvis, and calyces
IVModerate dilation with blunting of calyceal fornices
VGross dilation and tortuosity of ureter with loss of papillary impressions
Grades I–III: ~80% spontaneous resolution; managed with observation ± antibiotic prophylaxis. Grades IV–V: lower spontaneous resolution; consider surgical correction (ureteral reimplantation or endoscopic injection).
Circumcision reduces UTI risk ~10-fold in males during the first year of life. Uncircumcised febrile males <12 months have a UTI prevalence of ~20%, compared to ~2% in circumcised males. This influences the threshold for urine testing in the AAP algorithm.

22 Vomiting & Dehydration

Assessment of Dehydration Severity

FeatureMild (3–5%)Moderate (6–9%)Severe (≥10%)
Mental statusNormal, thirstyIrritable, restlessLethargic, obtunded
EyesNormalSlightly sunkenDeeply sunken
TearsPresentDecreasedAbsent
Mucous membranesSlightly dryDryParched
Skin turgorNormalDecreased (slow recoil)Tenting
Cap refill<2 seconds2–3 seconds>3 seconds
Urine outputSlightly decreasedDecreased (<1 mL/kg/hr)Minimal/absent
Heart rateNormalTachycardicTachycardic → bradycardic (preterminal)

Rehydration

SeverityApproach
MildORS (oral rehydration solution) 50 mL/kg over 4 hours + replace ongoing losses
ModerateORS 100 mL/kg over 4 hours; ondansetron 0.15 mg/kg ODT may facilitate oral rehydration; IV if ORS fails
SevereIV NS or LR bolus 20 mL/kg over 15–20 min (may repeat ×3); then replace deficit + maintenance; if signs of shock: immediate 20 mL/kg bolus

Pyloric Stenosis

Hypertrophic pyloric stenosis presents at 2–6 weeks of age (classic: firstborn male) with projectile, nonbilious vomiting after feeds, "hungry vomiter" who wants to feed immediately after vomiting. Physical exam may reveal a palpable "olive" in the right upper quadrant. Labs show hypochloremic, hypokalemic metabolic alkalosis (from loss of HCl in vomitus). Ultrasound diagnostic criteria: pyloric muscle thickness >3 mm, pyloric length >15 mm. Treatment: correct electrolytes and dehydration first, then Ramstedt pyloromyotomy.

Intussusception

Most common cause of intestinal obstruction in children 6 months–3 years (peak 5–9 months). Most cases are ileocolic and idiopathic (hypertrophied Peyer patches serving as lead point after viral illness). Classic triad (present in <50%): colicky abdominal pain (episodic, drawing up legs), "currant jelly" stools (blood and mucus), and sausage-shaped abdominal mass. Diagnosis: ultrasound showing "target sign" (concentric rings). Treatment: air or contrast enema (both diagnostic and therapeutic) — ~90% success rate; surgery if enema fails, peritonitis, or perforation.

A child >3 years with intussusception should raise concern for a pathologic lead point (lymphoma, Meckel diverticulum, polyp, HSP). These patients are more likely to require surgical reduction rather than enema reduction.

23 Abdominal Pain in Children

Appendicitis

Most common surgical emergency in children. Classic presentation: periumbilical pain migrating to right lower quadrant (McBurney point), anorexia, nausea/vomiting, low-grade fever. The Pediatric Appendicitis Score (PAS) and Alvarado score help risk-stratify. Diagnosis: ultrasound first in children (avoids radiation); CT if ultrasound equivocal. Nonperforated appendicitis: appendectomy (laparoscopic) within 24 hours; some centers now offer antibiotic-first approach for uncomplicated cases. Perforated: IV antibiotics (piperacillin-tazobactam or ceftriaxone + metronidazole) ± percutaneous drainage if abscess, with interval appendectomy 6–8 weeks later.

Meckel Diverticulum

The "rule of 2s": 2% of population, 2 feet from ileocecal valve, 2 inches long, presents by age 2, 2 types of ectopic tissue (gastric and pancreatic). Most common presenting symptom in children is painless rectal bleeding (dark red or brick-colored) due to acid secretion from ectopic gastric mucosa causing ulceration of adjacent ileal tissue. Diagnosis: Meckel scan (technetium-99m pertechnetate scintigraphy — tags ectopic gastric mucosa). Treatment: surgical resection.

Malrotation with Midgut Volvulus

Malrotation with Volvulus — Surgical Emergency

Malrotation results from incomplete rotation and fixation of the midgut during embryologic development. The narrow mesenteric pedicle predisposes to midgut volvulus — twisting of the bowel around the SMA — causing ischemia of the entire midgut. Presentation: bilious (green) vomiting in a neonate is volvulus until proven otherwise. Diagnosis: upper GI series (gold standard) showing abnormal position of duodenojejunal junction (ligament of Treitz). Emergency treatment: Ladd procedure (detorsion, lysis of Ladd bands, appendectomy, broadening of mesenteric base). Time is critical — delay leads to bowel necrosis and short gut syndrome.

Hirschsprung Disease

Congenital absence of ganglion cells in the distal colon (aganglionosis), most commonly affecting the rectosigmoid. Presents with failure to pass meconium within 48 hours of birth, abdominal distension, and bilious vomiting. Can present later with chronic constipation (ribbon-like stools, failure to thrive). Diagnosis: barium enema (transition zone), rectal suction biopsy (gold standard — absent ganglion cells, hypertrophied nerve trunks). Treatment: pull-through procedure (Soave, Swenson, or Duhamel).

Bilious (green) vomiting in a neonate is a surgical emergency until proven otherwise. The differential includes malrotation with volvulus, intestinal atresia, meconium ileus, and Hirschsprung disease with enterocolitis. An upper GI series should be obtained emergently to rule out malrotation.

24 Pediatric GI Emergencies

Necrotizing Enterocolitis (NEC)

NEC is the most common GI emergency in premature neonates (primarily <32 weeks GA and <1,500 g). Pathogenesis involves mucosal injury from ischemia, formula feeding, and bacterial invasion. Presentation: feeding intolerance, abdominal distension, bloody stools, bilious aspirates, and systemic signs (apnea, lethargy, temperature instability, DIC).

Modified Bell StagingClinicalRadiographicTreatment
Stage I (Suspected)Nonspecific signs, feeding intolerance, mild distensionNormal or mildly dilated loopsNPO, NGT decompression, IV antibiotics, serial exams
Stage II (Definite)Bloody stools, absent bowel sounds, abdominal wall erythemaPneumatosis intestinalis (pathognomonic); portal venous gasNPO 7–14 days, IV antibiotics (ampicillin + gentamicin + metronidazole), TPN
Stage III (Advanced)Peritonitis, hemodynamic instability, DICPneumoperitoneum (free air = perforation)Surgical consultation; laparotomy or peritoneal drain; resuscitation
Breast milk significantly reduces the risk of NEC. Exclusive human milk feeding (mother’s own milk or pasteurized donor milk) is one of the most evidence-based preventive strategies in neonatology. Probiotics may also reduce NEC incidence, though strain-specific recommendations remain under investigation.

Pyloric Stenosis — Quick Reference

See Section 22 for full details. Key points: projectile nonbilious vomiting at 2–6 weeks; "olive" mass; hypochloremic hypokalemic metabolic alkalosis; US >3 mm thickness, >15 mm length; pyloromyotomy after correcting metabolic derangements.

Intussusception — Quick Reference

See Section 22 for full details. Key points: 6 months–3 years; episodic colicky pain; currant jelly stools; US target sign; air enema reduction 90% success; surgery if failed enema or perforation.

25 Celiac Disease & Food Allergies

Celiac Disease

An immune-mediated enteropathy triggered by gluten (wheat, barley, rye) in genetically predisposed individuals (HLA-DQ2 or DQ8). Prevalence ~1% in Western populations. Classic presentation in children: chronic diarrhea, abdominal distension, failure to thrive, irritability, and iron deficiency anemia beginning after introduction of gluten-containing foods (typically 6–24 months). Older children may present with constipation, short stature, delayed puberty, or dermatitis herpetiformis.

Diagnostic TestDetails
Initial screenTTG-IgA (tissue transglutaminase IgA) + total serum IgA (to rule out IgA deficiency, present in 2–3% of celiac patients causing false-negative TTG-IgA)
If IgA deficientTTG-IgG or deamidated gliadin peptide (DGP) IgG
ConfirmatoryEsophagogastroduodenoscopy with small bowel biopsy showing villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis (Marsh classification)
TreatmentStrict lifelong gluten-free diet; monitor with TTG-IgA; screen for associated conditions (Type 1 DM, thyroiditis, IgA nephropathy)

Food Allergies

IgE-mediated food allergy affects ~6–8% of children <3 years. The most common allergens are cow’s milk, egg, peanut, tree nuts, soy, wheat, fish, and shellfish. Milk, egg, soy, and wheat allergies are usually outgrown by school age; peanut, tree nut, and shellfish allergies tend to persist.

Anaphylaxis Management in Children

Epinephrine IM (anterolateral thigh) is the first-line treatment: 0.01 mg/kg of 1:1,000 (0.1 mg/mL) solution, max 0.3 mg in children <30 kg, max 0.5 mg in adolescents. May repeat every 5–15 minutes. Position supine with legs elevated (unless vomiting or respiratory distress). After epinephrine: IV fluid bolus (20 mL/kg NS), albuterol for bronchospasm, H1/H2 blockers (diphenhydramine + ranitidine), methylprednisolone 1–2 mg/kg IV. Observe 4–6 hours for biphasic reaction. Prescribe epinephrine auto-injector at discharge.

The LEAP (Learning Early About Peanut Allergy) trial demonstrated that early introduction of peanut-containing foods (4–11 months) in high-risk infants (severe eczema or egg allergy) reduced the incidence of peanut allergy by ~80% compared to avoidance. This fundamentally changed the paradigm from "delay allergen introduction" to "early introduction."

26 Congenital Heart Disease — Acyanotic

Acyanotic (left-to-right shunt) lesions present with signs of pulmonary overcirculation: tachypnea, poor feeding, diaphoresis with feeds, recurrent respiratory infections, and failure to thrive. They do not cause cyanosis initially, but long-standing shunts can cause pulmonary hypertension and eventually Eisenmenger syndrome (shunt reversal → cyanosis).

LesionPathologyMurmurManagement
VSDMost common CHD (~30%); communication between ventricles; L→R shuntHolosystolic murmur at LLSB; louder murmur = smaller VSD (more turbulence)Small: observe (many close spontaneously by age 2). Large: diuretics, surgical closure if symptomatic HF
ASDCommunication between atria; L→R shunt; often asymptomatic in childhoodSystolic ejection murmur at LUSB (increased flow across pulmonic valve); fixed split S2Secundum type: transcatheter device closure if significant shunt (Qp:Qs >1.5:1); primum: surgical repair
PDAPersistent patency of ductus arteriosus; L→R shunt from aorta to PAContinuous "machinery" murmur at left infraclavicular area; bounding pulses, wide pulse pressurePreterm: indomethacin or ibuprofen (prostaglandin inhibition). Term: transcatheter or surgical closure if hemodynamically significant
Coarctation of AortaNarrowing of aorta, typically at insertion of ductus arteriosus (juxtaductal)Systolic murmur between scapulae; upper extremity hypertension + weak femoral pulses; BP gradient >20 mmHg arm-to-legNeonatal (critical): PGE1 to maintain ductal patency; surgical repair. Older: balloon angioplasty ± stent or surgical repair
Aortic StenosisObstruction at valvular (most common), subvalvular, or supravalvular (Williams syndrome) levelSystolic ejection murmur at RUSB radiating to carotids; ejection click if valvularBalloon valvuloplasty for severe valvular AS; surgical intervention for subvalvular/supravalvular
An infant with weak or absent femoral pulses and a BP differential between arms and legs has coarctation of the aorta until proven otherwise. This may present as shock in the first 1–2 weeks of life when the ductus closes. PGE1 (alprostadil) can be lifesaving by reopening the ductus arteriosus.
Diagram of a ventricular septal defect showing the abnormal communication between left and right ventricles with left-to-right shunt flow
Figure 3 — Ventricular Septal Defect (VSD). The most common congenital heart defect, showing abnormal communication between the left and right ventricles with left-to-right shunt. Source: Wikimedia Commons. Public domain.

27 Congenital Heart Disease — Cyanotic

Cyanotic CHD presents with hypoxemia that does not significantly improve with supplemental oxygen (the "hyperoxia test": PaO2 remains <150 mmHg after 10 minutes of 100% FiO2, suggesting intracardiac right-to-left shunt rather than lung disease). The "5 T’s" of cyanotic CHD:

LesionPathologyKey FeaturesManagement
Tetralogy of Fallot (TOF)VSD + overriding aorta + RV outflow tract obstruction + RV hypertrophyMost common cyanotic CHD beyond neonatal period; "boot-shaped" heart on CXR; "tet spells" (hypercyanotic episodes)Tet spell: knee-chest position, oxygen, morphine, IV fluid, phenylephrine. Definitive: complete surgical repair at 3–6 months
Transposition of the Great Arteries (TGA)Aorta arises from RV, PA arises from LV → parallel circuitsMost common cyanotic CHD at birth; cyanosis in first hours of life; "egg on a string" heart on CXRPGE1 to maintain PDA (allows mixing); balloon atrial septostomy (Rashkind); definitive: arterial switch operation (Jatene) within first 2 weeks
Truncus ArteriosusSingle great vessel overriding a VSD giving rise to aorta, PA, and coronary arteriesCyanosis + HF; single S2; associated with DiGeorge syndrome (22q11.2 deletion)Surgical repair in neonatal period
TAPVRAll pulmonary veins drain to systemic venous system (SVC, coronary sinus, IVC) instead of LACyanosis; survival requires ASD/PFO for mixing; obstructed TAPVR = emergency ("snowman" heart on CXR in supracardiac type)Surgical redirection of pulmonary veins to LA
Tricuspid AtresiaAbsent tricuspid valve; no connection between RA and RVCyanosis; requires ASD + VSD or PDA for blood flow; left axis deviation on ECG (unusual in CHD)Staged palliation: BT shunt → Glenn → Fontan
Tet Spells (Hypercyanotic Episodes) — Emergency

Occur in unrepaired TOF, typically in infants 2–4 months old, triggered by crying, feeding, or defecation. Mechanism: increased RV outflow tract obstruction → increased right-to-left shunt → profound cyanosis → metabolic acidosis → further RVOT spasm (vicious cycle). Management: (1) knee-chest position (increases SVR, decreases venous return), (2) supplemental O2, (3) IV fluid bolus, (4) morphine 0.1 mg/kg (reduces agitation), (5) phenylephrine 5–20 mcg/kg IV (increases SVR, reverses shunt), (6) emergent surgical consultation if refractory.

Prostaglandin E1 (PGE1 / alprostadil) maintains ductal patency and is lifesaving in duct-dependent cyanotic and obstructive lesions. Key side effects to monitor: apnea (12%), fever, hypotension. Always have intubation equipment ready when starting PGE1.

28 Kawasaki Disease

Kawasaki disease (KD) is an acute, self-limited vasculitis of medium-sized arteries with a predilection for the coronary arteries. It is the leading cause of acquired heart disease in children in developed countries. Peak incidence: 6 months to 5 years; male predominance (1.5:1); highest incidence in Asian/Pacific Islander populations.

Diagnostic Criteria (Classic KD)

Fever ≥5 days PLUS ≥4 of the following 5 criteria:

#CriterionDetails
1Bilateral conjunctival injectionNon-exudative, limbal-sparing
2Oral mucous membrane changesStrawberry tongue, erythematous/cracked lips, oropharyngeal erythema
3Extremity changesErythema/edema of hands and feet (acute); periungual desquamation (convalescent)
4Polymorphous rashNon-vesicular; often accentuated in groin; not specific
5Cervical lymphadenopathy≥1.5 cm, usually unilateral
Incomplete (Atypical) Kawasaki Disease

Suspect in children with fever ≥5 days and only 2–3 criteria, especially if <12 months (who are at highest risk for coronary aneurysms and most likely to have incomplete presentation). If CRP ≥3 mg/dL and/or ESR ≥40 mm/hr with 3 or more supplementary lab criteria (albumin ≤3.0, anemia, elevated ALT, platelets >450K after day 7, WBC ≥15K, urine WBC ≥10/hpf), treat as KD. Echocardiogram should be obtained — coronary abnormalities on echo are diagnostic.

Treatment

TherapyDetails
IVIG2 g/kg IV as single infusion over 10–12 hours; given within first 10 days of illness (ideally by day 7). Reduces coronary aneurysm risk from ~25% to <5%
AspirinHigh-dose (80–100 mg/kg/day divided QID) until afebrile ×48–72 hours, then low-dose (3–5 mg/kg/day) for 6–8 weeks (or indefinitely if coronary aneurysms present)
IVIG-resistant (≥36 hr persistent/recurrent fever after IVIG)Second IVIG infusion; consider IV methylprednisolone 30 mg/kg/day ×3 days; infliximab in refractory cases

Coronary Artery Follow-Up

Echocardiography at diagnosis, 1–2 weeks, and 6–8 weeks. Coronary artery aneurysms are classified by z-score: small (z 2.5–5), medium (z 5–10), giant (z ≥10 or absolute diameter ≥8 mm). Giant aneurysms require long-term anticoagulation (warfarin + aspirin) and carry risk of thrombosis, stenosis, and MI.

Kawasaki disease is the most common cause of acquired heart disease in children in developed countries, surpassing rheumatic heart disease. The key to preventing coronary aneurysms is early IVIG treatment within the first 10 days of fever. Infants <6 months are at highest risk for coronary complications and most often present with incomplete criteria — maintain a high index of suspicion.

29 Short Stature & Growth Disorders

Short stature is defined as height <3rd percentile or >2 SD below the mean for age and sex. The differential is broad, but most children have either constitutional delay of growth and puberty or familial (genetic) short stature, both of which are normal variants.

Differential Diagnosis

CategoryFeaturesBone Age
Constitutional delayShort for age but normal growth velocity; delayed puberty; family history of "late bloomers"; will reach normal adult heightDelayed (predicts more growth remaining)
Familial short statureShort parents; growing along low-but-consistent percentile; normal growth velocity; normal puberty timingNormal (matches chronologic age)
GH deficiencySevere short stature; declining growth velocity (<5 cm/yr after age 2); increased truncal adiposity; micropenis/midline defects; neonatal hypoglycemiaDelayed
HypothyroidismGrowth deceleration, weight gain, fatigue, constipation, delayed pubertyDelayed
Turner syndrome (45,X)Short stature, webbed neck, shield chest, coarctation, streak gonads, primary amenorrhea; affects girls onlyMildly delayed
Skeletal dysplasiasDisproportionate short stature (limb vs trunk); achondroplasia most commonVariable
Chronic diseaseIBD, celiac, renal failure, cystic fibrosis, chronic steroid useDelayed

Workup

Initial evaluation: growth velocity calculation (plot serial heights), bone age X-ray (left hand and wrist, Greulich-Pyle atlas), CBC, CMP, ESR, TSH/free T4, celiac panel (TTG-IgA), IGF-1 and IGFBP-3 (GH axis screening). If IGF-1 low, GH stimulation testing (clonidine or arginine) is the gold standard for GH deficiency diagnosis. Karyotype in all short girls (to rule out Turner syndrome).

Bone age is the single most useful test in the evaluation of short stature. A delayed bone age means the growth plates are still open and the child has more growth potential. A normal bone age in a short child suggests familial short stature (less "catch-up" potential).

30 Precocious & Delayed Puberty

Tanner Staging

StageGirls (Breast)Girls (Pubic Hair)Boys (Genitalia)Boys (Pubic Hair)
IPrepubertalNonePrepubertalNone
IIBreast buds (thelarche)Sparse, straight, medial labiaTesticular enlargement (>4 mL / >2.5 cm)Sparse, base of penis
IIIBreast elevationDarker, curlier, over monsPenile lengtheningDarker, curlier
IVAreola forms secondary moundAdult-type, not to thighsPenile widening, glans developmentAdult-type, not to thighs
VAdult contourAdult, extends to thighsAdultAdult, extends to thighs
Normal puberty onset: girls 8–13 years (thelarche first), boys 9–14 years (testicular enlargement first). Menarche occurs ~2.5 years after thelarche, typically at Tanner stage IV. Peak height velocity: girls at Tanner II–III (before menarche), boys at Tanner III–IV.

Precocious Puberty

Defined as onset of secondary sexual characteristics before age 8 in girls or 9 in boys.

TypeMechanismCausesWorkup / Treatment
Central (GnRH-dependent)Premature activation of HPG axis; follows normal pubertal sequenceIdiopathic (most common in girls); CNS tumors (hamartoma, astrocytoma), hydrocephalus, radiationBone age, LH/FSH (LH predominant), estradiol/testosterone, brain MRI; treat with GnRH agonist (leuprolide)
Peripheral (GnRH-independent)Sex steroids from gonads or adrenals, independent of HPG axisCAH, adrenal tumors, gonadal tumors, McCune-Albright syndrome, exogenous hormonesSuppressed LH/FSH with elevated sex steroids; adrenal/gonadal imaging; treat underlying cause

Delayed Puberty

No breast development by age 13 in girls; no testicular enlargement by age 14 in boys. Most common cause in both sexes: constitutional delay. Pathologic causes include hypogonadotropic hypogonadism (Kallmann syndrome — associated with anosmia), hypergonadotropic hypogonadism (Turner syndrome in girls, Klinefelter syndrome in boys), chronic disease, and eating disorders.

31 Pediatric Diabetes

Type 1 Diabetes

Autoimmune destruction of pancreatic beta cells; accounts for ~95% of diabetes in children <10 years. Presentation: polyuria, polydipsia, polyphagia, weight loss over days to weeks. ~30–40% present in DKA at diagnosis. Autoantibodies: GAD65, IA-2, insulin autoantibodies (IAA), ZnT8.

DKA Management in Children

Pediatric DKA — Cerebral Edema Risk

DKA is defined as glucose >200 mg/dL + pH <7.30 or bicarb <15 + ketonemia/ketonuria. The most feared complication of pediatric DKA treatment is cerebral edema (0.5–1% incidence, 21–24% mortality). Risk factors: young age, new-onset DM, severe DKA, rapid fluid administration, rapid glucose decline, failure of Na+ to rise with treatment. Management protocol: (1) IV NS bolus 10–20 mL/kg over 1 hour for hemodynamic instability (avoid rapid bolusing if hemodynamically stable); (2) Calculate fluid deficit and replace over 24–48 hours (not faster); (3) Start insulin infusion 0.05–0.1 units/kg/hr (no bolus) AFTER 1 hour of fluids; (4) Target glucose decline ≤50–100 mg/dL/hr; (5) Monitor neurologic status hourly.

DKA SeveritypHBicarbonateClinical
Mild7.20–7.3010–15 mEq/LAlert, tolerating oral fluids
Moderate7.10–7.195–9 mEq/LKussmaul respirations, may be drowsy
Severe<7.10<5 mEq/LObtunded, hemodynamically unstable

Type 2 Diabetes in Adolescents

Rising incidence parallel to the obesity epidemic, particularly in minority populations (Native American, Black, Hispanic, Asian/Pacific Islander). Typically presents in overweight/obese adolescents (age ≥10 or pubertal) with acanthosis nigricans, family history, and insidious onset. C-peptide is normal or elevated (vs. low in T1DM). Treatment: lifestyle modification + metformin (FDA-approved ≥10 years); insulin if HbA1c >8.5% or symptomatic hyperglycemia at presentation.

Always check for autoantibodies in obese children presenting with diabetes — up to 10% of children initially diagnosed with T2DM actually have T1DM (or "double diabetes"). Incorrect classification delays appropriate insulin therapy.

32 Febrile Seizures

Febrile seizures are the most common seizure type in children, affecting 2–5% of children ages 6 months to 5 years. They occur in the setting of fever (≥38°C / 100.4°F) without evidence of CNS infection or other defined cause.

Simple vs. Complex

FeatureSimple Febrile SeizureComplex Febrile Seizure
Duration<15 minutes≥15 minutes
TypeGeneralized (tonic-clonic)Focal features
Recurrence in 24 hrDoes not recurRecurs within 24 hours
PostictalBriefMay be prolonged; focal deficit (Todd paralysis)

Management

ScenarioApproach
Simple febrile seizure, well-appearing, recoveredReassurance; identify source of fever; NO EEG, NO imaging, NO LP (in ≥12 months fully immunized); counsel on recurrence risk
Complex febrile seizureConsider LP (especially if <12 months, partially immunized, or pretreated with antibiotics); consider EEG; neuroimaging if focal features
Febrile status epilepticus (>5 min)Benzodiazepine (midazolam intranasal 0.2 mg/kg or diazepam rectal 0.5 mg/kg); ABCs; identify/treat infection
Recurrence risk: ~33% after first simple febrile seizure (higher if <18 months at onset, lower temperature at seizure, or family history). Risk of epilepsy: simple febrile seizure → ~1% (same as general population); complex febrile seizure → 2–10%.
Antipyretics (acetaminophen, ibuprofen) treat fever for comfort but do NOT prevent febrile seizures. Parents should be counseled that febrile seizures, while frightening, are almost always benign, do not cause brain damage, and do not predict epilepsy in the vast majority of cases.

33 ADHD

Attention-deficit/hyperactivity disorder is the most common neurodevelopmental disorder in children, affecting ~8–10% of school-age children. Boys are diagnosed 2–3× more often than girls (partly due to more externalizing behavior; girls more often present with inattentive type).

DSM-5 Diagnostic Criteria

≥6 symptoms (or ≥5 if age ≥17) of inattention and/or hyperactivity-impulsivity, present for ≥6 months, in ≥2 settings (school, home, work), with onset before age 12. Symptoms must cause functional impairment and not be better explained by another mental disorder.

PresentationFeatures
Predominantly InattentiveDifficulty sustaining attention, careless mistakes, poor organization, loses things, easily distracted, forgetful
Predominantly Hyperactive-ImpulsiveFidgets, leaves seat, runs/climbs inappropriately, talks excessively, interrupts, difficulty waiting turn
CombinedMeets criteria for both inattention and hyperactivity-impulsivity (most common presentation)

Treatment

AgeFirst-LineDetails
4–5 yearsBehavioral therapy (parent training)Medication only if behavioral therapy fails; methylphenidate if needed
6–11 yearsFDA-approved medication AND/OR behavioral therapyStimulants are first-line: methylphenidate (Ritalin, Concerta) or amphetamines (Adderall, Vyvanse)
≥12 yearsFDA-approved medication with or without behavioral therapyStimulants first-line; non-stimulants (atomoxetine, guanfacine, clonidine) for those who cannot tolerate stimulants

Monitoring

Before starting stimulants: height, weight, blood pressure, heart rate, personal/family cardiac history. Monitor every 3–6 months: growth parameters (stimulants can suppress appetite/growth), BP, HR, symptom control, side effects (insomnia, appetite suppression, irritability, headache). No routine ECG required unless cardiac history or symptoms.

Stimulant medications are Schedule II controlled substances with potential for diversion and abuse. However, appropriately treated ADHD actually REDUCES the risk of substance use disorders compared to untreated ADHD. The benefit-risk ratio strongly favors treatment in appropriately diagnosed children.

34 Autism Spectrum Disorder

ASD is a neurodevelopmental disorder characterized by persistent deficits in social communication/interaction and restricted, repetitive behaviors/interests. Prevalence: ~1 in 36 children (CDC 2023), with 4:1 male-to-female ratio.

DSM-5 Criteria (Both Required)

DomainExamples
A. Deficits in social communication and social interaction (all three must be present)(1) Deficits in social-emotional reciprocity (back-and-forth conversation, shared interests, emotions). (2) Deficits in nonverbal communication (eye contact, gestures, facial expression). (3) Deficits in developing/maintaining relationships (adjusting behavior to context, sharing play, making friends).
B. Restricted, repetitive behaviors (at least 2 of 4)(1) Stereotyped movements, speech, or object use (echolalia, hand flapping, lining up toys). (2) Insistence on sameness, inflexible routines. (3) Highly restricted, fixated interests (abnormal intensity). (4) Hyper- or hyporeactivity to sensory input.

Screening & Diagnosis

AAP recommends universal screening with M-CHAT-R/F at 18 and 24 months. Early signs include lack of pointing by 12 months, no single words by 16 months, no 2-word phrases by 24 months, lack of joint attention, and regression of language or social skills. Diagnosis is made by comprehensive developmental evaluation (developmental pediatrician, child psychologist, or multidisciplinary team) using standardized tools (ADOS-2, ADI-R).

Management

InterventionDetails
Applied Behavior Analysis (ABA)Gold-standard behavioral intervention; intensive, early initiation (<3 years) yields best outcomes
Speech-language therapyFor communication deficits; augmentative/alternative communication (AAC) devices if needed
Occupational therapySensory integration, fine motor skills, daily living activities
MedicationsNo medication treats core ASD symptoms. Risperidone and aripiprazole are FDA-approved for irritability/aggression in ASD (age ≥5–6). SSRIs for anxiety, stimulants for comorbid ADHD.
Educational supportIEP (Individualized Education Program) under IDEA; structured environment; social skills training
Early intensive behavioral intervention (before age 3) can significantly improve cognitive, language, and adaptive outcomes in children with ASD. The window of maximal neural plasticity makes early identification and referral critical. "If in doubt, refer" — a negative evaluation is better than a missed diagnosis.

35 Pediatric Resuscitation

Pediatric cardiac arrest is most often due to respiratory failure or shock (asphyxia), unlike adult arrest which is usually primary cardiac (VF/VT). The most common preterminal rhythm in children is bradycardia progressing to PEA/asystole. Early recognition of respiratory distress and shock, before arrest occurs, is the most impactful intervention.

PALS Key Algorithms

RhythmManagement
Asystole / PEACPR (15:2 ratio with 2 rescuers); epinephrine 0.01 mg/kg (0.1 mL/kg of 1:10,000) IV/IO q3–5 min; identify and treat reversible causes (H’s and T’s)
VF / Pulseless VTCPR + defibrillation 2 J/kg → 4 J/kg → max 10 J/kg; epinephrine q3–5 min; amiodarone 5 mg/kg (max 300 mg) or lidocaine 1 mg/kg
Bradycardia with poor perfusionOxygenation/ventilation first; if HR <60 despite adequate ventilation with O2: start CPR; epinephrine 0.01 mg/kg; atropine 0.02 mg/kg (min 0.1 mg) if vagal
SVT with pulsesVagal maneuvers (ice to face in infants); adenosine 0.1 mg/kg rapid IV push (max 6 mg), may repeat at 0.2 mg/kg (max 12 mg); synchronized cardioversion 0.5–1 J/kg if unstable

Weight-Based Equipment & Dosing

The Broselow tape (length-based resuscitation tape) provides rapid weight estimation and corresponding drug doses, equipment sizes, and defibrillation energy for children up to ~36 kg. Weight estimation formula: weight (kg) = (age in years × 2) + 8 for children 1–10 years.

Vascular Access

If IV access cannot be obtained within 60–90 seconds in a critically ill child, intraosseous (IO) access should be established. Preferred site: proximal tibia (1–2 cm below tibial tuberosity on medial flat surface). Alternative sites: distal tibia, distal femur, humeral head. Any medication or fluid that can be given IV can be given IO.

The H’s and T’s of Pediatric Cardiac Arrest

H’s: Hypovolemia (most common treatable cause), Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia, Hypoglycemia (especially in infants). T’s: Tension pneumothorax, Tamponade, Toxins/poisons, Thrombosis (pulmonary embolism), Trauma.

In pediatric arrest, the compression-to-ventilation ratio is 15:2 for two-rescuer CPR (vs. 30:2 for single rescuer and for adults). This reflects the primacy of respiratory failure as the cause of pediatric arrest. Compression depth is at least 1/3 AP diameter of chest (~4 cm in infants, ~5 cm in children). Rate: 100–120/min.

36 Non-Accidental Trauma

Child abuse is tragically common: ~700,000 confirmed cases annually in the U.S., with ~1,750 fatalities per year. Children <3 years are at highest risk. All healthcare providers are mandatory reporters in all 50 states — suspected abuse must be reported even without proof. Reporting in good faith is legally protected.

Red Flags for Non-Accidental Injury

FindingSignificance
Injuries inconsistent with developmental stagee.g., "fell off couch" in a pre-mobile infant
Changing/inconsistent historyStory changes between caregivers or over time
Delay in seeking careSignificant injury presented hours to days later
Patterned bruisingBelt marks, loop marks, bite marks, hand prints; bruises in various stages of healing
Bruising in non-mobile infants"Those who don’t cruise rarely bruise" — any bruise in a pre-cruising infant is concerning
Specific fracture patternsClassic metaphyseal lesions (corner/bucket-handle fractures), rib fractures (especially posterior), spiral fractures of long bones in non-ambulatory children, multiple fractures in different stages of healing
Retinal hemorrhagesStrongly associated with abusive head trauma (shaken baby syndrome); multi-layer, bilateral; rare in accidental injury
Subdural hematomasEspecially bilateral or interhemispheric; in combination with retinal hemorrhages = highly suspicious for abusive head trauma
BurnsStocking/glove pattern (immersion), well-demarcated, circular (cigarette), pattern burns (iron, grill); sparing of flexion creases (child pulled limbs in)

Workup

Skeletal survey (full body radiographic series) in all children <2 years with suspected abuse. Head CT for all children <6 months with suspected abuse (or any age with neurologic symptoms). Ophthalmologic exam for retinal hemorrhages. Labs: CBC, CMP, coagulation studies, lipase, urinalysis (to rule out bleeding disorders and assess for occult organ injury).

The triad of subdural hematomas + retinal hemorrhages + encephalopathy in an infant, especially with no or inadequate accidental explanation, is the classic presentation of abusive head trauma (formerly "shaken baby syndrome"). This remains a clinical diagnosis — the specificity of this triad for abuse is >95% when accidental mechanisms and medical conditions are excluded.

37 Foreign Body Ingestion & Poisoning

Foreign Body Ingestion

ObjectUrgencyManagement
Button battery (disk/coin battery)EMERGENTIf in esophagus: endoscopic removal within 2 hours (generates hydroxide at negative pole → liquefactive necrosis → esophageal perforation, aortoesophageal fistula, death). If past esophagus: may observe if asymptomatic, but close follow-up. Honey (sucralfate in some protocols) can mitigate injury pre-removal.
Magnets (≥2 or magnet + metal)EMERGENTCan attract through bowel walls → pressure necrosis, perforation, fistula. Endoscopic or surgical removal.
CoinsModerateMost common ingested foreign body. Esophageal: endoscopic removal if symptomatic or stuck >24 hours. Gastric/distal: observe, most pass spontaneously in 1–4 weeks.
Sharp objects (pins, bones)HighEndoscopic removal if in esophagus or stomach (risk of perforation). If beyond reach of endoscope and asymptomatic, observe with serial radiographs. Surgical removal if signs of perforation.
Button Battery in Esophagus — Emergency

A button battery lodged in the esophagus can cause severe injury within 2 hours. It generates an electrical current and creates hydroxide at the negative pole, causing liquefactive necrosis. Complications include esophageal perforation, tracheoesophageal fistula, mediastinitis, and fatal aortoesophageal fistula. AP/lateral X-ray shows a "double ring" or "halo" sign (distinguishing it from a coin). Emergent endoscopic removal is mandatory. Do NOT induce vomiting.

Common Pediatric Poisonings

SubstanceKey FeaturesManagement
AcetaminophenMost common pediatric poisoning; toxic dose >150 mg/kg; liver failure if untreated; Rumack-Matthew nomogram guides treatmentN-acetylcysteine (NAC) within 8 hours of ingestion; 72-hour IV or 72-hour oral protocol
IronGI hemorrhage, metabolic acidosis, hepatotoxicity; abdominal X-ray may show pills; serum iron >500 mcg/dL = severeWhole bowel irrigation; deferoxamine chelation if serum iron >500 or symptomatic
LeadChronic: developmental delay, behavior changes, abdominal pain, anemia, basophilic stippling; Acute: encephalopathy (>70 mcg/dL)BLL 3.5–44: environmental investigation, follow-up. BLL 45–69: oral succimer (DMSA). BLL ≥70: IV CaNa2EDTA ± dimercaprol; hospitalize
HydrocarbonsAspiration pneumonitis is the main risk; do NOT induce emesis; CNS depression with high volatilitySupportive care; monitor for aspiration; do NOT give activated charcoal (risk of aspiration)
Caustics (alkali/acid)Alkali: liquefactive necrosis (deeper injury). Acid: coagulative necrosis (self-limiting). No emesis, no charcoal, no NG tubeEndoscopy within 12–24 hours to assess injury grade; supportive care
Poison Control Center: 1-800-222-1222 (U.S.). Call for any suspected poisoning. Available 24/7, staffed by pharmacists and toxicologists. Most pediatric ingestions can be managed at home with their guidance.
"One pill can kill" drugs in toddlers: sulfonylureas (hypoglycemia), calcium channel blockers (cardiovascular collapse), opioids (respiratory depression), tricyclic antidepressants (seizures, arrhythmias), clonidine (CNS depression, bradycardia), and camphor (seizures). A single tablet or teaspoon of these agents can be lethal in a 10 kg child.

38 Pediatric Vital Signs by Age

AgeHeart Rate (bpm)Respiratory RateSystolic BP (mmHg)Diastolic BP (mmHg)Weight (kg, est.)
Premature120–17040–7055–7535–451–2.5
Newborn (0–28 days)120–16030–6060–7630–452.5–4
1–6 months100–15025–5072–10437–564–7
6–12 months90–14025–4072–10437–567–10
1–3 years90–14020–3086–10642–6310–14
4–5 years80–12020–2589–11246–7214–20
6–9 years70–11018–2297–11557–7620–30
10–12 years60–10016–20102–12061–8030–45
13–18 years60–10012–20110–13164–8345–70

ETT Size by Age

AgeUncuffed ETT (mm ID)Cuffed ETT (mm ID)
Premature2.5–3.0
Newborn3.0–3.53.0
1–2 years4.0–4.53.5–4.0
>2 years(Age/4) + 4(Age/4) + 3.5
Quick formulas: Uncuffed ETT = (age/4) + 4; Cuffed ETT = (age/4) + 3.5; ETT depth (cm at lip) = 3 × ETT size. Suction catheter = 2 × ETT size.

39 Classification Systems

APGAR Score

See Section 08 for full APGAR scoring table. Assessed at 1 and 5 minutes. Score 7–10 = reassuring; 4–6 = moderately depressed; 0–3 = severely depressed.

Tanner Staging

See Section 30 for full Tanner staging table. Stages I (prepubertal) through V (adult) for breast/genital and pubic hair development.

WHO Dehydration Classification

ClassificationSignsTreatment Plan
No dehydrationNot enough signs to classify as some or severe dehydrationPlan A: ORS after each loose stool (10 mL/kg); continue feeding
Some dehydration (≥2 signs)Restless/irritable, sunken eyes, drinks eagerly/thirsty, skin pinch goes back slowlyPlan B: ORS 75 mL/kg over 4 hours; reassess
Severe dehydration (≥2 signs)Lethargic/unconscious, sunken eyes, unable to drink, skin pinch goes back very slowly (≥2 sec)Plan C: IV Ringer’s lactate 100 mL/kg over 3–6 hours (age-dependent); NGT or ORS if IV unavailable

Asthma Severity Classification

See Section 13 for full classification table (Intermittent, Mild Persistent, Moderate Persistent, Severe Persistent).

VUR Grading (International Reflux Study)

See Section 21 for full VUR grading table (Grades I–V based on VCUG findings).

Modified Bell Staging for NEC

See Section 24 for full NEC staging (Stage I = suspected, Stage II = definite with pneumatosis, Stage III = advanced with perforation).

Westley Croup Score

Parameter01235
Chest wall retractionsNoneMildModerateSevere
StridorNoneWith agitationAt rest
CyanosisNoneWith agitation / at rest (4/5)
Air entryNormalDecreasedMarkedly decreased
Level of consciousnessNormalAltered (5)
Westley score: ≤2 mild, 3–7 moderate, ≥8 severe. Maximum score = 17.

40 Medications Master Table

Common Pediatric Antibiotics (Weight-Based Dosing)

DrugDoseRouteCommon Indication
Amoxicillin40–90 mg/kg/day ÷ BID-TIDPOAOM (80–90 mg/kg/day), pharyngitis (50 mg/kg/day), pneumonia, UTI
Amoxicillin-clavulanate90 mg/kg/day of amoxicillin component ÷ BIDPOResistant AOM, sinusitis, bite wounds
Azithromycin10 mg/kg day 1 (max 500 mg), then 5 mg/kg (max 250 mg) days 2–5POAtypical pneumonia, pertussis, Chlamydia trachomatis
Cephalexin25–50 mg/kg/day ÷ BID-QIDPOSkin/soft tissue, UTI, pharyngitis (penicillin-allergic)
Ceftriaxone50–100 mg/kg/day ÷ QD-BID (max 4 g/day)IV/IMMeningitis (100 mg/kg), pneumonia, UTI; avoid in neonates <28 days
Cefdinir14 mg/kg/day ÷ QD-BID (max 600 mg/day)POAOM, sinusitis (penicillin-allergic); turns stools red (not blood)
TMP-SMX8–12 mg/kg/day of TMP component ÷ BIDPOUTI, MRSA skin infections (in children >2 months)
Clindamycin30–40 mg/kg/day ÷ TID-QIDPO/IVMRSA, bone/joint infections, dental infections

Antipyretics & Analgesics

DrugDoseIntervalNotes
Acetaminophen10–15 mg/kg/dose (max 75 mg/kg/day or 4 g/day)q4–6hUse from birth; no anti-inflammatory effect; hepatotoxic in overdose
Ibuprofen10 mg/kg/dose (max 40 mg/kg/day or 2.4 g/day)q6–8hUse from age ≥6 months; anti-inflammatory; avoid in dehydration (renal risk)

Asthma Medications

DrugDoseNotes
Albuterol (MDI)4–8 puffs via spacer q20min ×3 (acute); 2 puffs q4–6h PRN (maintenance)Use spacer + mask in children <5 years
Albuterol (nebulizer)2.5 mg (<20 kg) or 5 mg (>20 kg) q20min ×3 (acute)Continuous nebulization 0.5 mg/kg/hr for severe exacerbation
Ipratropium bromide0.25–0.5 mg nebulized q20min ×3Only for acute exacerbation; not for maintenance
Prednisolone/Prednisone1–2 mg/kg/day (max 60 mg) ×3–5 daysOral; no taper needed for short course
Dexamethasone0.6 mg/kg ×1–2 doses (max 16 mg)Alternative to 5-day prednisone course; better compliance
Montelukast4 mg (2–5 yr), 5 mg (6–14 yr), 10 mg (≥15 yr) QHSLTRA; FDA black box warning for neuropsychiatric events

PALS Resuscitation Drugs

DrugDoseIndication
Epinephrine0.01 mg/kg (0.1 mL/kg of 1:10,000) IV/IO q3–5 minCardiac arrest, symptomatic bradycardia
Amiodarone5 mg/kg IV/IO (max 300 mg); may repeat ×2VF/pulseless VT refractory to defibrillation
Adenosine0.1 mg/kg (max 6 mg) rapid IV push; repeat: 0.2 mg/kg (max 12 mg)SVT (with pulses)
Atropine0.02 mg/kg (min 0.1 mg, max 0.5 mg child / 1 mg adolescent)Symptomatic bradycardia (vagal)
DextroseD10W: 5 mL/kg (neonates); D25W: 2–4 mL/kg (infants/children)Hypoglycemia
Naloxone0.1 mg/kg IV/IM/IN (max 2 mg); may repeatOpioid reversal
Calcium chloride 10%20 mg/kg (0.2 mL/kg) slow IV pushHyperkalemia, calcium channel blocker overdose, hypocalcemia
Magnesium sulfate25–50 mg/kg IV (max 2 g) over 15–20 minTorsades de pointes, severe refractory asthma
Broselow tape being used alongside a child to estimate weight and determine appropriate equipment sizes and drug doses
Figure 4 — Broselow Tape. A length-based resuscitation tape used to rapidly estimate a child’s weight and determine age-appropriate equipment sizes and drug doses in emergency situations. Source: Wikimedia Commons. Licensed under CC BY-SA 3.0.

41 Abbreviations Master List

AAPAmerican Academy of Pediatrics ABRAuditory brainstem response ACIPAdvisory Committee on Immunization Practices ADHDAttention-deficit/hyperactivity disorder AGAAppropriate for gestational age AOMAcute otitis media APGARAppearance, Pulse, Grimace, Activity, Respiration ARFAcute rheumatic fever ASDAtrial septal defect / Autism spectrum disorder BPDBronchopulmonary dysplasia CAHCongenital adrenal hyperplasia CDCCenters for Disease Control and Prevention CFCystic fibrosis CHDCongenital heart disease CMVCytomegalovirus CoNSCoagulase-negative Staphylococci CPAPContinuous positive airway pressure DKADiabetic ketoacidosis DMSADimercaptosuccinic acid (renal scan) DTaPDiphtheria, tetanus, acellular pertussis vaccine ECMOExtracorporeal membrane oxygenation ELBWExtremely low birth weight (<1,000 g) ETTEndotracheal tube FTTFailure to thrive GAGestational age GASGroup A Streptococcus GBSGroup B Streptococcus GHGrowth hormone HFNCHigh-flow nasal cannula HibHaemophilus influenzae type b HMDHyaline membrane disease (RDS) HPVHuman papillomavirus HSVHerpes simplex virus IAPIntrapartum antibiotic prophylaxis ICSInhaled corticosteroid IEPIndividualized Education Program iNOInhaled nitric oxide IOIntraosseous IPVInactivated poliovirus vaccine IVHIntraventricular hemorrhage IVIGIntravenous immunoglobulin KDKawasaki disease LABALong-acting beta-agonist LAIVLive attenuated influenza vaccine LTRALeukotriene receptor antagonist MASMeconium aspiration syndrome M-CHATModified Checklist for Autism in Toddlers MMRMeasles, mumps, rubella vaccine NAEPPNational Asthma Education and Prevention Program NATNon-accidental trauma NECNecrotizing enterocolitis NICUNeonatal intensive care unit OAEOtoacoustic emissions ORSOral rehydration solution PALSPediatric Advanced Life Support PATPediatric Assessment Triangle PCVPneumococcal conjugate vaccine PDAPatent ductus arteriosus PGE1Prostaglandin E1 (alprostadil) PKUPhenylketonuria PMAPostmenstrual age PPHNPersistent pulmonary hypertension of the newborn RDSRespiratory distress syndrome RSVRespiratory syncytial virus RUSPRecommended Uniform Screening Panel SABAShort-acting beta-agonist SBISerious bacterial infection SCIDSevere combined immunodeficiency SGASmall for gestational age TGATransposition of the great arteries TOFTetralogy of Fallot TORCHToxoplasmosis, Other (syphilis), Rubella, CMV, HSV TPNTotal parenteral nutrition TTG-IgATissue transglutaminase IgA TTNTransient tachypnea of the newborn VCUGVoiding cystourethrogram VLBWVery low birth weight (<1,500 g) VSDVentricular septal defect VURVesicoureteral reflux VZVVaricella-zoster virus

42 Growth Charts & Screening Schedules

Well-Child Visit Schedule (AAP / Bright Futures)

VisitAgeKey Activities
Newborn3–5 daysWeight check, jaundice assessment, feeding evaluation, newborn screen results
1 month1 monthGrowth, HepB #2, feeding, development
2 months2 monthsDTaP #1, IPV #1, Hib #1, PCV #1, RV #1; developmental surveillance
4 months4 monthsDTaP #2, IPV #2, Hib #2, PCV #2, RV #2
6 months6 monthsDTaP #3, Hib #3, PCV #3, HepB #3; start flu vaccine; introduce solids
9 months9 monthsDevelopmental screening (ASQ); developmental surveillance
12 months12 monthsMMR #1, Varicella #1, HepA #1, Hib booster, PCV booster; lead/Hb screen
15 months15 monthsDTaP #4; developmental surveillance
18 months18 monthsHepA #2; M-CHAT autism screen; developmental screening
24 months24 monthsM-CHAT autism screen; developmental screening; lead screen
30 months30 monthsDevelopmental screening
Annual visits3–21 yearsGrowth, BP (starting age 3), vision (3–5 yr), dental referral, anticipatory guidance, age-appropriate vaccines
11–12 yearsPreadolescentTdap, HPV, MenACWY; lipid screen (9–11 yr); depression screen starts at 12

Growth Chart Reference Points

MilestoneExpected
Birth weight doubles4–5 months
Birth weight triples12 months
Birth weight quadruples24 months
Birth length increases 50%12 months
Birth length doubles4 years
Adult height = 2 × height at age 2Rough estimate
Head circumference at birth~35 cm (equals chest circumference)
Anterior fontanelle closes9–18 months (average 12–14 months)
Posterior fontanelle closes2–3 months
CDC growth chart for boys aged 2 to 20 years showing height and weight percentile curves
Figure 5 — CDC Growth Chart. Example of a CDC growth chart for boys aged 2–20 years showing stature-for-age and weight-for-age percentiles. Growth charts are the primary tool for monitoring growth in pediatrics. Source: Wikimedia Commons, CDC. Public domain.

References

  1. American Academy of Pediatrics. Bright Futures: Guidelines for Health Supervision of Infants, Children, and Adolescents, 4th ed. AAP, 2017.
  2. Kliegman RM, St Geme JW, et al. Nelson Textbook of Pediatrics, 21st ed. Elsevier, 2020.
  3. American Academy of Pediatrics, Subcommittee on Hyperbilirubinemia. "Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation." Pediatrics. 2004;114(1):297–316.
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