Pediatrics Cardiology

1. Acute rheumatic fever

a. Patho: infection with GABHS proceeding onset of RF by 2-6 weeks. Stimulates Ab production to host tissues and
damages organ directly
b. Etiology: MC between 5-15 YO
c. Complications: mitral (8o%), aortic (30%), tricuspid/pulmonic (5%) valvular dz. recurrences common if
myocarditis during initial infection
d. DX: Jones criteria:
i. Major Criteria: Joints (migratory polyarthritis), active carditis (mitral-80%/aortic-30%), nodules (subQ),
erythema marginatum (trunk), Sydenham’s chorea (purposeless movements-Saint Vitus dance).
ii. Minor criteria: include fever, ESR, prolonged PR interval
iii. Must also have recent evidence of GAS.
e. Symptoms:
i. Polyarthritis: 2 or more joints or migratory (UE->LE). Medium/large joints MC. Heat, redness, swelling,
severe tenderness
ii. Erythema marginatum: macular, erythematous, non-pruritic annular rash with sharp demarcated
borders (central clearing +/-). MC in trunk/extremities, not face. Hours to days
iii. Nodules: seem on extensor surfaces, scalp, spine
iv. Chorea: can occur 1-8 months after initial infection. Usually resolves on its own
v. Carditis
vi. Additional: abdominal pain, facial tics, epistaxis
f. TX: Aspirin +/- steroids if severe. Penicillin G abx of choice (erythromycin if allergy) both during and after acute
episode.
g. NOTE: Patients who have suffered acute rheumatic fever should receive secondary prophylaxis against group A
Streptococcus. For patients who are not allergic to penicillin, the prophylactic treatment of choice is with
penicillin G benzathine, administered intramuscularly every 21–28 days. The duration of prophylactic therapy
depends upon the age and health status of the patient at presentation. For a patient who has rheumatic fever
with carditis and echocardiographic evidence of persistent valvular disease, current recommendations call for
prophylaxis to continue for ten years or until age 40, whichever is longer. If NO carditis then give for 5 years or
until 21 YO.
2. Atrial Septal defect
a. Patho: hole in the atrial septum. 2nd MC cause of CHD 2/2 to VSD
b. Types: Ostium secundum (MC), ostium primum (MR?), sinus venosus, coronary sinus
c. Symptoms: (noncyanotic) most asymptomatic or minimal until >30 YO. May have recurrent respiratory
infections or failure to thrive. In adults->palpitations, atrial arrhythmias, syncope, HF, paradoxus embolism
d. PE: systolic ejection crescendo-decrescendo flow murmur @ LUSB (similar to PS). Wide split fixed S2 (does not
vary with respirations). Loud S1/hyperdynamic RV
e. DX: XR- cardiomegaly. ECG- incomplete RBBB, Crochetage sign (notching of the peak of R wave in inferior leads).
Echo is GS
f. TX: spontaneous closure likely in one year->observe if small. Otherwise surgery between 2 and 4 YO
g. Note: the murmur a mid-systolic pulmonary flow or ejection murmur with a fixed split second heart sound due
to the associated increased flow across the pulmonary valve caused by the left-to-right shunt (the defect itself
does not usually cause an audible murmur). The recommended approach to monitoring is pediatric cardio f/u
for clinically significant atrial septal defects, specifically defects greater than 3 mm in diameter. For pts with
smaller defects, no special follow-up is needed unless new signs or symptoms develop
3. Coarctation of the aorta
a. Patho: narrowing descending thoracic aorta. *Inc LV afterload w SNS and RAAS activation cause HTN, LVH, CHF
b. Symptoms: (noncyanotic) secondary HTN, bilateral claudication, syncope, infants may show failure to
thrive/poor feeding/shock. Think in->baby with HTN, claudication (refusal to walk, relief with sitting)
c. Types: Infantile-> preductal. Adult->postductal
d. PE: systolic murmur that radiates to the back/scapula/chest. BP in UE>LE. Delayed weak femoral pulses.
e. DX: XR- rib notching, ‘3 sign’ on narrowed aorta, ECG-LVH. Angiogram is Gold Standard.
f. TX: surgical correction; balloon angioplasty + stent. Prostaglandin E1 given preoperatively
4. Hypertrophic cardiomyopathy
a. Patho: genetic disorder caused by mutations in sarcomere proteins
i. Subaortic outflow obstruction: 2/2 to hypertrophied septum + SAM of mitral valve and papillary
muscle displacement.
1. SAM increased with contractility (digoxin, beta agonist, exercise) and decreased with dec LV
volume (dehydration, Valsalva)
ii. Diastolic dysfunction-> stiff ventricle causes impaired relaxation/filling
b. Symptoms: sudden cardiac death (esp with excursion due to Vfib), dyspnea (MC), chest pain, syncope,
arrhythmias (afib, VF/VT), palpitations
c. PE: harsh systolic crescendo-decrescendo murmur at LLSB (similar to AS) that is decreased with
squatting/supine/handgrip and increases with valsalva/standing. May have loud S4
d. DX: Echo shows asymmetrical wall thickness (septal), systolic anterior motion of the mitral valve, small LV
chamber, +/- MR. ECG- LVH, anterolateral and inferior pseudo q eaves
e. TX: ICD placement, counsel to avoid dehydration and extreme exertion. BB are 1st line medical tx (cation with
digoxin, nitrates, diuretics as they dec vent volume). Myomectomy if severe/refractory. Alcohol septal ablation
alternative to sx

5. Kawasaki disease (Mucocutaneous lymph node syndrome)

a. Patho: MC in children < 5 (Asian boys). Possible respiratory agent or viral pathogen with propensity towards
vascular tissue->small and medium necrotizing vasculitis of CORONARY arteries
b. Symptoms: (CREAM) conjunctivitis (bilateral and nonexudative), polymorphous rash, extremity changes
(desquamation/edema/erythema of pals and soles, Beau’s lines, arthritis), adenopathy (cervical), mucus
membrane (pharyngeal erythema, lip swelling and fissures, strawberry tongue)
c. DX: 5 day Fever plus 4 out of 5 above ^. Inc ESR/CRP, reactive thrombocytosis. Sterile pyuria. Do echo/angio if
heart involvement suspected
d. Complications: coronary artery arteritis-> coronary artery aneurysm, MI, pericarditis myocarditis, peripheral
artery occlusion
e. TX: IV immune globulin + high dose aspirin is mainstay. Steroids if refractory

6. Patent ductus arteriosus

a. Patho: communication between the descending thoracic aorta and PA
b. Symptoms: (noncyanotic) mostly asymptomatic, poor feeding, weight loss, pulmonary congestion.
c. Eisenmengers syndrome (pul HTN-> left to right shunt becomes right to left cyanotic shunt)
i. *also seen in TOF, VSD, PDA, +/- ASD*
d. PE: continuous machinery murmur loudest at pulmonic area, wide pulse pressure with bounding peripheral
pulses (loud S2). Eisengmener (normal hands, cyanotic toes)
e. DX: XR- normal. ECG- LVH/LAE. Echo is GS
f. TX: IV indomethacin 1st line. Surgical correction if failure (do before ages 1-3)

7. Syncope
a. Sudden, brief LOC assoc w/ loss of postural tone, with spontaneous recovery (NO post-ictal phase)
b. Etiology: usually benign, but must rule out life threatening
i. MCC in adolescents: dehydration – followed by: fear, pain medications
c. Life threatening conditions: Abrupt decrease in CO, either from arrhythmia or structural cardiac disease
i. Arrhythmias: typically tachycardia
1. Exogenous causes (metabolic disturbance or drug ingestion)
2. Inherited electrophysiologic abnormality
a. Brugada syndrome
i. ECG: pseudo-RBBB and persistent ST elevation in V1, V2, V3
b. Catecholaminergic polymorphic VTACH
c. Preexcitation syndrome (WPW)
d. Congenital short QT syndrome (QT <.30 sec)
ii. Structural heart disease: myocarditis or repaired congenital heart disease
1. HCM: common autosomal dominant disorder, asymmetric hypertrophy of L. ventricle, PT’s may
experience exertional syncope (athletes), MC cause of sudden cardiac death with exercise
 2. Coronary artery anomalies: teens and young adults; an abnormally located coronary artery (ex:
btw aorta and pulmonary artery) may become compressed during exercise →
MI/syncope/death
3. Arrhythmogenic R ventricular cardiomyopathy
4. Valvular aortic stenosis: typically asymptomatic in kids, but 5% have sudden cardiac death
5. Dilated cardiomyopathy: typically idiopathic, but may develop due to viral myocarditis, severe
anemia, muscular dystrophy
6. Pulmonary HTN: usually have exertional dyspnea prior to onset of syncope
7. Acute myocarditis: common viruses- coxsackie A and B, adenovirus
iii. Other: aortic stenosis or HCM as result of L ventricular outflow tract obstruction and compromised
systemic blood flow
iv. Heat illness:
1. Heat syncope occurs when athletes are unable to stand/walk due to lightheadedness or
syncope
2. Usually occurs immediately after completing race/workout, common at distance running events
3. Mechanism: abrupt decrease in venous return once athlete has finished event
4. Heat stroke may also cause collapse in assoc w/ progressive AMS, seizures or coma (elevated
core temp, tachypnea, tachycardia with hypotension, nausea, vomiting and diarrhea)
5. Prevention
a. drink electrolyte replacement solutions if practice is longer than 60 min
b. Wear lightweight, moisture wicking clothing
c. Avoid practicing mid day when temps are the highest
d. Water break intervals every 20-30 mins
v. Anaphylaxis: assoc w/ subtle early sxs->flushing, itching, hives, cough and bronchospasm, or abdominal
cramping
d. Common conditions causing syncope
i. Vasovagal syncope
1. MC cause of syncope in children (>50%)
2. Typically involves precipitating event and prodrome
a. Ppt: standing or stress (physical or emotional)
b. Prodrome: lightheadedness, dizziness, visual changes (decr acuity, tunnel vision or
double vision), nausea, pallor and diaphoresis
3. Mechanism: exaggeration of reflex-mediated alterations in vasomotor tone and HR normally
responsible for maintaining BP
ii. Breath holding spells
1. Typically 6-24 months of age, triggered by emotional insult (pain, anger, fear)
2. Cyanotic: breath holding → cyanosis → LOC
3. Pallid: LOC → breath holding
4. Brief posturing or tonic-clonic activity may occur with either type
5. Spells usually stop by 5 YO But child may develop vasovagal syncope
iii. Orthostatic hypotension
1. Syncope which occurs with postural change related to an abrupt drop in BP
2. Can result from volume depletion (hemorrhage or dehydration), pregnancy, anemia, anorexia
nervosa, meds (CCB, vasodilators, phenothiazines, diuretics)
iv. Toxic exposure
1. Decreased CO (barbs, TCA’s, phenothiazines)
2. Sudden LOC (cocaine, EtOH, marijuana, inhalants, opiates)
3. Severe CO poisoning → QT prolongation → syncope
a. Look for history of exposure, HA, nausea
v. Other
1. Hypoglycemia
a. Insulin-dependent diabetics
b. Prior to syncope feel weak, hungry, sweaty → agitation, confusion, AMS
2. Arrhythmias (non life threatening): SVT, bradycardia
3. POTS (postural tachycardia syndrome)
a. Form of orthostatic hypotension
 b. Excessive increase in HR (>40 bpm over baseline in kids and >30 bpm or to >20 bpm in
adults) that occurs with postural change
c. Common in teenage girls → palpitations, anxiety, dizziness, tremulousness
d. Dx: tilt table test
e. Tx: avoid precipitating factors, medications, dehydration and inactivity should be
avoided
i. Exercise
ii. Oral volume expansion (increased water and high salt diet) and
fludrocortisone
e. DDX:
i. Seizure: assoc w/ aura, prolonged tonic clonic activity and postictal phase
ii. Migraine syndromes: basilar migraines may present with LOC, ataxia, vertigo; LOC usually longer than
several seconds
iii. Hysteria/conversion disorder: MC in adolescents, events occur in the presence of an audience; no
hemodynamic or autonomic changes; may be prolonged, rarely result in injury
iv. Hyperventilation: assoc w/ emotional distress; pt may complain of chest pain, chest tightness, SOB,
lightheadedness, paresthesia, visual disturbances
v. Intentional strangulation activities: “the choking game”, game to produce euphoria caused by cerebral
hypoxia
vi. Narcolepsy: cataplexy, emotionally triggered muscle weakness w/ collapse that may mimic syncope;
assoc w/ chronic daytime sleepiness, hypnagogic hallucinations or sleep paralysis
1. Dx: nocturnal polysomnography and multiple sleep latency tests
2. Tx: behavioral and lifestyle modifications
a. Regular sleep-wake schedules, planned naps
b. Regular exercise
c. Safety considerations are important!

8. Tetralogy of Fallot
a. Patho: MC cyanotic congenital heart disease, right to left
i. RV outflow obstruction (PA stenosis) + RV hypertrophy + VSD + overriding aorta
b. Symptoms: (cyanotic) blue baby syndrome, exertional dyspnea, tet-spells (older kid, cyanosis relieved by
squatting)
c. Associations: Downs and DiGeorgi syndrome
d. PE: harsh holosystolic murmur @ LUSB (similar to PS), RV heave, clubbing
e. DX: XR- boot shaped heart (prominent RV), ECG- RVH/RAE. Echo is Gold Standard.
f. TX: surgical repair preformed in first 4-12 mos. Can give PGE1 infusion to keep ductus arteriosus patent in
cyanotic patient
g. Acute tx: The most readily available maneuver is to place the patient in a knee-to-chest position, which will
increase systemic vascular resistance. Next, oxygen can be administered which leads to decreased pulmonary
vascular resistance due to vasodilation. If these maneuvers are unsuccessful, subsequent treatment is to
administer morphine, which calms the pt, decreases tachycardia and normalizes the systemic venous return.

9. Ventricular septal defect

a. Patho: hole in ventricular septum, MC CHD. Left to right shunt/noncyanotic
b. Types:
i. Perimembranous (MC)- hole in LV outflow tract near tricuspid valve
ii. Muscular: multiple holes in a swiss cheese pattern
iii. Inlet/posterior- post to the septal leaflet of tricuspid valve
iv. Outlet/supacristal- beneath the pulmonic valve (AI?)
c. Symptoms:
i. Small-asymptomatic, may close on own. Restrictive-normal pressure maintained between ventricles
ii. Mode- excessive sweating and fatigue during feeds (from inc SNS 2/2 to dec CO), fatigue with feeding,
lack of growth, respiratory infections
iii. Large- more severe symptoms. nonrestrictive
d. PE: loud high pitched harsh holosystolic murmur at LLSB. If moderate may have +/- thrill, diastolic rumble at
mitral area (inc flow across area). If large may have signs of CHF
 e. DX: Echo preferred over cath. ECG-LVH, +/- combined RVH/LVH (Katz-Watchtel phenomenon). MRI or cath done
if other tests non diagnostic
f. TX: Restrictive VSD (left to right) had good prognosis. Most small ones close w/in 10 years. Otherwise, patch if
symptomatic or uncontrolled CHF/growth delays/recurrent resp infections. Large ones repaired by 2 YO to
prevent Pul HTN.

Murmur Pearls
a. S1: AV closure, loudest at apex. Exercise increases ventricular contraction  increased S1 intensity
b. S2: Semilunar closure, loudest at base. Physiologic split of S2 on inspiration. Fixed split seen with ASD/VSD or delayed P2
closure (Pul HTN, mitral regurg). Paradoxical split on expiration with delayed closure (prolonged LV emptying, LBB, aortic
stenosis)
c. S3: Normal in young-physiologic S3 disappears when patient sits or stands or low HR. If over 30 YO its protodiastolic
gallop and indicative of LV systolic failure
d. S4: may be heard/normal in infants and adults over 50. Pathologically seen with hypertension, LVH & artic stenosis
e. Harsh/rumbles=think stenosis. Blowing=think regurgitation
f. Location: Aortic-R 2nd ICS; Pulmonary- L2nd ICS, Tricuspid-L 4th ICS, mitral- 5th ICS (midclavicular) apex
g. Systolic murmurs grade 1-3/6 do not need investigation

Pediatric Function Murmurs

a. Stills murmur: MC innocent murmur, heard from 2 years of age-pre-adolescent. Early mid-systolic musical, vibratory,
noisy, twanging, high pitched murmur. Loudest at inferior aspect of LLSB & apex. Cause->Vibration of valve leaflets
b. Venous Hum: 2nd MC Cause->blood flowing from head to neck returning to heart. Grade 1-11 harsh systolic ejection
murmur. Best heard in ULSB/URSB (intraclavicular) and can be diastolic (only non-patho diastolic murmur)
c. Pulmonary ejection murmur: Cause->blood flowing across pulmonary valve into PA. Heard in mid-systole in second left
intercostal space Harsh

Congenital Cyanotic Heart Diseases

a. Truncus arteriosus
b. Transposition of great arteries
c. Tricuspid atresia
d. TOF
e. Total anomalous pulmonary venous return
Pediatric Endocrinology

1. DM
a. BG goals
i. Children <5: maintain blood glucose between 80-180
ii. School aged children: 80-150
iii. Adolescents: 70-130
b. Screening in children:
i. BMI for age/sex >85th % OR
ii. Weight for height > 85th % percentile OR
iii. Weight >120%
iv. PLUS 2 risk factors
v. Start at age 10/9-11 (puberty), screen with A1c, fasting glucose, or 2 hr OGTT, if normal repeat x 2-3
years
c. Diabetes Mellitus
i. Types
1. Type 1: pancreatic beta cell destruction. MC in children (<30)
a. Type 1a=autoimmune beta cell destruction triggered by environmental factor
b. Type 1 B: non-autoimmune beta cell destruction
2. Type 2: insulin resistance + relative impairment of secretion. MC over 40 and due to genetic
and environmental factors (weight gain + dec activity)
3. Gestational: during pregnancy
ii. Symptoms (type1) most are asymptomatic. Polyuria, polydipsia, polyphagia, weight loss, failure to
thrive. Most recognized symptoms are secondary to hyperglycemia (general malaise, headache,
weakness, irritable, ill-tempered), and glycosuria (increased frequency and volume, nocturia)
d. DX:
i. 8 hr Fasting plasma glucose >126 on 2 occasions is gold standard
ii. 2 hr oral glucose tolerance test >200 , normal <140(3hr GGT GS in gestational diabetes);
iii. Hgb A1C > 6.5% , normal <5.7(average BS over 10-12 weeks/3 months)
iv. Random plasma >200 AND symptoms of diabetes. No confirmation test needed
v. Measure antibodies: (GAD 26, IA-2) in Type 1
e. Screening: all adults >45 YO q3 yrs or any adult with BMI>25 + 1 risk factors
f. TX: Diet, exercise and lifestyle changes first in Type 11 DM->oral antihyperglycemic. Insulin therapy if cannon
control and is initial tx in Type 1 DM
g. Goals: Hgb A1C <7 (check every 3 months), LDL <100, TG<150, post-prandial glucose <180, pre-prandial 80-130
h. Oral Medications
i. Metformin: Dec hepatic production.1st line PO med. No hypoglycemia or weight gain. C/I in hepatic or
renal impairment due to lactic acidosis
ii. Sulfonylureas (Glipizide): stimulate pancreatic insulin secretion. Hypoglycemia MC s/e, weight gain, GI
upset
iii. A-glucosidase inhibitors (acarbose): delays intestinal absorption of glucose; S/E of hepatitis, diarrhea
iv. Thiazolidindeiones (Pioglitazone): increased insulin sensitivity @ peripheral receptor site (no pancreatic
cells). S/E of edema, cardiac toxicity (MI)
v. GP1- agonist/Glucagon like Peptide 1 agonist (exenatide): increase insulin secretion, dec glucose
production, delays gastric emptying. S/E of hypoglycemia, wt. loss. CI if gastroparesis
vi. DPP-4 inhibitor (sitgliptin): inhibits degradation of GLP-1. CI in renal failure, pancreatitis
vii. SGLT-2 inhibitors (Canagliflozin): lowers glucose renal threshold->urinary glucose excretions. S/E thirst,
UTI’s, DKA!!
i. Insulins:
i. Rapid acting (5-15 min): Lispro/Humalog, Aspart/Novolog->3-4 hr duration, given at meal
ii. Short acting (30-1hr): Regular/Humulin-R->4-6 hr, given 30-60 min prior to meal
iii. Intermittent (2-4 hr): NPH/Humalin -N, Lente->16-20 hr, covers insulin for half day or overnight
iv. Long acting (6-8 hr): Detemir/Levemir, Glargine/Lantus-> 20-30 hr, covers for full day (basal insulin)
and should not be mixed with other types of insulin in same syringe
 j. Other
i.failure of 2+ orals should prompt insulin therapy
ii.In hospital, stop orals, start insulin
iii.Life style reduce A1c by 1%, orals by 3%. Insulin should be started if A1C>9%
iv. If using insulin, use self-monitoring glucose checks. Start with pre-prandial, once under control but A1C
still high, add post-prandial checks
v. .5units/kg
*.3units/kg if Cr>1.3, Age >65, or BG<180
* Every 1 unit of insulin decreased BG by about 50 mg/d

2. Hypercalcemia
a. Etiology:
i. PTH mediated: Primary hyperparathyroidism MC overall (inc Ca + intact PTH + dec phosphate), +/-
secondary if compensated, tertiary
ii. PTH independent: Malignancy->mets or PTH-rp, vit D excess, thiazides, lithium, vit A excess, milk alkali
syndrome, familial hypcolciuric hypercalcemia, immobilization (2/2 bone turn over), vit D excess
(sarcoid,TB)
b. Symptoms: increases excitation threshold->stronger stimulus needed for contraction; most are asymptomatic.
Stones, painful bones/fractures (inc remodeling), abdominal ileus/constipation/N/V, and psychiatric moans
(weakness, fatigue, AMS, decreased DTR, depression, blurred vision)
c. DX: increased ionized Ca, total Ca corrected, 24 hr urinary Ca, 1,25 vit D levels, shortened QT interval with
prolonged PR interval and WRS widening
1. In the neonate also check serum protein, phosphate and PTH levels as well as the maternal
levels of calcium and PTH
d. TX: Severe-> IV saline->furosemide 1st line (loops diuretic enhance secretion). Avoid hydrochlorothiazide (inc Ca)
Can also give calcitonin in immediate case. Bisphosphonates and vigorous fluids are best for sustained
reduction. If mild  no treatment

3. Hypothyroidism
a. Definition: aka cretinism
i. Diagnosed by a decreased free T4 and may be the result of diseases of the thyroid gland (primary
hypothyroidism), abnormalities of the pituitary gland (secondary) or abnormalities of the hypothalamus
(tertiary).
ii. Congenital or acquired and may be associated with a goiter
1. MC cause is Hashimoto thyroiditis, in areas where iodine is deficient endemic cretinism is MC
iii. Congenital hypothyroidism: low T4, high TSH
iv. Isolated secondary or tertiary hypothyroidism: T4 is normal or low
b. Etiologies
i. Hypoplasia or aplasia of the thyroid gland
ii. Failure to secrete hormone secondary to enzyme deficiency
c. Clinical manifestations
i. Hypothermia, acrocyanosis, respiratory distress, large fontanelles, abdominal distension, lethargy and
poor feeding, prolonged jaundice, edema, umbilical hernia, mottled skin, constipation, large tongue,
dry skin, hoarse cry, somnolent, sluggish mental/physical, slow reflexes, decreased HR
ii. Acquired hypothyroidism should be suspected in any child who has a decline in growth velocity
especially if not associated with weight loss
iii. Untreated acquired hypothyroidism is associated with permanent developmental delay
iv. Hashimoto thyroiditis: firm, non tender euthyroid, hypothyroid or rarely hyper thyroid diffuse goiter
with a pebble like surface
a. Onset occurs after 6 years of age, more common in females
v. Specific symptoms and signs of hypothyroidism:
1. Ectodermal: poor growth, dull facies, dry scaly skin, sparse brittle hair, diminished sweating,
carotenemia, vitiligo
2. Circulatory: sinus bradycardia/heart block, cold extremities, cold intolerance, pallor, ECG
changes
 3. Neuromuscular: muscle weakness, hypotonia: constipation, potbelly, umbilical hernia,
myxedema coma, pseudohypertrophy of muscles, myalgia, physical and mental lethargy,
developmental delay, delayed relaxation of reflexes, paresthesia, cerebellar ataxia
4. Skeletal: delayed bone age, epiphyseal dysgenesis
5. Metabolic: myxedema, serous effusions, hoarse voice, weight gain, menstrual irregularity,
arthralgia, elevated CK, macrocytosis, hypercholesterolemia, hyperprolactinemia, precocious
puberty in severe cases
d. Laboratory tests and imaging
i. Newborn screening, crucial to make an early diagnosis and initiate thyroid therapy before 1 MONTH of
age
1. Heel stick test to evaluate TSH values
ii. When tertiary or secondary hypothyroidism is detected assessment of other pituitary hormones via MRI
is indicated
iii. Hashimoto thyroiditis- confirm diagnosis by serum antithyroid peroxidase and antithyroglobulin
antibodies.
1. Neither biopsy nor thyroid scan is indicated
iv. Obtain bone scan for baseline bone age and thyroid scan before starting tx
e. Treatment
i. levothyroxine
1. If initiated is 1 month or less, the prognosis for normal intellectual development is excellent,
screening programs usually offer therapy within 1-2 weeks of birth
2. If therapy is instituted after 6 months when severe sx present, intellectual fxn likelihood is decr
3. Test TSH and free T4 every 6-12 months

4. Hyperthyroidism
a. overview
i. MCC: Grave’s disease
ii. Elevated T3 and T4, decreased TSH
iii. Congenital hyperthyroidism: results from transplacental passage of maternal TSIs (thyroid stimulating
immunoglobulin) and may be masked for several days until the short lived effects of the transplacental
maternal antithyroid medication wear off
iv. Clinical hallmarks: irritability, tachycardia, polycythemia, craniosynostosis, bone age advancement,
poor feeding, failure to thrive
v. treatment : Methimazole, beta blocker, could have spontaneous resolution after 2-3 months
b. Clinical manifestations
i. Personality changes, mood instability, and poor school performance are common initial problems
ii. Tachycardia, palpitations, appetite changes, diarrhea, DOE, fatigue, heat intolerance
iii. Tremor, anxiety, inability to concentrate and weight loss
iv. Physical exam
1. Firm goiter is usually present, many patients complain of neck fullness
a. Palpitation of the thyroid gland is best performed with the examiner’s hands around
the neck from the back, watch the patient swallow
b. Auscultation may reveal a bruit over the gland
2. Pretibial myxedema, exophthalmos, lid lag, hyperreflexia
c. Laboratory tests and images
i. Elevated T3/T4, decreased TSH
ii. Monitor CBC, if WBC is suppressed stop anti-thyroid treatment- methimazole can cause
granulocytopenia
d. Treatment: 3 treatment choices are available--pharmacologic, radioactive iodine and surgical
i. Medical therapy:
1. Methimazole (first line) or propylthiouracil (second line because of liver injury/liver failure)
2. Beta blocker used to control cardiac manifestations- propranolol or atenolol
3. Medication is continued for 1-2 years
ii. radioiodine - takes longer to work and may cause permanent hypothyroidism
iii. Surgery- partial or complete thyroidectomy
e. Complications
 i. Thyroid storm: medical emergency consisting of tachycardia, disorientation, elevated blood pressure
and hyperthermia
1. Treatment includes:
a. Reducing hyperthermia with a cooling blanket
b. giving beta blockers
c. iodine may be given after an antithyroid medication
d. Hydrocortisone may be indicated for relative adrenal insufficiency
e. heart failure includes diuretics and digoxin

5. Obesity
a. BMI >95th %
b. Growth chart: >85% percentile
c. DX: 85-95th percentile (fasting lipid levels,), 94-95th percentile (lipids, AST/ALT/glucose) >95th (same)
d. Screen: age 2
e. Goals: <12 1lb/mo >12 2lb/mo
f. TX: >/= 5 servings of fruits/veggies, no more than 2 hours of screen time per day, minimized sweetened
beverages, address eating behaviors (avoid skipping breakfast), >1 hr of mod physical activity per day, involve
whole family in lifestyle changes
i. *only med >12 YO is Orlistat (lipase inhibitor)*
g. Prader-Willi syndrome is the most common syndromic form of obesity. The syndrome is caused by absence of
expression of the paternally active genes on the long arm of chromosome 15, also known as maternal
uniparental disomy. Indications for genetic testing in children ages 2 to 6 years old include hypotonia with a
history of poor suck and global developmental delays. May also see hypogonadism and behavioral issues

6. Short stature
a. Etiology:
i. Abnormal growth velocity:
1. CA>BA: malnutrition, chronic disorder, endocrine (hypothyroid, GH def)
2. CA=BA: malnutrition, chromosomal disorder (Pradar-Willi syndrome, Turner syndrome,
achondroplasia)
ii. Abnormal Growth velocity (Beyond 1-2 YO):
1. Family (genetic) short stature: CA=BA
2. Constitutional short stature (delay of growth and puberty): CA>BA
a. normal size at birth with decline at 3-6 months and attain normal growth as adult
b. Symptoms: height is 2 SD below the mean (< 5th % on growth chart) for individuals of same sex and
chronological age
c. Clinical manifestations (specifics)
i. Constitutional growth delay (CA>BA)
1. MCC of short stature and pubertal delay
2. Pts attain normal height by 18 YO
3. Growth charts show the following:
a. Normal birth wt and ht
b. Drop in % between 6mo and 3yrs
c. Reestablished growth velocity, following at 5th and 10th%
d. Will have normal growth spurt and adult height
ii. GH deficiency (CA>BA)
1. Infants with congenital GH deficiency achieve a normal birth length/ weight at term, but the
growth rate slows after birth (most noticeable after age 2-3)…normal growth spurt and adult
hood not achieved as in Constitutional growth delay?
2. Children appear chubby and short, cherub appearance (chubby, immature appearance), may
note increased truncal adiposity, with a high pitched voice resulting from an immature larynx
3. Normal intellectual growth and age appropriate speech most of the time
iii. Laron dwarfism- autosomal recessive disease (CA=BA)
1. Mutations of the GH receptor; growth hormone insensitivity
 2. Presents with a prominent forehead, hypoplastic nasal bridge, delayed dentition, sparse hair,
blue sclerae, delayed bone maturation and osteoporosis, progressive adiposity,
hypercholesterolemia and low blood glucose
iv. DX: evaluate growth rate (height velocity)-more sensitive indicator, check bone age, check nutrition.
Serial growth measurements.
a. If the height velocity is less than expected for age then further evaluation is necessary.
Another valuable calculation is projected height compared to midparental height. The
next step is a radiograph of the left wrist and hand, read by a radiologist trained in
determining bone age.
d. TX: GH therapy for children with GH deff, reassurance if constitutional
Pediatric Dermatology

1. Acne vulgaris
a. Patho: increased sebum production (androgens->puberty/POS/Cushing’s) OR clogged sebaceous glands
(proliferation of follicular keratinocytes) OR Propionibacterium acne overgrowth (P.acne in normal flora
overgrows in blocked pore->lipase production converts to fatty acids that damage healthy cells->inflammation
response) OR inflammatory response
b. Symptoms: Common in face/chest/back/upper arms where there are more sebaceous glands.
i. Comedeone: small noninflammtory bumps of clogged pores
1. Open (black heads)->incomplete blockage
2. Closed (white heads)-> complete blockage
ii. Inflammatory: papules or pustules with surrounding inflammation
iii. Nodular or cystic acne: heals with scarring
c. DX: Clinical-> Mild (comedones), Mod (comedones + large amount of papules/pustules), Severe (nodular, >5
mm) or cystic acne
d. TX:
i. Mild: topical retinoids (Retin-A) - good for inflammatory/noninflammtory acne. Benzoyl Peroxide-dec
Propionibacterium concentration. Topical abx (clindamycin) mc used with benzoyl peroxide to reduce
resistance. OCPs in pubertal women
ii. Mod: above + oral abx (doxycycline or minocycline) +/- anti-androgen agents (spironolactone). Abx best
for pregnancy as others are CI
iii. Severe: Isotretinoin’s (effect all patho mechanisms).
1. S/E psychiatric, hepatitis and increased TG/cholesterol, arthralgia, leukopenia, premature bone
closure, dry skin. Very teratogenic (2 preg test before use and monthly while being treated + 2
forms of contraception 1 month prior to initiation and 1 month after discontinuation)
2. Androgenetic alopecia
a. Patho: progressive loss of terminal hairs on the scalp 2/2 to Dihydrotestosterone (DHT)
b. Symptoms: varying degrees of hair thinning and nonscarring hair loss MC on temporal scalp, midfront scalp and
vertex area of scalp. Appears as central balding with floating hairs (loss of melanocytes at base of hair follicle)
c. TX: Minoxidil (Rogan) topically and oral Finasteride (5-a reductase inhibitor) which inhibits the conversion to
DHT. Women treated with OCP and spironolactone

3. Atopic Dermatitis (eczema)

a. Patho: altered immune reaction to genetically susceptible people when exposed to certain triggers (increased
IgE production)
i. Triad: eczema, allergic rhinitis, asthma
b. Triggers: heat, perspiration, allergens and contact irritants (wool, nickel, food)
c. Symptoms: pruritus hallmark. Acute lesions-> erythematous ill-defined blisters/papules/plaques that dries and
crusts over and scales. MC in FLEXOR creases

i. Nummular eczema: sharply defined discoid/coin shaped lesions, common on dorsum of hands, feet and
extensor surfaces (knees, elbows)
d. TX: topical steroids for acute scenario, antihistamines for itch. Alternative to steroids is topical calcineurin
inhibitors (Tacrolimus) which do not atrophy skin but run risk of lymphoma/skin cancer.
i. Chronic lesions->daily hydration and emollients
ii. Avoid triggers/irritants like soap and frequent baths. Maintain skin hydration.

4. Burns
a. Minor: <5% TBSA in young (10 for adults), isolated, not involving face/hands/feet/perineum, not cross major
joints, not circumferential
b. Major: >20% TBSA in kids (25% for adults), >10% full thickness burn, burns involve face/hands/perineum/feet,
cross major joints, circumferential
c. Classification
1st degree-superficial (sunburn) Erythematous, dry, PAINFUL, + cap refill with blanching.
7 days to heal

*epidermis

2nd degree-superficial partial thickness Erythematous/pink, Moist, weeping, blistering, MOST

PAINFUL, + cap refill with blanching. Heals 14-21 days.
Possible pigment changes
*epidermis + superficial dermis (papillary)

2nd degree-deep partial thickness Red, yellow, pink, dry, blistering. Usually NOT painful,
decreased 2 point discrimination, - cap refill with NO
blanching. Heals 3wks-2months, scarring. +/- skin
*epidermis into deep dermis (reticular) grafting/excision

3rd degree-full thickness Waxy, white, leathery. Dry. PAINLESS. – Cap refill. Heals
in months but not well

*extends through the entire skin

4th degree=extension into deep tissue Black, charred, dry. PAINLESS. – Cap refill. Does not heal
well, life threatening.

*entire skin into underlying bone, muscle, fat

d. DX: Lund-Browder chart (rules of 9%)

Head-> 18

Chest/back->18

Perineum-> 1

Legs-> 14 x 2

Arms->9 x 2

e. TX:
i. Cleaning: mild soap and water. DO NOT apply ice directly. If chemical irrigate profusely with running
water x 20 min
ii. Debridement: escharotomy recommended for circumferential burns to prevent compartment
syndrome. Debri necrotic/sloughed skin
iii. Blisters: remove ruptured blisters
iv. Pain: Tylenol, nsaids, opiates
v. Abx: on Nonsuperficial burns; silver sulfadiazine. Silvadine CI in sulfa allergy, pregnancy, children <2
months and DO NOT apply to face due to discoloration effect. For Superficial burns can use aloe vera or
bacitracin
vi. Dressings: NOT on superficial burns. Cover with nonadherent gauze and elastic gauze. Wrap fingers and
toes individually
vii. Fluids: Parkland Formula=> 4ml x kg x %TSA IV LR over first 24 hours (1/2 on first 8 hrs, second ½ in
following 16 hrs)

5. Contact Dermatitis
 a. Patho: IRRITANTS such as chemicals, detergents, cleaners, acids, prolonged water exposure, metals.
i. Diaper rash->prolonged exposure to urine/feces
b. Symptoms: burning, itching, erythema to affected area, dry skin, eczematous eruption. Red rash may take on
shape of an object
c. TX: avoid irritants. High potency topical steroids (Clobetasol propionate 0.05% ointment twice daily for 14
days). Protective/wet dressings PRN
i. Avoid topical abx as allergic reactions are common to topical antibiotics containing neomycin and
bacitracin.

6. Dermatitis (diaper, perioral)

a. Diaper Rash
i. Etiologies: wearing diapers (contact dermatitis, miliaria, candida). If rash in diaper AND other areas
(atopic dermatitis, seborrheic dermatitis). If affecting diaper area regardless of diaper use (scabies,
bullous impetigo)
ii. Risk: friction and moisture from urine/feces
iii. TX: frequent diaper changes every 2 hours or when soiled. Open air exposure. Zinc oxide or petroleum
jelly application. Can use 1% hydrocortisone cream (<2 weeks)
b. Perioral Dermatitis
i. Patho: MC seen in young women, +/- hx of topic steroid use
ii. Symptoms: papulopustules on an erythematous base which may become confluent into plaques with
scales. +/- Satellite lesions. Usually spares vermillion boarder (directly around lips)
iii. TX: flagyl or erythromycin (topical), tetracycline (oral). AVOID topic steroids.
c. Seborrheic Dermatitis
i. Patho: hypersensitivity to Malassezia furfur (fungal skin commensal)
ii. Commonly resolves weeks to months after birth
iii. Symptoms:
1. Cradle cap: infants, erythematous plaques with fine white scales. Can be yellow greasy plaques
that develop on scalp, ears, eyelids, cheeks, and nasal folds
iv. TX: parents can apply baby or vegetable oil to scalp before bath to loosen scales and then gently brush.
1. +/- baby shampoo, steroids, ketoconazole cream/shampoo

7. Drug eruptions
a. Most are self-limited if drug is discontinued
b. Patho:
i. Type 1: IgE mediated. Immediate. Ex. urteicaria and angioedema
1. Bee sting, latex, penicillin
ii. Type 11: cytotoxic, Ab- mediated
1. Hemolytic, good pastures, graft rejection
iii. Type 111: autoimmune antibody-antigen complex. Ex. drug mediated vasculitis and serum sickness
1. SLE, polyarteritis nodosa
iv. Type IV: delayed (T cell mediated) morbiliform reaction. Ex. Erythema Multiforme
1. PPD, nickel, poison ivy, eczema
c. Symptoms:
 i. Exanthematous/Morbiliform rash: MC skin eruption. Generalized distribution of bright-red macules and
papules that coalesce to form plaque. 2-14 days after medication ignition. (abx, NSAID, allopurinol, THZ)
ii. Urticarial: 2nd MC, occurs within minutes to hours. (abx, NSAID, opiates, radiocontrast)
iii. Erythema multiform: 3rd MC, target lesions not always present during drug induced EM (sulfonamides,
penicillin’s, Dilantin, phenobarbital)
iv. Any: can have fever, abdominal pain, joint pain
d. TX: Discontinue med. Oral antihistamines for exanthems/morbiliform. Systemic Steroids for urticaria.
Symptomatic tx for erythema minor. If anaphylaxis reaction give intramuscular epinephrine!

8. Erythema multiforme
a. Patho: acute self-limited type IV hypersensitivity reaction. Resolves over 3-5 days and persists about 2 weeks
b. Associations: HSV MC, mycoplasma (common in kids), S. pneumo, sulfa drugs, beta lactam, phenytoin,
autoimmune
c. Symptom’s: target (iris) lesions-> dull dusty-violet red, purpuric macules/vesicles or bullae in the center
surrounded by edematous rim and peripheral halo

i. EM minor: distributed acrally. NO mucosal membrane lesions

ii. EM major: involvement of >/= 1 mucous membrane (oral, genital, ocular), <10% BSA acrally->centrally.
NO EPIDERMAL DETACHMENT.
d. TX: symptomatic->discontinue offending drug, antihistamine, analgesics, skin care. Steroid/lidocaine
mouthwashes for oral lesions. Systemic steroids if severe.

9. Exanthemas
a. Macular and popular eruptions
i. Scarlatiniform: eruptions consist of confluent blanching erythema, “sandpaper”
1. Scarlet fever->associated with strep pharyngitis
a. Presentation: Skin eruption follows fever→ fine erythematous papules. Mucous
membranes erythematous w/ petechiae, and the tongue has white membrane
(strawberry tongue), first on upper part of trunk, then more general. Face flushed w/
circumoral pallor
b. Tx: IM benzathine PCN G or p.o. PCN VK
2. Toxic Shock Syndrome: acute febrile illness caused by toxin-producing strains of S. aureus (less
commonly Strep)
a. Presentation: fever, rash, hypotension, involvement of multiple organs (lungs, kidney,
liver, GI tract). Desquamation of palms and soles follows onset by 1-2 weeks .Diffuse
macular erythema w/ flexural accentuation, mucous membrane erythema, severe
conjunctival involvement
3. Kawasaki disease
ii. Morbilliform: eruptions consist of erythematous macules and papules (resemble measles)
1. Measles
2. Rubella
3. Erythema infectiosm (fifths disease)
4. Roseola/ 6ths disease (exantham subitum)
5. EBV and PCN
iii. Papular eruptions
1. Molluscum contagiosm
a. Presentation: Firm, smooth, flesh-colored umbilicated papules, 2-6 mm diameter, in
groups or widely disseminated on skin/mucosa. May appear anywhere on the body
except the palms and soles
2. Warts (verruca vulgaris)
b. Vesicular & Pustular exanthems
i. Varicella and herpes zoster
ii. Hand foot mouth disease
10. Impetigo
a. Patho: contagious superficial vesicularpustular skin infections, common at site of superficial skin trauma (insect
bite) on exposed surfaces of the face/extremities
b. Risk: warm, humid conditions, poor personal hygiene
c. Types:
i. Nonbullous (MC type): vesicles/pustules  characteristic ‘honey colored crust’. Associated with
regional lymphadenopathy (staph MC, GABHS 2nd MC)
ii. Bullous: vesicles form large bullae  rupture  thin ‘varnish-like crusts’. Fever, diarrhea. (Staph aureus
MC, strep). Rare.
iii. Ecthyma: ulcerative pyoderma (deeper erosions) caused by GABHS. Uncommon.

d. TX: Mupirocin (Bactroban) TOC x 10 days. Bacitracin. Wash with soap and water
i. If extensive/fever: Cephalexin (Keflex) 1st line. Clindamycin, erythromycin azithromycin, clarithromycin,
dicloxacillin (penicillinase resistant)
ii. Note: Children may return to school 24 hours after antibiotics are started and should cover any lesions
that are actively draining.

11. Lice (Pediculosis)

a. Types: head louse (pediculus humanus capitus); body louse (pediculus humanus corporis), pubic louse (phthirus
pubis)
b. Transmission: person to person. Fomites (hats, headsets, clothing, bedding)
c. Symptoms: intense itching (occipital area), popular urticarial near the lice bites. May have scaly patches with
alopecia and black dots with cervical lymphadenopathy
i. Nits: white oval shaped egg capsules at the base of hair shafts. Removed with comb
d. TX:
i. Permethrin topical TOC
1. Capitus: permethrin shampoo left x 10 min
2. Pubis/corporis: permethrin lotion x 8-10 hours (safe in kids >2)
ii. Lindane- neurotoxic if used after shower. Oral Ivermectin used in refractory cases
iii. Bedding/clothing laundered in hot water with detergent and dried in hot drier for 20 minutes. Toys that
can be washed are placed in air tight bag x 14 day
e. Note: Spreads through direct contact of scalp and most children with nits do not develop active infection so DO
NOT withhold from school

12. Lichen planus

a. Patho: idiopathic cell-mediated immune response (Hep C increased incidence!)
b. Symptoms: 5p’s: purple, polygonal, planer, pruritic papules with fine scales and irregular boarders. MC on flexor
surfaces (skin, mouth, scalp, genitals, nails)
i. Wickham striae: fine white lines on skin lesions or the oral mucosa. Nail dystrophy
ii. +/- Koebners phenomenon: new lesions at sites of trauma
c. TX: topical steroids 1st line. Can give antihistamine for itching. PO steroids 2nd line, UVB therapy, retinoids.
d. Prog: resolves 8-12 months

13. Pityriasis rosea

a. Patho: unknown, possibly viral infections (HHV7) that occur mostly in children/young during spring/fall. *can
mimic syphilis*
b. Symptoms: Herald patch (salmon colored macule) on trunk 2-6 cm->general exanthema 1-2 week later (pruritic
1 cm round/oval salmon colored papules with white circular scaling along cleavage lines in a Christmas tree
pattern). The face is usually spared, predominantly trunk/extremities and resolves in 6-12 weeks.
i. The pigmentation of the center of the herald patch gradually regresses. As it does, center of lesion
clears, and margin develops a scale. New lesions may progress caudally or centrifugally in crop-like
formations
c. TX: none needed. Can give antihistamines, steroids, and oatmeal baths for itching. +/- UVB phototherapy if
severe and started early in course.
14. Scabies
a. Patho: mites that are transmitted through prolonged close skin-skin contact or fomites (bedding/cloths). Female
mites burrow into the skin to lay eggs, feed and defecate
i. Scybala-fecal particles that create hypersensitivity reaction on skin
b. Symptoms: intensely pruritic lesions (papules/vesicles/linear burrows found in intertriginous zones such as webs
spaces between fingers/toes, scalp) w/ increased intensity at night. Red itchy pruritic papules or nodules on the
scrotum, glans, and penile shaft, body folds are patho for scabies
c. DX: clinical. Skin scrapping of burrows with mineral oil to identify mites or eggs under microscope
d. TX: Permethrin topical TOC for 8-14 hours before showering with repeat application 1 week later. Can also use
Lindane which is cheaper, but if used after shower it can cause seizure due to absorption threw pores (CI-
teratogenic, breastfeeding, <2 YO).
i. Place all clothing/bedding in plastic bag x 72 hours then washed and heat dried
ii. Pregnant/infants: 6-10% sulfur in petroleum jelly. Extensive- oral Ivermectin

15. SJS and TEN

a. Patho: MC after drug eruptions (sulfa and anticonvulsants MC). Can be from NSAIDs, Allopurinol, abx,
infections-mycoplasma/HIV, malignancy, idiopathic
b. SJS-> sloughing <10% body surface areas
c. TEN->sloughing >30%.
d. Symptoms: fever, URI->widespread blisters on trunk/face, erythematous/pruritic macules >/= 1 mucous
membrane (Hemorrhagic erosions w a greyish white membrane) with epidermal detachments (+ Nikolsky sign)
e. TX: treat like severe burn (burn unit), pain control, withdraw of offending agent ASAP, fluids/electrolyte
replacements, wound care
f. Note: The FDA has recommended that anyone of Asian or South Asian descent be genetically tested for HLA-
B*15:02 prior to starting on carbamazepine. (2nd most common cause is mycoplasma pneumoniaie).
g. Prognosis: Use SCORTEN score

16. Uticaria (Hives)

a. Type 1 HSN (IgE) or complement mediated edematous reaction to the dermis/SQ tissue
b. Triggers: foods, meds, infections, insect bites, drugs, environmental, stress, heat, cold
c. Patho: Mast cells release histamine (causing vasodilation of venules->edema of dermis/SQ tissues)
d. Symptoms: Uticaria->blanchable edematous pink papules, wheals or plaques that may coalesce. Hives disappear
within 24 hours
i. Dermatographism: local pressure to the skin may cause wheals in that area
ii. Dariers sign: localized urticarial appearing where the skin is rubbed
e. TX: oral antihistamine TOC. Eliminate triggers. Steroids if needed.

17. Verrucae
a. Actinic Keratosis
i. Patho: premalignant condition to SCC (MC premalignant skin condition)
ii. Epi: fair skinned elderly with prolonged exposure
iii. Symptoms: dry rough scaly sandpaper skin lesions with erythematous hyperkeratotic (pigmented)
plaques +/- horn projection on skin
iv. DX: punch or shave BX showing atypical epidermal keratinocytes and cells with large hyperchromatic
pleomorphic nuclei rom basil layer upward
v. TX: observe or cryosurgery. Topical 5-fluorouracil
b. Seborrheic Keratosis
i. Patho: MC benign skin tumor in fair skinned elderly with prolonged skin exposure
ii. Symptoms: small papule/plaque velvety warty lesion with greasy-stuck on appearance
iii. TX: none. Cosmetically can do cryotherapy
c. HPV
i. Patho: HPV infects keratinized skin causing excess proliferation and retention of the striatum corneum
leading to papule formation
1. Cutaneous: verruca, vulgaris (common), plantar, flat/plana
2. Mucosal: genital warts (condyloma acuminate), cervical dysplasia/cancer and anogenital
carcinoma (intraepithelial)
 d. Benign types:
1. Common-vulgaris/plantar: firm, hyperkeratotic papules 1-10 mm with red-black/brown
punctuates/dots (thrombosed capillaries). Common on hands
2. Plana: numerous, small discrete flesh colored papules measuring 1-5 mm in diameter and 1-2
mm in height. Common on face, hands, shins
3. Genital: tiny, painless papules evolve into soft, fleshy cauliflower-like lesions occurring in
clusters in genital or oropharynx region
ii. DX: whitening of lesions with acetic acid application on mucosal. Histology shows koilocytic squamous
cells with hyperplasic hyperkeratosis
iii. TX: most resolve on own within 2 years
1. Reassurance and watchful waiting is the most appropriate course of action for a young child,
because the majority of children will experience a spontaneous remission of the lesion within
two years
2. Plantaris/vulgaris: salicylic acid. Cryotherapy (liquid nitrogen)
3. Condyloma acuminate: chemical, salicylic acid, cryo
iv. Prevention: Gardasil vaccine in women 11-26 protects against 70% of strains (6, 11, 16, and 18).
Gardasil 9 covers that + (31,33, 45, 52, 58)

18. Tinea
a. Risk: increased skin moisture, immunodeficiency (HIV, DM), PAD
b. DX: Woods lamp with green fluorescence due to microsporum  KOH smear
c. Symptoms/TX:
i. Tinea Capitus (ring worm): annular, scaling lesions and broken hair shafts. Inflamed plaques with
multiple pustules with scarring and alopecia.
1. TX: PO Griseofulvin 1st line. Fluconazole 2nd line.

ii. Tinea barbae: papules, pustules and hair follicles

iii. Tinea Pedis (athletes food): pruritic scaly eruption between toes
1. TX: topical antifungal. Keep cool and dry

iv. Tinea cruris (jock itch): diffusely red rash on the groin or scrotum
1. TX: topical antifungal

v. Tinea corporis: erythematous plaques (circular rash with clear center and defined boarders) scaling,
cracking. Presence of SCALES=tinea corporis (diff between erythema migrans)
1. Tinea corporis will NOT cause the appearance of additional crops of papules in a linear
distribution like pityriasis rosea
2. TX: topical antifungal (clotrimazole)

vi. Onychomycosis: nail infection by various fungi. Occurs MC on great toe. Opaque thickened, discolored
and cracked nails with subungual hyperkeratinization
1. TX: PO itracanozle and Terbinafine (associated with hepatotoxicity and drug interactions)
Pediatric GI
1. Appendicitis
a. Presentation by age group
i. 0-30 days: rare->due to anatomic differences/soft diet/diarrheal illness/recumbent positioning.
Abdominal distention, vomiting, decreased feeding, resp distress, lethargy, abd wall cellulitis
ii. < 5 YO: uncommon, abdominal pain, fever, vomiting, diffuse abdominal wall tenderness
iii. 5-12 YO: most frequent in this age group abdominal pain over RLQ, diffusely walking, nausea, anorexia
b. DX: WBC >18K, CRP, US
c. TX: appendectomy, single prophylactic dose of cefoxitin or ceftriaxone + flagyl 3-60 min before operation, IV
fluids, pain control (ketorolac). Post op abx not needed unless perf. Note-can use FQ + flagyl or clindamycin if
PCN allergy

2. Colic
a. Etiology: 2wk-3/4 mo. M=F. Thought to be related to feeding techniques, under/over feeding, infrequent
burping, swallowing air, cow’s milk protein intolerance, lactose, hypermotility of intestine
b. Wessel Criteria: child cries for 3 + h/d, 3 + d/wk for at least 3 wks *rules of 3*
c. Symptoms: occurs suddenly in the evening. Triggered when hungry, sick, hot/cold, allergy to formula.
Hypertonia, circumoral pallor, tense abdomen, knees drawn up, fists clenched, stiffening of arms, arching of back
d. DX: clinical, benign condition that resolves with time
e. TX: soothing techniques (rub abdomen, white noise, rhythmic motions, pacifier, warm bath). Change feeding
habit (don’t rush, bottle feed in vertical positon with frequent burping). If refractory try cow’s milk elimination
f. Health maintenance: normal to cry for 2 h/d esp in first 3 mo of life. DO NOT give dicylomine/phenobarbital

3. Constipation
a. Patho: 90% functional with no patho. Painful BM with voluntary withholding of feces.
b. Triggers: toilet training, changes in routine/diet, stress, unavailable toilets
c. Cause: toilet phobia, avoidance, parental intervention, dryness

d. Criteria: (2 + the following x 2 mo) <3 BM/wk, 1+ episode of encopresis/wk, impaction of rectal with stool, stool
that obstructs toilet due to volume, fecal withholding, pain with defecation
i. Longer stool stays->more water taken out->harder it gets. Stool may sneak around and cause
intermittent diarrhea and encopresis
e. Symptoms: pain, straining, decreased frequency or incontinence. Ask about stressors-functional cause OR
history of delayed meconium-organic cause
f. TX: <1 YO glycerin suppository. >1 YO enema/mineral oil/saline/milk & molasses. +/- PO Senna/PO Mg Citrate. In
adults- fiber + fluids, osmotic stool softeners, Senna. May require disimpaction in the OR

4. Dehydration
a. Risk: gastroenteritis, fever, burn, illness, diarrhea
b. Volume depletion measured by change in weight from baseline
c. Symptoms:
i. Mild-> inc thirst, normal pulse, pressure, RR
ii. Mod: rapid pulse, lower pressure, deeper RR, dry mucosa, reduced tugor and UO, irritable
iii. Severe: rapid and weak pulse, low pressure, tachy/absent RR, parched mucosa, cool/tenting/mottled
skin with increased cap refil >3 sec, anuria, lethargy
d. DX: hypernatremia, HCO3 <17, urine sodium <25 and osmolality >450 (normal 275-295)
i. Sodium bicarb best indicator of dehydration
e. TX:
i. Fluid repletion:
 1. Mild-> oral intake, 50 ml/kg over 4 hrs
2. Mod-> 100 ml/kg over 4 hrs + maintence. + 10 ml/kg ORT for each stool. Resume feeding, no
bowel rest in all ages
3. Severe: rapid IV 20 ml/kg over 20-30 min of isotonic saline, repeated PRN. ORT
ii. Fluid Maintence (divide daily volume by 24. Max 2400 ml daily). Can also use 4/2/1 Holliday Segar
method.
1. 3.5-10 kg-> 100 ml/kg
2. 11-20 kg-> 50 ml/kg for every kg over 10 + 1000 ml
3. >20 kg -> 20 ml/kg for every kg over 20 + 1500 ml

5. Duodenal atresia
a. Patho: complete absence or closure of a portion of the duodenum -> gastric outlet obstruction. (failure of the
bowel to recanalize after endodermal epithelial proliferation)
b. Epi: polyhydramnios (inc amniotic fluid) seen during pregnancy. Inc incidence in Down syndrome
c. Symptoms: intestinal obstruction shortly after birth, distention, BILIOUS vomiting first day of life
d. DX: abdominal XR shows distended duodenum and distention sep by pyloric valve-> double-bubble sign + no
distal air
e. TX: decompression of GI tract, electrolyte and fluid replacement. Duodenoduodenostomy.
f. NOTE: Intestinal atresia is seen with double bubble signs + mult-air fluid levels. Caused by cocaine/tobacco use-
>vascular accidents in utero. TX is surgery

6. Encopresis
a. Etiology: males MC, ages 5-6 YO, constipation (90%)
b. Symptoms: repeated passage of feces in inappropriate places (soiling). Stool is foul smelling and dark.
c. Criteria: 1 event per month x 3 months and at least 4 YO
d. DX: T4/TSH, IgA TG Ab, Ca and lead levels, KUB
e. PE: palpable mass in LLQ, stool smearing around anus
f. TX: evacuation behavior strategies (sit on toilet for 10 min after meal). <1 YO osmotic
laxative/suppositories/enema. >1 YO osmotic laxative, lubricants/stimulants/enema
i. Daily doses of polyethylene glycol to be given for at least six months 2 x per day->enema (even when
the problem resolves), regular toileting behaviors should be reinforced for a period of at least six
months. Often, a longer period is required to ensure complete and long-term resolution. *fleet enema
CI in infants due to hypocalcemia

7. Foreign body

8. Gastroenteritis
a. Norovirsu MCC in patients >2 YO
b. Rotavirus MC cause <2 YO
i. Etiology: 3-15mo, winter, fecal-oral, 1-3 day incubation
ii. Symptoms: vomiting, diarrhea (4-8 days, nonbloody), low grade fever, nasal symptoms precede GI.
Metabolic acidosis from bicarb loss
iii. DX: hypo or hypernatremia from dehydration. PCR of stool
iv. TX: supportive (pedialyte), reduce fat intake, NO antidiarrheal
v. Health maintenance: vaccinate @ 2, 4, 6 mo

9. GERD
a. GER (normal)
i. Etiology: weak LES, well nourished “happy spitter” MC around 4 mo
ii. Risk: overfeeding, anatomic abnormalities
iii. Symptoms: frequent regurg, good weight gain, feeds well, burping, reswallowing. Sandifer syndrome->
arching of back w/ chin lifting/screaming 2-6 h/spitting up
iv. DX: mostly clinical
v. TX: life style changes (hypoallergic formula, eliminate beef if breast feeding, thickened feeds, 2wk trial
of acid suppression therapy, avoid tobacco exposure). Acid suppression not useful if <1 YO with
 uncomplicated GER->however, do 2 wk trial in infants with mild esophagitis on endoscopic bx or
failed conservative tx (PPI preferred)
vi. Prog: resolves 9-12 mo of age (max 2 YO), no intervention needed if gaining weight
b. GERD in preschool:
i. Symptoms: intermittent regur past 2 YO, decreased PO intake, poor weight gain, food aversion,
recurrent pneumonia, hoarseness/stridor
ii. DX: empiric acid suppression->UDG if persistent or dysphagia->pH monitoring. Barium swallow to
exclude anatomic cause
iii. TX: lifestyle, acid suppression 2-4 wks, prokinetic agents, refer to GI if alarm symptoms (including
weight loss)
c. GERD in school sage
i. Symptoms: similar to adults- heart burn, dyspepsia, regrug, cough, hoarseness
ii. DX: Barium contrast first line study to r/o complications/CA. EDG with bx if refractory to tx is
confirmatory. 24 hour pH is GS
iii. TX: Diet changes-> H2 blockers->switch too PPI->add promotility agent->Nissan fundoplication

10. Hepatitis
a. Fulminant (acute hepatic failure)
i. Patho: Rapid liver failure and encephalopathy within 8 weeks of liver injury in previously healthy
patient
ii. Etiology: Acetaminophen MC, drug reactions (ex. rifampin), viral hepatitis (A-E), liver ischemia, Reye
syndrome (aspirin use during viral infection), pregnancy fatty liver

iii. Symptoms: encephalopathy-AMS, seizures, asterixis, hyperreflexia, cerebral edema, inc ICP, inc
ammonia. Coagulopathy, hepatomegaly, jaundice
iv. DX: inc ammonia, inc PT/INR > 1.5, LFT’s, hypoglycemia
v. TX: Lactulose to neutralize ammonia; rifaximin or neomycin decrease ammonia producing bacteria;
protein restriction; liver transplant is definitive tx
b. Viral
i. Symptoms: prodromal phase->malaise, arthralgia, fatigue, decreased smoking, N/V, abdominal pain,
(Hep A=spiking fever). Icterus phase-> jaundice usually once fever subsides (rare to get to this phase)
ii. Lab values: Inc ALT> AST (<500 if chronic), +/- increase bili
iii. Prognosis: recovery within 3-16 weeks. 10% HBV and 90% HCV->chronic
iv. Types:
1. Chronic hepatitis
a. >6 months duration. Only HBV, HCV, HDV associated. Can lead to ESLD or HCC
2. Fulminant: encephalopathy, coagulopathy, jaundice, edema, ascites, asterixis, hyperreflexia
3. HAV
a. Transmission: fecal-oral. Think if water/food outbreak during international travel; day
care; gays; shellfish
b. Symptoms: Children usually asymptomatic (MC adult source). Prodromal phase-
>spiking fever, loss of appetite, malaise, nonbloody diarrhea->icterus phase (rare)
c. DX: IgM HAV ab (IgG HAV ab if past exposure)
d. TX: self-limiting. May give HAV immune globulin + vaccine for post exposure
prophylaxis within 2 weeks. Hep A vaccine giving in high risk population or travelers
>2weeks before trip
4. HEV
a. Transmission: fecal oral, associated with waterborne outbreaks
b. DX: IgM anti-HEV
c. TX: self-limiting. High mortality rate during 3rd trimester (pregnancy) due to fulminant
hepatitis risk
5. HCV
 a. Transmission: parenteral (IVDU, blood transfusion before 92’) Sexual or perinatal
(uncommon)
b. DX: anti HCV in 6 weeks (HCV RNA better then HCV ab)
i. Acute: + HCV RNA, +/- Anti-HCV
ii. Resolved: - HCV RNA, +/- Anti-HCV (doesn’t imply recovery)
iii. Chronic: + HCV RNA, + anti-HCV
c. TX: PEGylated interferon alpha-2b AND ribavirin
d. Screening: HCC via alpha-fetoprotein and US
6. HDV
a. Transmission: requires HBV to cause coinfection or superimposed infection
b. More severe, faster progression to cirrhosis
7. HBV
a. Transmission: parenteral, sexual, perinatal, percutaneous
b. Symptoms:
i. Acute: 80% subclinical, 30% jaundice .Mainly in adults because strong immune
system->jaundice,LFTs in 1000s

ii. Chronic carrier (asymptomatic): 10% adult, 90% perinatal acquired. High HCC
risk. DNA normal, normal LFT’s. Asymptomatic but CAN transmit

iii. Chronic infection: + HBsAg with increased AST/ALT, + HBV DNA +

hepatocellular liver damage on bx

iv. Serology:
1. HBsAg: 1st evidence of infection (or infectivity). >6 M=chronic
infection
2. HBsAb (anti-HBs): recovered OR vaccinated. Lack of antiHBS in
6M=chronic infection
3. HBcAB: IgM=acute infection (only marker in window period).
IgG=chronic infection or distant resolved
4. HBeAG: inc viral replication and infectivity
5. HBeAB: waning viral replication, decreasing infectivity
6. HBV DNA: correlates with active replication in liver
v. TX:
1. Acute: supportive.
2. Chronic (IF inc ALT/inflammation on bx or + HBeAG): alpha-interferon
2b (CI in decompensated) + antiviral (Lamivudine, Adefovir). Newer
options- Tenofovir and entecavir
vi. Prevention: Hep B vaccine @ 0, 1, 6 months (CI in makers yeast allergy)
11. Hirschprung disease
a. Congenital absence of ganglion cells  fecal obstruction MC in distal colon and rectum
b. Patho: absence of enteric ganglion cells (aurbach & Meissner plexuses), functional obstruction due to failure of
relaxation of the aganglionic segment, enterocolitis with V/D and signs of megacolon.
c. Epi: males, downs syndrome
d. Symptoms: neonatal intestinal obstruction (meconium ileus failure of passage >48 hrs), BILIOUS vomiting,
abdominal distention, failure to thrive. Chronic constipation. Megacolon/sepsis picture +/-
e. DX: XR: first step  dilated proximal colon (normal) and normal looking distal colon (abnormal). Rectal BX is
definitive dx (shows absence of ganglion cells)
i. Failure to pass meconium ileus  Contrast enema (initial) showing caliber change at transition zone
ii. Overflow incontinence (stool eruption on DRE in older child)  Anorectal manometry used as
screening — shows lack of relaxation in internal sphincter/increased tone.
f. TX: surgical resection of effected bowel-pull through procedure

12. Inguinal hernia

a. Patho: protrusion of contents of the abdominal cavity through the inguinal canal
b. Types:
i. Indirect: through the internal inguinal ring, lateral to the inferior epigastric artery. Congenital due to
persistent patent process vaginalis. MC in young children and young adults (MC overall in M and F. MC
right side).
1. Painless inguinal swelling that retracts when cold, active, frightened
ii. Direct: protrude medial to IEA within Hesselbacks triangle (rectus abdominis, IEA, Pouparts ligament)
2/2 to weakness in floor of inguinal canal
c. Symptoms: Asymptomatic-scrotal swelling with indirect hernia, fullness. Incarcerated- painful, enlargement of
an irreducible hernia, N/V. Strangulated- Ischemic with systemic toxicity, severe painful BM.
d. TX: Can try manual reduction if incarcerated after sedation in Trendelenburg position (not if 12 + hrs or bloody
stool).Inguinal require sx, if strangulated-emergency

13. Intussusception
a. Patho: intestinal segment invaginates into adjoining intestinal lumen leading to bowel obstruction and vascular
compromise
b. Epi: children 6-18 months, males. MC at ileocolic junction post viral infection
c. Symptoms: Triad of-> vomiting + abrupt onset of abdominal pain + passage of blood per rectum (currant jelly
stool). Abdominal pain is colicky and can cause lethargy. Kids assume the knee-chest position
d. PE: Dances sign (sausage shaped mass in URQ or hypochondrium & emptiness in RLQ)
e. DX: Ultrasound-sensitive, may show target sign. If dx or high suspicion->air contrast barium enema.
f. TX: barium or air insufflation, IV fluids, sx resection if refractory
g. Other causes of blood in stool
i. NEC->premature infant. DX with babygram/xray. TX with NPO + TPN + IV abx
 ii. Meckel’s diverticulum-> remnant of the Vitelline duct (omphalomesenteric duct) which contain gastric
tissue->ulcers->bleeding. + FOBT, IDA or hematochezia. Bleeding is painless, intermittent (rules of 2’s).
Dx with techonium scan. TX with surgery
iii. IDB
iv. Infectious colitis: bloody diarrhea + fever, +/- hx of travel/outbreaks. TX with hydration and electrolyte
+/- abx
v. Milk protein allergy: 6 mo, hematochezia and FTT. TX by switching to hydrolyzed formula. Avoid cows
milk til 2-3 YO
vi. Swallowed blood: Do Apt test to see if mothers or fetal blood
vii. Anal fissure

14. Jaundice
a. Normal (indirect/unconjugated) is elevated in newborn 2/2 to immature liver which cannot conjugate bili due to
lack of UGT enzyme activity. Increased in days 3-5 and falls by ½ during 1st week.
b. Pathologic: if jaundice in 1st 24 hours (think hemolysis or hereditary spherocytosis), persistent 10-14 days,
conjugated >2mg/dl, total bili >12.
i. Note-increased direct is always pathologic, indirect can be physiologic
ii. Bili >20 can cause kernicterus and neurotoxicity (deposition in basal ganglia, pons, cerebellum)
c. Increased Indirect: Dec rate of conjugation
i. MC physiologic/prematurity: after 24 hours and not past 3-5 days
ii. Breast feeding (poor quality or quantitiy)
iii. Crigler-Najjar, Gilberts, Cretinism (congenital hypothyroidism)
iv. Hemolytic anemia: hereditary spherocytosis, G6PD deff-> presents in 1st 24 hours)
v. ABO incompatibility/Rh isoimmunization
d. Increased Direct:
i. Dubin-Johnson syndrome,
ii. Roto syndrome
iii. Infections
e. Symptoms: yellow skin of mucus and sclera (esp when bili >5). Usually progresses from head to toe.
f. Complication: Kenicterus-cerebral dysfunction and encephalopathy->seizures, lethargy, hearing loss, mental
development disorders
g. DX: Bhutani nomogram (hyperbilirubinemia >35 wk if TB >95% nomogram). Measure TB if extends below the
umbilicus?
h. TX:
i. Phototherapy: when bili>15 or not descending for cases like G6PD/physiologic/breast feeding
(conjugates bili, so does not help in direct hyperbili as it is already conjugated)
ii. Exchange transfusion: in severe cases like ABO incompatibility/hemolysis/Rh
isoimmunization/spherocytosis.
iii. Breast feeding: supplement breast milk, feed every 2h, phototherapy if >15

15. Lactose intolerance

a. Patho: inability to digest low levels of lactase enzyme
b. Symptoms: loose stools, abdominal pain, flatulence and borborygymi after ingestion of milk containing products
c. DX: hydrogen breath test is TOC (H produced when colonic bacteria ferment the undigested lactose)-done after
lactose free diet trial.
d. TX: lactase enzyme. Lactaid (prehydrolyzed milk). Diet.
 e. Note: Lactase breaks down lactose in to glucose and galactose simple sugars

16. Niacin (B3) deficiencies

a. Patho: often due to diets high in corn (maize) or diets that lack tryptophan. Can be due to inborn errors of
metabolism
b. Symptoms: Early-> anorexia, weakness, mouth soreness. Late-> Pellagra (3D’s-> diarrhea, dementia, and
dermatitis), glossitis, and irritability.
c. DX: N-methylnicotinamide measured in urine
d. TX: nicotinic acid or nicotinamide. Diet (red meat, fish, poultry, fortified breads/cereals, enriched pasta, peanuts).

17. Pyloric Stenosis

a. Patho: hypertrophy of the muscular layers of the pylorus causing functional obstruction. Inc incidence with
erythromycin use
i. 95% present in 1st 3-12 weeks of life (rare >6 months)
b. Epi: white males 4:1
c. Symptoms: NONBILIOUS vomiting/regurgitation->projectile after feeding, child still hungry. Hypochloremic
metabolic alkalosis (2/2 vomiting), jaundice, dehydration, malnutrition. Olive shaped non-tender mobile hard
pylorus. Visible peristaltic waves.
d. DX: Ultrasound 1st line- pyloric thickness of 3-4 mm, overall pyloric length greater than 14 mm and pyloric
diameter of 10-14 mm +/- donut sign. Upper GI contrast shows an elongated pyloric channel (string sign), a
bulge of the pyloric muscle into the antrum (shoulder sign), and parallel streaks of barium seen in the narrowed
channel creating a "double tract” sign.
e. TX: IV fluids 1st ! (to fix metabolic derangement), K repletion. Pylormyotomy is definitive.
f. NOTE: other cause of nonbilous vomiting are tracheoesophageal fistula->will vomit everything from birth. . Look
for bubbling and gurgling with respirations. Place NG tube and obtain x-ray, NG will coil up. Call surgery.
g. NOTE: it is normal to ‘spit up’ formula colored non projectile small volume during early days of birth

18. Umbilical hernia

a. Patho: through the umbilical fibromuscular ring due to failure of closure, congenital (MC in full term A.A infants)
b. TX: observation-usually resolves by 2 YO. Repair via sx if still present after 5 YO to avoid complications

19. Vit A deficiency

a. Patho: Vit A effects vision, immune function, embryo development, hematopoiesis, skin and cellular health.
Found in the kidney, liver, egg yolk, butter, green leafy vegetables
b. Risk: liver disease, alcoholics, fat free diets (rice diets)
c. Symptoms: visual changes/nyctalopia (nigh blindness!), dry eyes/xerophthalmia, dry skin, impaired immunity
(wound healing), poor bone growth, taste loss, squamous metaplasia (eyes, resp, urinary tract)
i. Bilots spots: white spots on conjunctiva due to squamous metaplasia of cornea
d. DX: serum retinol levels (20 ug/dL) on fasting
e. TX: high dose vit A (200K IU) PO, repeat dose every 4-6 months, carotenoids in diet
f. Too much-> teratogenicity, alopecia, ataxia, visual changes, skin disorders, hepatotoxicity

20. Vit C deficiency (ascorbic acid)

a. Risk/cause: diets lacking raw citrus fruits and green veggies, smoking, alcohol, malnourished, elderly
b. Symptoms: (Scurvy- 3 Hs) Hyperkeratosis, hemorrhage (vascular fragility in gums, skin/perifollicular, joints-
>impaired wound healing), hematologic (anemia, glossitis, weakness, inc BT)
c. DX: Ascorbic acid <.1 mg/dL, noticeable at levels <2
d. TX: Ascorbic acid 300-1000 mg PO (adults), citrus fruits and veggies
i. Vitamin C 100 mg three times daily for one week, then once daily (children)?

21. Vit D deficiency

a. Risk/cause: deficient intake or metabolism results in low serum calcium. Meds?- phenobarbital, phenytoin,
aluminum antacids
b. Source: Fortified milk and sun exposure
c. Symptoms: dental carries, hypocalcemia symptoms, inability to walk, pneumonia, diarrhea, rachitic rosary (rib
expansion), craniotabes, genu valgum/varum
d. Rickets (kids): softening of bone causing bowed legs, fractures, costochondral thickening, dental issues, and
developmental delays.
e. Osteomalacia (adults): diffuse body pains, weakness, looser lines (radiolucencies)
f. DX: high PTH, XR-thick growth plates with fraying/cupping/widening of distal metaphysis. 25-hydroxyvitamin D
levels
g. TX: Ergocalciferol (Vit D) 2000-5000 IU/d for 4-6 weeks then 400 IU daily
Pediatric Hematology

1. Anemia
a. Refer to heme study guide
b. Sideroblastic Anemia
i. Only microcytic anemia with INCREASED iron
ii. DX: bone marrow biopsy
iii. Etiology: lead, EtOH, ISH, B6 metabolic disease, AML
iv. TX: Get them away from lead, give them B6, BM BX for cancer
c. Autoimmune Hemolytic Anemia (hemolytic)
i. Patho:
1. Cold: caused by Mycoplasma and Mono which produce IgM against RBC at cold temps
2. Warm: caused by any rheumatic disease, drugs (PCN, sulfa), and cancer producing IgG against
RBC at warm temp
ii. DX: coombs test
iii. TX: steroids, IVIg when acute, and splenectomy if refractory
d. Hereditary Spherocytosis (hemolytic)
i. Patho: mutation of the RBC membrane (missing piece- spectrin or Ankyrin) causing a defect in cell
membrane proteins->spleen lyse these cells
ii. DX: spherocytosis on smear, confirm with osmotic fragility test. Microcytic or normocytic anemia with a
normal hematocrit and is the only disorder that will cause an increase in mean corpuscular
hemoglobin concentration
iii. TX: folate, splenectomy if severe. Can observe if compensated.
e. Physiologic anemia
i. The MCC of anemia in young infants between six and nine weeks of age. The cause of physiologic
anemia is the decrease in erythropoiesis due to increased tissue oxygenation. In a healthy newborn, the
hemoglobin level is elevated to greater than 14 g/dL. There is a rapid decline that reaches its lowest
point, near 11 g/dL, at between six and nine weeks.
f. Alpha Thalassemia
i. Decreased a-globulin chain production
ii. Epi: MC in Asians, Africans, Mediterranean’s
iii. Types
1. Silent carrier (1/4)->clinically normal
2. Alpha minor/trait (2/4)->mild microcytic anemia
3. Alpha intermedia/Hgb H disease (3/4)->chronic anemia, pallor, hepatosplenomegaly,
frontal/maxillary bony overgrowth, fractures, pigmented gallstone, iron overload
4. Hydrops Fetails (4/4)-> Hgb Barts gama tetramers associated with still birth
iv. DX:
1. CBC-hypochromic, microcytic anemia (MCV 60-75) with normal or inc RBC and normal or inc
iron
2. Peripheral smear with target cells, Heinz bodies in Hgb H disease
3. Hgb electrophoresis show normal Hgb ratios in adults (all 3 Hgb types contain 2 alpha chains so
dec alpha production affects are proportionate)
v. TX:
1. Mild (trait)->none
2. Mode->folate, avoid stress (sulfa drugs) and avoid iron overload
3. Severe-> weekly transfusions, vit C and folate supplementation. Iron chelating agents
(deferoxamine), +/- splenectomy, marrow transplant is definitive
g. Beta Thalassemia
i. Decreased production of B-globin chains->excess a-chains
ii. Epi: MC in Mediterranean, Africans, and Indians
iii. Types
1. Trait/minor (1/2)->asymptomatic, can be mild anemia
 2. Intermedia (mild homozygous form)->milder then major, anemia, hepatosplenomegaly and
bony disease
3. Major/Cooley’s anemia (2/2)->asymptomatic at birth->sx at 6 months when HgbF declines-
>ineffective erythpoiesis, erythroid hyperplasia and extramedually hematopoiesis (frontal
bossing), hepatosplenomegaly, severe hemolytic anemia, osteopenia, gallstones, iron overload
iv. DX:
1. CBC-same as alpha thalassemia
2. Peripheral smear-same
3. Hemoglobin electrophoresis (inc HgbA2 and HgbF due to dec B chains causing excess coupling
with delta and gamma chains)
a. Minor-> inc HgbF and HgbA2, dec HgbA (dec beta chain production)
b. Major-> inc HgbF and HgbA2, little to no HgbA
4. Skull XR-bossing with hair on end appearance
5. TX: Minor->none, genetic counseling. Major-> periodic blood transfusions, vit C and folate
supplementation, deferoxamine, splenectomy if refractory. Bone marrow transplant definitive
h. Sickle cell
i. Disease-> autosomal recessive genetic disorder of HgbSS.
ii. Trait->heterozygous HgbS asymptomatic unless hypoxia/dehydration, may have episodic hematuria and
inability to concentrate urine. Rarely sickles. Increase risk for renal vein thrombosis.
iii. Patho: dec solubility of HgbS under hypoxic conditions->rbc sickling causing micro thrombosis. Oxidative
stress causes HgbS to polymerize and sickle which gets trapped in capillaries leading to hemolysis and
microvascular occlusion.
iv. Triggers: hypoxia, infection, DKA, dehydration
v. Symptoms:
1. Early=6 M, dactylitis MC first presentation
2. Infection=salmonella osteomyelitis, functional asplenia, aplastic crisis associated with
Parovirus B19 infections
3. Microthrombosis=Skeletal H shaped vertebrae, splenic sequestering crisis->acute splenomegaly
and dec Hgb->infarction (requiring annual vaccinations), skin ulcers on tibia , painful occlusive
crisis (acute chest syndrome, back, abdominal, bone pain triggered by cold weather, stress,
dehydration, infection), aseptic necrosis of hip/femur (requiring dexa scans annually)
vi. Low reticulocyte count=acute aplastic crisis (Parovirus B19), folate deficiency
vii. High reticulocyte count= chronic anemia
viii. DX: CBC with peripheral smear->dec Hgb/Hct, inc reticulocytes, sickled erythrocytes, Howell-jolly
bodies. Hgb electrophoresis GS (HgbS, no HgbA, inc Hgb F)
ix. TX:
1. Pain control with IV hydration and oxygen first step in pain ciris (avoid meperidine-seizure!)
2. hydroxyurea reduces pain frequency crisis by inc HbF which cannot sickle
3. folic acid starting at 1 YO and prophylactic Pen V starting at 2 Mo (usu stopped by 5 years old)
4. ferrous sulfate not recommended
5. vaccine kids with S.pneumo/H.influenza/N.menigiococal
6. RBC transfusion in severe crisis, stem transplant only curative management
2. Bleeding disorders
a. Von Willebrand Disease
i. Patho: ineffective platelet adhesion due to autosomal dominant disorder with deficient vWF
(responsible for platelet adhesion and prevents FV111 degradation)
ii. Epi: MC hereditary bleeding disorder
iii. Symptoms: superficial/mucosal bleeding (bruising, epistaxis, gums, menorrhagia, GI), bleeding after
minor lacerations, petachiae common
iv. DX: Dec vWF levels on assay, +/- prolonged PTT (corrected with mixing study), bleeding time and PTT
prolonged and worse with aspirin. Dec Ristocetin activity test is GS (no platelet aggregation with abx
Ristocetin-normally should). Remember platelet count is normal.
v. TX: avoid aspirin. Mild  none. Mod  DDAVP. Severe  Factor V111 concentrates (also contain
vWF), recombinant vWF
vi. Mixing study distinguished factor deficiency from + factor inhibitors (ex. Lupus, antiphospholipid
syndrome) in which it does not correct when mixed with normal plasma
b. DIC
i. Patho: pathologic activation of coagulation system->widespread microthrombi (consume coag proteins
and platelets) ->severe thrombocytopenia with diffuse bleeding. Fibrin clots that consume both
platelets and factors.
ii. Etiology: Infections (sepsis), malignancy (AML), preeclampsia, septic abortion, abdrupto placente,
burns, liver disease, ARDS
iii. Symptoms: widespread hemorrhage (venipuncture sites), thrombosis (renal, hepatic, resp dysfunction,
gangrene)
iv. DX: inc thrombin formation= dec fibrinogen, inc PTT/PT/INR, thrombocytopenia. Peripheral smear with
schistocytes. Fibrinolysis->inc D-Dimer
v. TX: Tx underlying cause, FFP if severe bleeding , cryo replaces fibrinogen, platelet transfusion if
<20,000, +/- heparin for severe thrombosis
c. Thrombotic Thrombocytopenic Purpura (TTP)
i. Patho: Dec ADAMTS13 (vWF cleaving protease) -> vWF adhere to platelets and cause adhesion->small
vessel thrombosis->damaged RBC due to occluded vessels->hemolytic anemia. Hyaline clots that do
not consume factors.
ii. Pentad: Thrombocytopenia (petachiae, mucocutaneous bleeding) + microangioplathic hemolytic anemia
(anemia, schistocytes) + kidney failure + neurologic symptoms + fever (difference from HUS). Think FAT
RN-fever, anemia, thrombocytopenia, renal failure, neurologic
iii. PE: splenomegaly
iv. Etiology:
1. Primary: idiopathic/autoimmune-> AB vs ADAMTS13
2. Secondary: malignancy, marrow transplant, SLE, estrogen, pregnancy, HIV
v. DX:
1. Labs-thrombocytopenia, normal coags (PT/PTT), prolonged bleeding time
2. Hemolytic anemia- Peripheral smear (inc reticulocytes, schistocytes), Inc LDH and indirect bili,
dec haptoglobin (binds to free hgb to prevent oxidative toxicity), neg coombs
vi. TX: Plasmapheresis TOC (removes ab and adds serum), steroids, NO platelet transfusion (thrombosis)
d. Idiopathic (autoimmune) Thrombocytopenic Purpura (ITP)
i. Patho: autoimmune ab reaction vs platelets with splenic platelet destruction following acute infection
(ex. viral)  AB vs GP11b/IIIa receptor on platelets
ii. Etiology:
1. Primary: idiopathic
2. Secondary: immune mediated with underlying d/o (SLE, HIV, HCV – hep c?)
iii. Acute vs chronic
1. Acute: MC in children after viral infection
2. Chronic: MC in adults, women <40, males >70
iv. Symptoms: often asymptomatic, increased mucocutaneous bleeding, NO splenomegaly
v. DX: isolated thrombocytopenia with normal coag tests. Smear may show megakaryocytes. Really is a
diagnosis of exclusion. NO neuro/fever
 vi. TX: observe in children +/- IVIG acutely to get platelets up faster. Steroids in adults->IVIG-
>splenectomy if refractory. Transfusion only if <20,000 to prevent spontaneous ICH. If all else fails-
Rituximab
e. Hemolytic Uremic Syndrome
i. Triad: thrombocytopenia (petachiae, mucotaneous bleeding), microangipathic hemolytic anemia
(anemia, jaundice, schistoytes), kidney failure/uremia (more common in HUS then TTP)
1. No fever, or neuro symptoms
ii. Etiology: predominantly seen in children, usually preceded by Enterohemorrhagic E.coli 0157:H7,
Shigella or Salmonella gastroenteritis. Suspect in HUS in renal failure in children with diarrhea prodrome
iii. Patho: platelet activation by exotoxins. Toxins enter blood where it damages vascular endothelium and
activates platelets (microthrombi formation) ->platelet depletion->thrombocytopenia. Toxins damage
kidney. Small vessel thrombosis causes RBC damage->hemolytic anemia
iv. DX: same labs/smear as TTP. Increased BUN/CR
v. TX: observation in most children, IV fluids for renal profusion. If severe-> plasmapheresis
1. NOTE: abx may worsen condition (inc verotoxin release as a result of cell lysis)

3. Brain tumors
a. Etiology: 60% infratentorial
i. Pilocytic astrocytoma: Astrocytoma; MC overall. Benign, cystic, slow growing (TX->surgical resection)
ii. Medulloblastoma: Cerebellar Primitive Neuroectodermal Tumor; MC malignancy. Forms in the
posterior fossa. (TX->XRT/chemo, resection)
b. Symptoms:
i. Infant: large head, bulging fontanelle, anorexia/FTT, loss of milestones, shrill cry, resistance to being
held
ii. Child: morning HA, vomiting (w/o nausea), drowsiness, decreased academics, personality change
iii. Other: vision changes, altered speech/handwriting, CN deficit, head tilt, altered fait and ataxia, DI
c. DX: neuro exam, head CT/MRI->BX
d. TX: surgery
e. Specific Tumors:
i. Ependyoma
1. Patho: ependymal cells lining ventricles and spinal column. MC seen in 4th ventricle, +/-
medulla, SC. Cauda equine in adults
2. Epi: MC in children
3. Symptoms: (infants) increased head size, sleeplessness. (older kids/adults) N/V, H/A
4. DX: CT shows hypointence T1, hyperintence T2.
a. Biopsy shows perivascular pseudorosettes (tumor cells surrounding blood vessel)
5. TX: sx resection->XRT. Chemo NOT helpful
ii. CNS Lymphoma
1. Patho:
a. Primary: no systemic dz, variant of extranodal NHL
b. Secondary: MC, mets from another site esp diffuse large B cell lymphoma and
Burkett’s lymphoma
2. Risk: immunocompromised, EBV + in 90%
3. Symptoms: Focal deficit, ocular symptoms
4. DX: CT shows hypointence ring enhancing lesion; also include work up of
abdomen/pelvis/bone
5. TX: chemo (methotrexate TOC) followed by radiation/steroids. Sx resection usually ineffective
iii. Astrocytoma
1. Patho: astrocytes support endothelial cells of BBB, provide nutrients for cell, maintain
extracellular ion balance, repair brain after injury
2. Epi: infratentorial in children, suprtentorial in adults
3. Types:
a. Pilocytic/Grade 1/Juvenile: most benign, MC in children and young adults
i. TX: sx excision +/- radiation
b. Diffuse/Grade 11:invade surrounding tissue but slow
i. TX: sx if respectable, radiation if not
 c. Anaplastic/Grade 111: rare, aggressive
i. TX: sx->XRT +/-chemo
d. Glioblastoma Multiform/Grade IV: MC primary CNS tumor in adults
i. TX: sx->XRT + chemo
4. Symptoms: Focal deficits MC, HA worse in morning and can wake pt up at night. Mass effect-
>HA, N/V, ataxia, papilledema
5. DX:
a. CT/MRI with contrast (Grade 111,IV are enhancing).
b. Brain biopsy: Grade 1->cystic, Rosenthal fibers; Grade 11->microcysts and mucus fluid;
Grade 111->tentacle like projections hard to remove; Grade IV->cystic material,
calcium deposits, blood vessels
iv. Meningioma’s (2nd MC primary)
1. Patho: arise from meningothelial arachnoid cells of meninges covering brain and SC that
normally act as barrier for CNS system usually BENIGN, associated with neurofibromatosis,
MC arise from dura or sites of dural reflection
2. Epi: MC in women, estrogen receptors on tumor cells
3. Symptoms: most asymptomatic, can have focal sx
4. DX:
a. CT shows intensely enhancing, well defined lesion often attached to the dura
b. Biopsy->spindle cells arranged in whorled pattern. Psammoma bodies (round
calcifications)
5. TX: observe if small/asymptomatic, sx removal or radiation if not sx candidate

4. Hemophilia
a. Hemophilia A (V111 Deficiency)
i. Patho: MC hemophilia, X linked recessive trait or can also be caused by spontaneous mutation. Effects
intrinsic pathway->failure to form hematomas
ii. Symptoms: Hemarthrosis (bleed in ankles, knees, elbows)->arthropathy. Hematoma.
Excessive/prolonged hemorrhage in response to trauma and surgery (can present as urinary tract
hemorrhage), less commonly have petechial so spontaneous hemorrhage uncommon
iii. DX: Low factor V111, prolonged PTT, normal PT/bleeding time/fibrinogen/platelets. *mixed study
corrects PTT
iv. TX: Factor V111 infusion, DVVAP (inc V111 and vWF)
v. All daughters of a hemophilic male are carriers of hemophilia, whereas all sons are normal. Sons of
female carriers have a 50% chance of being affected and daughters of carriers have a 50% chance of
being carriers themselves.
b. Hemophilia B (Christmas Disease, IX deficiency)
i. Patho: x linked recessive trait
ii. Symptoms: same as Hemophilia A, deep tissue bleeding.
iii. DX: Dec Factor IX, prolonged PTT (corrects with mixing study)
iv. TX: Factor IX infusion, DDAVP not helpful

5. Lymph Poisoning (Plumbism)

a. Patho: causes cell death, shortens lifespan of RBC and inhibits multiple enzymes needed for heme synthesis-
>acquired sideroblastic anemia (MC in kids)
b. Symptoms: abdominal pain with constipation, neurological symptoms (ataxia, learning disabilities, coma, shock)
c. DX: serum lead and inc serum iron. Dec TIBC & inc Ferratin (similar to AOCD except inc serum Fe, not dec).
i. Peripheral smear-> microcytic, hypochromic anemia with basophilic stippling (denatured dots of RNA)
and ringed sideroblasts (iron accumulation in mitochondria due to failure of incorporation of iron into
Hgb)
ii. Xray: shows lead line (linear hyperdensities @ metaphyseal plates). May see lead line in gums in adults
iii. All pts w/ elevated BLLs on capillary samples must have confirmatory venous blood testing - Gold
standard
d. TX: remove source of lead. +/- chelation therapy
 i. Detectable BLL <5: Education, get rid of source, nutrition, annual blood testing until age 6, close
monitoring
ii. Detectable BLL 5-14: Retest 1-3 months, then every 3 months after
iii. Detectable BLL 15-44 : Have confirmatory venous BLL within 1-4 weeks
iv. Detectable BLL >45 – 69: Have confirmatory venous BLL within 48 hours. Chelation therapy, Measure
BLL weekly.
1. IV calcium disodium edetate [antidote] + dimercaprol (BAL). Can also use oral succimer
v. Detectable BLL >70: Repeat BLL within 24 hours, hospitalization, chelation therapy

6. Leukemia
*Acute will be sick (fever, night sweats, bleeding infx). Chronic will be asymptomatic, found on routine exam in late stage
*Myelogenous is Neutrophils, Lymphocytic is Lymphocytes
a. AML
i. Patho: CA of Immature neutrophils in the blood that crowd out healthy cells
ii. Epi: MC acute form in adults. >50 YO. Can be de novo or exposure to radiation, benzene, chemo, or
transformation of other marrow cancers (CML)
iii. Symptoms: Bleeding, bruising, petechiae, pallor, fever set in rapidly. Pancytopenia (splenomegaly,
gingival hyperplasia), leukostasis WBC >100,000, CNS-HA, Pulmonary-dyspnea
iv. DX: Peripheral smear shows blasts. Confirm with bone marrow bx showing >20% blasts and cytogenic
analysis revealing neutrophils
v. M3 type (Promyelocytic): special subtype, dx by presence of Auer Rods
vi. TX: combination chemo (idarubicin + Ara-C) +/- allogenic bone marrow transplant after remission. For
M3 type, give Vit A to induce development out of the blast phase by all-trans retinoic acid.
b. CML
i. Patho: Cancer of matured neutrophils in the blood. granulocyte proliferation, >50 YO
ii. Symptoms: asymptomatic until blastic crisis (acute leukemia), splenomegaly
iii. DX: diff with strikingly inc WBC counts with abnormal neutrophils (>60-% WBC, >90% PMNs). Confirm
with bone marrow BX and Cytogenetics. Associated with Philadelphia chromosome. Dec leukocyte
alkaline phosphatase, <5% blasts
iv. TX: Chemo- Tyrosine-kinase inhibitor (Imatinib) or (hydroxyurea), stem cell transplant if severe or failed
chemo
v. Prog: Inevitably becomes resistant, progresses to AMK, and patient succumbs.
c. ALL
i. Patho: Immature lymphocytes in the blood that crowd out the health cells. CA of lymphoid stem cells in
marrow->lyph nodes, spleen, liver
ii. Epi: mc childhood malignancy (3-7), increased incidence of ALL in kids >5 within down syndrome
iii. Symptoms: pancytopenia (fever MC), bleeding, bone pain, CNS symptoms. CNS and testis MC mets site
iv. DX: Bo Peripheral smear shows blasts. Confirm with bone marrow bx showing >20% blasts and
cytogenic analysis revealing lymphocytes.
v. TX: oral chemo (cyclophosphamide, doxorubicin, methotrexate). Highly responsive to combo chemo
with 90% remission rate. Consider Intrathecal methotrexate for CNS dz because CNS is a sheltered
region for ALL to hide while undergoing therapy.
1. Benign Leukmoid Reaction: increased WBC in response to stress/infection. Usually no
splenomegaly, increased Alk Phos, hx of precipitating factor
d. CLL
i. Patho: Mature lymphocytes in the blood. B cell clonal CA
ii. Epid: MC leukemia in adults overall
iii. Symptoms: asymptomatic inc WBC , fatigue, dyspnea, lymphadenopathy
iv. DX: peripheral smear with well differentiate lymphocytes with scattered smudge cells (fragile B cells).
However defining the disease is made with diff showing absolute lymphocyte cout >50 and bone
marrow bx.
v. TX: observation if indolent, chemo is symptomatic (Fludarbine), stem cell transplant is curative (if <65
YO)
 vi. Prog: 10 year survival is average, if there old do nothing

7. Lymphoma
a. Small lymphocytic lymphoma
i. Patho: closely related to CLL, indolent course. More common in elderly
b. Follicular, small, cleaved-cell lymphoma
i. Patho: a common form of NHL, indolent course
ii. Symptoms: presents with painless, peripheral lymphadenopathy
iii. TX: cured with radiotherapy, 15% have localized disease
c. Diffuse, large B-cell lymphoma
i. Symptoms: Presents as large extranodal mass
ii. TX: 85% cure rate with CHOP
d. Lymphoblastic lymphoma (T cell)
i. Patho: more common in children, may progress to T-ALL
ii. TX: aggressive, may respond to chemo
e. Burkett lymphoma
i. Etiology: African version like EBV
ii. Symptoms: African version-> involves facial bone and jaw. American version->rapidly expanding
abdominal mass, GI sx, marrow or CNS dz
iii. DX: Starry sky appearance
iv. TX: grave prognoses, treat aggressively with chemo
f. Hodgkin Disease
i. Patho: lymphocytic neoplasm that is of a contiguous orderly spread in upper body lymph nodes (neck,
axilla, shoulder, abdomen)
ii. Etiology: peaks at 20 and then again after 50, associated with EBV, MC in males
iii. Symptoms: Painless lymphadenopathy of post cervical and supraclavicular nodes (firm, mobile) that
may be increased pain with alcohol
1. Systemic B symptoms (advanced): Pel-Ebstein fever (cyclic fever with night sweats), weight
loss, anemia
iv. DX: Excisional bx (FNA insufficient) showing Reed-Sternberg cell-abnormal B cells/large cell with owl
eye appearance. If it is negative for lymphoma consider mets and infections.
v. Staging: any lymphoma start with chest x-ray then perform either a Pet/Ct or CT of
chest/abdomen/pelvis. If everything is negative a bone marrow bx must be performed to exclude bone
marrow involvement.
vi. TX: chemo-radiation regardless of stage
vii. Staging:
g. Non Hodgkin
i. Patho: Lymphocytic neoplasm with diffuse B cell, T cell, and follicular involvement seen in PERIPHERAL
lymph nodes. MC>50
ii. Risk: age, immunosuppression (HIV), connective tissue disease, FH, radiation
iii. Symptoms: painless lymphadenopathy (extranodal site common-GI,skin,CNS); Burkitt lymphoma;
systemic B symptoms (rarer in NHL)
iv. DX: lymph bx shows starry sky patter
v. Types:
1. Burkitt Lymphoma = abdominal pain, rapidly growing lymphadenopathy, spontaneous tumor
lysis syndrome
a. Males 4-6 y/o - “boys and belly pain”
b. Aggressive type of B-cell lymphoma
2. Diffuse large B cell lymphoma = rapidly enlarging symptomatic mass
3. T cell lymphoblastic lymphoma = peripheral lymphadenopathy, respiratory distress, wheezing,
superior vena cava syndrome
a. Males, medium dx 12 y/o
4. Anaplastic large cell lymphoma = painless lymphadenopathy, can have skin/subcutaneous
involvement, constitutional symptoms
a. Medium dx 12 y/o

vi. TX: Follicular->Rituximab (ab vs CD20 on B cells). Diffuse Large B cell-> MC and aggressive but curable
with chemo (Rituximab, Cyclophosphamide, Hydroxydaunorubicin, Oncovorin, Prednisone)

vii. TX side efefcts:

8. Neutropenia
a. Aplastic Anemia
i. Etiology: radiation, infection, toxins, drugs, can be congenital
ii. Symptoms: weakness, fatigue, palpitations, DOE, tinnitus, bleeding & bruising, infections
iii. DX: CBC-anemia, neutropenia, thrombocytopenia. Peripheral smear-> hypocellularity
iv. TX: Transfusions. Immunosuppression (cyclosporine x 1 year, steroids). Cure is allogenic stem cell
transplant
b. Myeloma
Pediatric HEENT

1. Acute Otitis media

a. Infection of the middle ear, temporal bone and mastoid hair cells.
b. Patho: URI causes Eustachian tube edema  negative pressure  fluid/mucus in middle ear  bacteria *MC
preceded by viral URI*
i. S.pneumo MC, H. influenza, Moraxella catarhalis, Strep pyogens
c. Risk: ET dysfunction (narrow), day care, pacifier use, parents smoke, on breastfed
d. Symptoms: otalgia, fever, ear tugging-causes relief, conductive hearing loss. Usually quick onset
i. If TM perf  rapid relief + otorrhea, heals 1-2 days
ii. If effusion  asymptomatic +/- no inflammation
e. PE: bulging, erythematous TM with effusion, DECREASED TM mobility with otoscopy. * If bullae on TM  think
Mycoplasma pnuemo
f. TX: Amoxicillin TOC 10-14 days. In children use Cefexime. Augmentin is 2nd line, use if reoccurs/recent abx use.
If PCN allergy can use azithro, Erythromycin-Sulfisoxazole, cefdinir, azithromycin
i. Recurrent: myringotomy (drainage) or tympanostomy. *think about IDA workup + CT*  can also do
tympanocentesis to identify exact causative organism
ii. With effusion: observation
iii. If present with conjunctivitis as well, likely H.influenza origin which produce beta lactamase so give
Augmentin

2. Acute pharyngotonsilitis
a. Patho: viral MC overall cause (adenovirus, rhinovirus, enterovirus, EBV, RSV, influenza). Bacterial- GABHS being
MC
b. Symptoms: sore throat, pain on swallowing or with phonation, ANTERIOR adenopathy
c. DX: rapid-strep tests is specific. If neg but high suspicion, send for culture
d. TX: symptomatic (fluids, saline gargle, lozenges, NSAIDS). If S.pyogens give penicillin-amoxicillin (erythromycin
or clinda if allergy)

e. Test vs Don’t Test:

f. Note: children with strep throat can return to school 24 hours after antimicrobial therapy AND afebrile

3. Allergic rhinitis
a. Patho: MC overall type, IgE mediated-> mast cell histamine release
b. Symptoms: pale/violaceous boggy “bluish” turbinates, nasal polyps with cobblestone of post oropharynx,
allergic shiners, salute sign (transvers line across nose)
c. DX: clinical. Skin testing 1st line as RAST serum testing may overcall allergens
d. TX: intranasal corticosteroids. Avoidance and environmental control. Can use oral antihistamine (no congestion
effect) and decongestants (no rhinorrhea/sneezing effect) but look out for rhinitis medicamentosa/rebound
congestion of >3-5 day use. +/- Leukotriene antagonist.
 i. 2nd gen H1 antihistamines>1st gen H1 antihistamines; less sedation effect since it does not cross the
BBB (* H2 blockers effect gastric parietal cells)
1. Examples: Loratadine (Claritin), Cetiriizine (Zyrtec), Fexofenadine (Allegra)

4. Conjunctivitis
a. Viral: MC is adenovirus due to swimming pool
i. Symptoms: foreign body sensation, erythema, itching, NORMAL vision. +/- viral sx
ii. PE: preauricular lymphadenopathy, watery discharge, scanty mucoid discharge, bilateral. Punctate
staining on slit lamp.
iii. TX: supportive (cool compress, artificial tears), antihistamines if itchy
b. Allergic:
i. Symptoms: bilateral conjunctival erythema (red injection), +/- rhinorrhea, discharge, cobblestone
mucosa of inner/upper eyelid, itching, tearing +/- chemosis (swelling on conjunctiva), allergic shiners
(venous congestion under eyes)
ii. TX: Avoid triggers, combination eye drops (antihistamine + mast cell stabilizer), artificial tears, +/- oral
2nd gen H1 blockers.
c. Bacterial: MC S.aurus, Strep pnuemo via direct contact
i. Symptoms: purulent discharge, lid crusting, NO visual changes, absence of ciliary injection. Use
fluorescein to detect abrasion or keratitis
ii. TX: topical abx-> erythromycin, moxifloxacin, sulfonamides (polymyxin B Sul-Trimethroprim).
1. If contact/lens: must cover pseudomonas with quinolone or aminoglycoside.
2. If chlamydia or gonorrhea: admit for IV abx (ceftriaxone/azithro) and DON’T use steroids
d. Opthalmia Neonatorium
i. Definition: neonatal conjunctivitis
ii. Patho: Day 1->silver nitrate/chemical use. Day 2-5 -> gonococcal. Day 5-7-> chlamydia. Day 7-11-> HSV
iii. TX:
1. Standard prophylaxis: given immediately after birth with topical erythromycin ointment (only
works for gonorrhea-NOT chlamydia). Topical tetracycline, or silver nitrate (outdated) to
prevent corneal ulceration or blindness
2. TX once infected: For Gonorrhea->Ceftriaxone IM. For Chlamydia-> Erythromycin PO

5. Epiglottitis
a. Patho: inflammation of epiglottitis that can interfere with breathing (emergent). H.Influenza MC-non Hib seen
commonly in adults with crack/coke use
i. In immunocompromised hosts, epiglottitis may be caused by other microbes such as Pseudomonas
aeruginosa and Candida species. Most commonly caused by Strep, Staph, H.influenzae (prior to the Hib
vaccine)
b. Epi: kids 3m-6 /6-12?YO, males 2x MC
c. Symptoms: (3 D’s) dysphagia, drooling, distress. Odynophagia, inspiratory stridor, muffled voice, tripoding. NO
prodrome (bacterial no viral) but high fever and rapid onset
 d. DX: Direct visualization with Laryngoscopy is definitive (see cherry red epiglottis with swelling), lateral cervical
xray (see thumb sign). DO NOT attempt to visualize with tongue depressor to avoid spasm.
e. TX: areaway maintenance (+/-controlled intubation in OR), can begin bag-valve mask until air way secure.
Dexamethasone to reduce edema. 2nd/3rd generation cephalosporin (ceftriaxone or cefotaxime) +/- penicillin
for staph coverage
f. Prevention: vaccinate against H.Influenza

6. Epistaxis
a. Patho:
i. Anterior (MC): nasal trauma, low humidity in hot environments, rhinitis, ETOH, platelet dysfunction
(*kiesselbach’s plexus mc site of bleeding*)
ii. Posterior: HTN and atherosclerosis mc risk factors (*palatine artery mc site of bleeding*)…look for
bleeding in both nares and posterior pharynx
b. TX: Direct pressure is 1st line (10-15 min leaning forward) +/- with petroleum guaze. Topical decongestants like
phenylephrine or Afrin. Cauterization if failed and site can be seen. Nasal packing if severe/refractory->
*consider cephalexin or clindamycin to prevent Toxic Shock Syndrome*
c. Adjunctive TX: Avoid exercise/spicy foods and use humidifiers/bacitracin for moistening of mucosa
d. Complications: septal hematoma may cause loss of cartilage if hematoma not removed. Silver nitrate not used in
children due to nasal septal perforation risk
e. Note: rare in children <2 YO so suspect trauma or systemic illness. Hematemesis indicates swallowed blood 
likely posterior bleed

7. Hearing Impairment
a. Sensorinueroal (inner ear): lateralizes to normal ear with Webber and has normal AC>BC with Rinne test.
Difficulty hearing own voice
i. Etiology: presbyacuisis MC, loud noise exposure, acoustic neuroma, labrynthitis, Meniere syndrome
b. Conductive (ext/middle ear): lateralizes to effected ear with Webber and BC>AC with Rinne test
i. Etiology: cerumen impaction MC, defect in sound conduction (foreign body or cerumen impaction),
damage to ossicles (cholesteatoma), mastoiditis, otitis media
ii. Cerumen impaction: tx with hydrogen peroxide 3% or Carbamide peroxide. Can de aural toilet
(irrigation and curette removal of cerumen with suction. Only if no TM perf and water at body temp)
iii. Tympanic Membrane Perforation: refer to # 14
iv. Cholesteatoma:
1. Patho: abnormal keratinized collection of desquamated squamous epithelium->mastoid bone
erosion. (Granulation tissue that erodes ossicles->conductive hearing loss)
2. Etiology: Repeated middle ear infection. MC due to chronic ET dysfunction (neg pressure
inverts TM).
3. Symptoms: painless otorrhea (brown/yellow discharge with odor)
4. DX: otoscope shows granulation tissue +/- conductive hearing loss
5. TX: surgical excision and ossicle reconstruction
v. Otosclerosis: abnormal bony overgrowth->slowly progressing conductive hearing loss, tinnitus (not
vertigo).TX with stapedectomy with prosthesis, hearing aid
vi. Foreign body: ear pain drainage, conductive hearing loss. TX with removal and asses TM for rupture.
1. Foul smelling unilateral rhinorrhea, ear pain, aspiration
2. If bug, unilateral scratching or buzzing and should be treated with lidocaine/warm mineral
oil/ethanol and retrieval but never light
c. Note: In an infant with suspected hearing loss an ophthalmology exam should be part of the physical exam.
There is an increased risk of ophthalmologic abnormalities in children with sensorineural hearing loss
(webber/rennie/aduiometery require behavioral response and is not useful in young children)
 d. Vertigo
i. Peripheral: labyrinth or vestibular nerve
a. Clinical: horizontal nystagmus (away from effected size) that is fatigable. Sudden onset
of tinnitus and hearing loss.
2. BPV: episodic vertigo (10-60 sec) provoked by head position and NO hearing loss caused by
displaced otoliths
a. DX: dix-hallpike elicits fatigable horizontal nystagmus
b. TX: epley maneuver, antihistamine
3. Meniere: episodic vertigo (min-hours) + tinnitus + ear fullness+ fluctuating hearing loss due to
idiopathic distension of endolymphatic compartment of inner ear by excess fluid. May see
horizontal nystagmus and N/V
a. DX: transtympanic electrochleography. Loss of nystagmus with caloric test.
Audiometry with loss of low tones.
b. TX:
i. Symptomatic:
1. Antiemetics-> antihistamines (Meclizine), benzos, anticholinergics
(scopolamine).
2. Decompression-> with tympanostomy tube if refractory
ii. Prevention: diuretics (HTZ). Avoidance of salt/caffeine/chocolate/ETOH
c. Syndrome has identifiable cause, Disease is idiopathic
4. Vestibular Neuritis: continuous vertigo and NO hearing loss due to inflammation of vestibular
portion of CN 8 after viral infection. May see dizziness, N/V, gait disturbances.
5. Labrynthitis: continuous vertigo + hearing loss/tinnitus from cochlear involvement
ii. Central vertigo: brainstem, or cerebellar
a. Etiology: Migraine, cerebellopontine tumors, CV dz, MS, vestibular neuroma
b. Clinical: vertical nystagmus that is nonfatgiable and continuous. Gait problems more
notable, gradual onset, + CNS symptoms
2. Acoustic (vestibular) CN V111 Neuroma
a. Patho: CN 8 Schwannoma- benign tumor of Schwann cells
b. Symptoms: unilateral sensorineural hearing loss in an acoustic neuroma until proven
otherwise. Tinnitus, facial numbness, continuous disequilibrium
c. DX: MRI. If bilateral suspect Neurofibromatosis type 11
d. TX: surgery or focused radiation

8. Mastoiditis
a. Patho: inflammation on mastoid hair cells in temporal bone
b. Etiology: usually a complication of prolonged or inadequately treated otitis media
c. Symptoms: deep ear pain (worse a night), fever, anteriorly rotated ear, mastoid tenderness
d. Complications: hearing loss, labrynthitis, vertigo, CN V11 paralysis, abscess
e. DX: CT 1st line
 f. TX: IV abx; vanco + cefepime/ceftazidime (if recent abx use or recurrent AOM to cover P. aeruginosa) + middle
ear/mastoid drainage (myringotomy +/- tympanostomy tube placement). Prompt surgical evaluation needed
i. Refractory: mastoidectomy

9. Oral candidiasis/thrush
a. Patho: caused by Candida albicans which is part of the normal flora but can be pathogenic due to local or
systemic immunosuppressed states (HIV, chemo, steroid inhaler w/o spacer, abx use, DM, dentures)
b. Symptoms: mouth or throat pain
c. DX: clinical- white-curd like plaques that bleeds when scraped. KOH smear- budding yeast/pseudohypae
d. TX: nystatin liquid TOC , oral fluconazole

10. Orbital cellulitis

a. Patho: 2/2 to sinus infection (ethmoid 90%). Can be caused by dental/facial infections or bacteremia
b. Etiology: MC in kids 7-12 YO
c. Symptoms: decreased vision, pain with ocular movement, proptosis (bluffing eye), erythema and edema.
d. DX: High resolution CT scan showing infection of fat and ocular muscles
e. TX: IV abx (vanco, clindamycin, unasyn)
f. NOTE: preseptal cellulitis is infection of eyelid and periocular tissue with ocular pain and swelling but NO visual
changes and NO pain with ocular movement

11. Otitis externa (swimmers ear)

a. Patho: excess H20 or local trauma changes pH of ear causing bacterial overgrowth.
i. Pseudomonas MC, proteus, S.aurus, S.epidermis, GABHS
b. Symptoms: unilateral ear pain, pain on palpation of pinna (unlike media) pruritus in ear canal, auricular
discharge, pressure/fullness. *Hearing is usually preserved*
c. PE: pain on traction of the ear canal/tragus, external auditory canal erythema/edema/debris
d. TX: Cipro/dexamethasone. If TM perf may use Ofloxacin. May also use aminoglycoside combination if TM perf
NOT suspected (due to ototoxicity risk)
e. Malignant otitis externa: osteomyelitis at skull base 2/2 to pseudomonas (common in DM and
immunocompromised). TX with IV antipseudomonal such as Piperacillin or Ceftazadime + Quinolone or
aminoglycoside

12. Peritonsillar abscess

a. Patho: tonsillitis  cellulitis  abscess formation. MC strep pyogens (GABHS), staph aureus, polymycrobial (+
anaerobes)
b. Symptoms: dysphagia, pharyngitis, muffled hot potato voice, difficult handling oral secretions, trismus, uvula
deviation to contralateral side, tonsillitis
c. DX: CT 1st line
d. TX: abx (unsays or clinda or flagyl) and aspiration or I & D. Can do tonsillectomy if recurrent strep infections or
chronic tonsillitis

13. Strabismus
a. Patho: misalignment of the eyes (presents around 2-3 months)
i. Esotropia: convergent strabismus-deviates inward (cross eyed)
ii. Exotropia: divergent strabismus-deviates outward
b. Symptoms: Diplopia, scotomas or amblyopia
c. DX: Hirschberg corneal light reflex testing (screen). Cover-uncover to determine angle of strabismus.
Convergence testing
d. TX: Patch therapy (on normal eye-strengthens effected one). Corrective surgery if unresponsive
e. Complication: if not corrected by 2 YO, amblyopia can occur and visual acuity be unfixable

14. Tympanic membrane perforation

a. Patho: MC due to penetrating or noise trauma (at pars tensa), otitis media
b. Symptoms: acute ear pain, hearing loss +/- blood otorrhea, tinnitus, vertigo
c. DX: otoscope examination +/- conductive hearing loss
d. TX: heal spontaneously, follow up requires in four weeks. Avoid water/moisture/topical aminoglycosides in ear
with TM rupture. Should be treated with ofloxacin otic drops if contaminated.
Pediatric Infectious Diseases

1. Atypical mycobacterial disease

a. Mycobacterium Marinum (fish tank granuloma)
i. Patho: found in fresh and salt water. Inoculation of a skin abrasion or puncture in a patient with
contact of an aquarium, salt water, or marine animal (fish, turtle)
ii. Risk: occupational hazard for aquarium handlers, marine workers, fisherman, seafood workers
iii. Symptoms: local cutaneous dz (erythematous bluish papule or nodule at site of trauma). Subsequent
lesions may occur along path of lymphatic drainage.
iv. DX: culture
v. TX: tetracycline, quinolone, macrolides, sulfonamides.

2. EBV
a. Transmission: saliva, especially 15-25 YO
b. Symptoms: fever, sore throat, POSTERIOR cervical lymphadenopathy, malaise, splenomegaly, petechial rash (esp
if Ampicillin given)
c. Manifestations: associated with Hodgkin Lymphoma, may cause Burkitts lymphoma and CNS lymphoma in
patients with AIDS
d. DX: heterophile (monospot) ab test is + within 4 wks. Rapid Viral Capsid Antigen test. Peripheral smear has
>10% atypical lymphocytes (>50% lymphocytes)
e. TX: supportive. Steroids only if airway obstruction. Avoid trauma and contact sports at least 1 month if
splenomegaly

3. Erythema infectiousum (fifth disease/slapped check)

a. Patho: Parovirus B19, 4-14 day incubation
b. Symptoms: asymptomatic, coryza, fever->slapped cheeck rash on face with circumoral pallor 2-4 days) -> lacy
reticular rash on extremities. Spares palms and soles. Resolves 2-3 weeks
i. Arthroplasty/arthralgia’s in older kids and adults. Associated with fetal loss in regency
c. DX: serology
d. TX: supportive
e. Complication: PVB 19 may cause aplastic crisis in patients with sickle cell disease or G6PD deficiency. If baby
gets sick near mom while pregnant-can cause hydrops fetalis in new baby. Arthritis in adults

4. Coxackie virus
a. Patho: part of the enterovirus family. MC in kids <5 YO. Spread fecal-oral and oral-oral. MC in late summer/early
fall
b. Type: A
i. Hand-foot-mouth dz
1. Symptoms: Mild fever, URI, dec appetite 3-5 days->vesicular lesions with erythematous halos in
oral cavity (mucosa, tongue)->exanthem 1-2 days after on distal extremities (including palms
and soles) +/- buttocks
a. Lesions on mouth may be described as small greyish vesicles and punched out ulcers
on the posterior pharynx
ii. Herpangina: sudden onset of high fevers, stomatitis (small vesicles on soft palate, uvula, tonsillar pillars
that ulcerate then heal)
c. Type: B
i. Pericarditis and myocarditis: MC cause
ii. Pleurodynia: fever and severe pleuritic chest pain and paroxysmal spasms of chest/abdomen muscles
d. TX: supportive (antipyretic, topical lidocaine)

5. Herpes simplex
a. Symptoms: prodromal symptoms 24 hours prior (burning, paresthesia’s, tingling)->painful grouped vesicles on
erythematous base *Herpes Hurts*
 i. Oral lesions: acute herpetic gingovstomatitis (fever, gingivitis, yellowish vesicles on tongue/lip), acute
herpetic phatyngotonsillitis (greyish exudate from rupture vesicles), herpes labialis (cold sores, fever
blisters with stress)
ii. Genital lesions: MC in HSV-2
iii. Herpes keratitis: shown on slit lamp via dendritic ulcers->tx with Trifluridine or Ganciclovir eye drops.
Oral acyclovir
iv. Bell’s palsy, HSV esophagitis (small deep ulcers), herpetic whitlow on nail, finger), encephalitis (MC
cause)
b. DX: PCR most sensitive and specific. Tzanck smear with multinucleated giant cells and intranuclear inclusion
bodies (not really used anymore)
c. TX: acyclovir (IC if encephalitis), valacylovir

6. Influenza
a. Types: A (Hemagglutinin (H) and Neuraminidase (N)) and Type B are season epidemics, Type C cause mild
respiratory illness
b. Symptoms: 1-4 day incubation, fever, cough, sore throat, HA, fatigue, diarrhea, vomit,
c. Complication: most recover <2 weeks, pneumonia, bronchitis, sinus infection, CHF worsen
d. Prevention: annual vaccine for anyone >6 months
*recommended groups: 6-59 months, >/= 50, chronic pulmonary condition, DM, immunocompromised,
pregnant, caregivers and contacts
1. Inactivated influenza vaccine (IIV)
a. Should be given to pregnant women, NOT LAIV
b. Adults >/= 65 should get standard or high dose IIV or RIV
c. Give to immunocompromised
d. <2, >50
2. Recombinant influenza vaccine (RIV)
a. >18 YO
3. Live attenuated influenza vaccine (LAIV)
a. Nasal spray, can be given to those 2-49 and not pregnant
b. DON’T give to ,<2,>50, pregnant, immunocompromised
e. DX: nasopharyngeal test (NAAT>RIDT in outpatient, RT-PCR in hospitalized)
f. TX: begin within 48 hrs of symptoms->Oseltamivir (Tamiflu) TX for 5 days
i. Post-exposure prophylaxis for 7 days , test for influenza if become symptomatic during treatment and
switch to xofluza
ii. Prexposure prophylaxis: at least 3 months of age and if high risk of complications and not vaccinated,
transplant s/p 6-12 months. Start when community outbreaks start, and 10 days after last know case.
iii. Zanamivir (Relenza) may cause Bronchospasm, HA, throat discomfort
iv. Peramivir (Repivab) for 18 YO+, not established for serious illness
v. Consider bacterial if severe or no improvement in 3 days, repeat PCR, could be NTI resistant->treat with
Baloxavir (Xofluza)
 g. Note: In the first season in which they are vaccinated for seasonal influenza, two doses of influenza vaccine are
recommended for children six months to eight years old. This approach optimizes the immune response.

7. Rubeola (Measles)
a. Patho: Paramyxovirus with 10-12 day IP
b. Transmission: respiratory droplets.
c. Symptoms: URI prodrome (high fever, 3 C’s- cough, coryza, conjunctivitis)-> kapolik spots (small spots in buccal
mucosa with pale blue/white center that proceeds rash by 1-2 days and lasts 2-3 days)-
>morbiliform/maculopapular brick-red rash on face beginning @ hairline->extremities that darkens
(palms/soles seen last). Rash lasts 1 week and fever usually with it
d. TX: supportive. Vit A reduces mortality
e. Complications: diarrhea, otitis media, pneumonia (MC complication leading to death), conjunctivitis,
encephalitis/ Subacute sclerosing panencephalitis

8. Mumps
a. Patho: Paramyxovirus
b. Transmission: patients infected 48 hours prior to and 9 days after onset
c. Symptoms: low grade fever, myalgia, HA->parotid gland enlargement
i. initial unilateral involvement is followed by contralateral involvement a few days later in 90% of cases
d. DX: serology. Inc amylase. Clinical MC
e. TX: Supportive
f. Complications: orhcitis in males, MC cause of acute pancreatitis in children. Deafness, infertility, arthritis.
g. Prevention: MMR vaccine 12-15 months with second dose at 4-6 YO

9. Pertussis (whooping cough)

a. Patho: high contagious 2/2 to Bordetella pertussis (gram neg), MC in children <2
b. Symptoms: Catarrhal phase (URI symptoms 1-2 weeks)->paroxysmal phase (coughing fit with inspiratory
whooping sound, 2-4 weeks)->convalescent phase (resolution of coughing phase)
i. associated with cyanosis, apnea, a final audible “whoop,” and posttussive emesis
c. DX: PCR of nasopharyngeal swab is GS. Lymphocytosis
d. TX: Supportive is mainstay, abx shortens duration within 1st 7 days of sx onset (Macrolide/erythromycin TOC,
Bactrim 2nd line)-also lessen contagiousness so give even after 7 days
e. Complications: pneumonia, otitis media, sinusitis, seizures, mortality in infants due to cerebral hypoxia

10. Pinworms (Enterobiasis vermicularis)

a. transmission feco-oral (hand->mouth) in school aged kids/daycare
b. symptoms: perianal itching esp. nocturnal (eggs being laid)
c. DX: Scotch tape test to look for eggs, not passed in stool so stool sample is not useful
d. TX: Albendazole, Mebendazole. Pyrantel 2nd line. Treat entire family.

11. Roseola (sixths disease, exanthema subitum)

a. Patho: Human Herpes virus 6 or 7 (antigen-antibody complex since rash appears after ‘infection’)
b. Transmission: respiratory droplets, MC < 5 YO, 10 day incubation
c. Symptoms: prodromal with high fever 3-5 days which resolves before onset of-> rose, pink
macupapular,blanchable rash on the trunk/back that spread to face x 1-2 days
i. Only childhood exanthema that starts on trunk and spreads to face. May be ‘well and alert during febrile
phase’
d. TX: supportive, anti-inflammatories, antipyretics
e. Complications: febrile seizures

12. Rubella (German Measles)

a. Patho: Togarovirus family
b. Transmission: respiratory droplets, 3 day rash*
c. Symptoms: low grade fever, cough, lymphadenopathy (post cervical, post auricular) -> pink, light red spotted
maculopapular rash on face->extremities x 3 days (rubella spreads more rapidly than measles and does not
darken or coalesce)
 i. Forchhimer spots: small red macules or petechiae on soft palate
ii. Transient photosensitivity and joint pain may be see (young women MC)
d. DX: clinical. Rubella-specific IgM ab via enzyme immunoassay
e. TX: supportive, less complications compared to Rubeola/measles
f. Complications: tetotrogenic in 1st trimester (congenital rubella)-> sensorineural deafness, cataracts ,TTP
(blueberry muffin rash), mental retardation, heart defects

13. Varicella Infection

a. Transmission: respiratory droplets, direct contact, 10-20 day incubation
b. Symptoms:
i. Chicken pox: primary infection, fever, malaise, vesicles on erythematous base in different stages
(macules, papules, pustules, crusted) starting on face/trunk->extremities->can lead to bacterial infection
complication. Described as a dew drop on a rose petal.
ii. Shingles->reactivation along one dermatome (disseminated in HIV)
iii. Herpes Zoster ophthalmicus->involving one division of the trigeminal nerve (CN V), will see dendritic
lesion on slit lamp.
iv. Ramsy-Hunt syndrome->facial nerve (V11) involvement causing otalgia, lesions on ear/canal/TM, facial
palsy, tinnitus, vertigo, deafness
v. Post herpetic neuralgia-> pain>3 months, hyperesthesia’s and dec sensation
c. TX: (chicken pox) symptomatic, (shingles) acyclovir within 72 hours, (RHS) oral acyclovir + steroid, (PHN)
Gabapentin or TCA
d. Complications: scarring and secondary infections (staph, GAS)
Pediatric Neurology

1. Anticipatory guidance
a. Safety recommendations
i. Infants and toddlers: rear facing car seats until 2 YO or 35 lb
ii. 2 YO: forward facing car seat with harness->belt positioned booster
iii. 8-12 YO or 4.9 ht. : child can sit in back seat with belt
b. SIDS prevention
i. Encourage
1. Tummy time - allows infant to develop strength to avoid situation that may compromise
breathing
2. Pacifiers - to help avoid bottle feedings as a sleep aid as this is assoc with increased risk (use
during nap/bedtimes)
3. Back to sleep
ii. Discourage
1. Excess warmth and blankets
2. Home monitors are not effective in prevention
c. CRAFFT questionnaire for drugs and alcohol
i. Have you ridden in a CAR with someone who was high/been using?
ii. Do you use it to RELAX?
iii. Do you use it ALONE?
iv. Do you FORGET things when you use
v. Do your FAMILY/FRIENDS tell you to cut back?
vi. Have you gotten in TROUBLE for using
vii. **if 2 or more = treatment needed
d. Screening
i. TB: assess with questionnaire on first contact, 6 months, and one years old. Only test if suspected.
ii. Lipid profiles: (2-8) selective fasting lipid profile based on FH; (9-11) universal non-fasting lipid
screening; (12-16) don’t test because of puberty changes; (17-21) universal screening
iii. Lead: screen for risk at 6, 9, 12, 18, and 24 months of age, and annually thereafter through six years of
age (old house, renovation). Check BLL if risk detected (BLL >5=poisoning)
iv. BP: measured annually beginning at 3 YO
v. STI: may test based on parental hx (sexual partners ect.)
vi. Alc/drug/smoking: screening begins at 11 YO
e. Breast feeding
i. LACKS vitamin D - 400 IU daily for breastfed infants
f. Developmental delays
i. screen at 9, 18, 24/30 months
ii. motor, language, cognitive, social, emotional are significantly delayed compared to the expected level
for age (25% or more difference or 1.5-2 SD from normal
iii. Tools
1. PEDS (birth-8YO): 5th grade reading level, 10 question/2 minutes, identifies children as low,
moderate, or high risk
2. ASQ (4-60 months): 3rd-12th grade reading level, parent reports on 25 items/15 minutes,
generates pass/fail score for cognitive, motor, self-help, and language
3. Direct Elicitation screens: timely, several attempts. Denver Developmental screening: originally
developed to demonstrate rate of achievement of milestones
4. Behavior screening: M-CHAT (checklist for autism in toddlers): used 16-30 months, takes 5
minutes
iv. if screen is positive: (0-36 months)->early intervention is provided through state agencies, (3-5 YO)
Preschool special education services available through state-run agencies, (5+) Public school system

2. Down syndrome
a. Patho: trisomy 21 due to nondisjunction in meiosis
 b. Risk: advanced maternal age during pregnancy
c. Complications: congenital heart disease
d. Symptoms: flat nasal bridge, transverse palmer crease (simian crease), upward slanting palpebral fissure,
protruding/wide tongue, wide gap between 1sr and 2nd toes, umbilical hernia, clinodactyly
e. DX: 1st trimester CVS + karyotype. Low AFP, low sterol, high beta-HCG
f. Screening
i. All pregnant women
ii. < 20 weeks gestation (usually between 10-13 weeks)
iii. Types of tests
1. Assessment of maternal serum levels = most widely used
2. Measurement of cell-free DNA in blood
3. First trimester combined test = sonography (looking for nuchal translucency) + PAPP-A and hCG

3. Febrile seizures
a. Definition: a seizure associated with a fever in a child usually btw 6 mo and 6 yrs
b. Presents: within the first 24 hr of fever, due to rapid change in body temp, usually > 102.2 F
c. MC triggers: viral URI, acute otitis media, roseola (HSV 6)
d. Types
i. Simple = Generalized seizures
1. <15 min
2. Not recurring during 24 hr
3. No prior neuro condition
ii. Complex = Focal seizures
1. >15 min, eye rolling
2. Recurring during 24 hr
3. Known neuro condition (ie. Cerebral palsy)
e. Risk factors
i. Initial
1. viral infx (HHV6 = MCC),low grade fever, day care attendance, developmental delay, neonatal
nursery hospitalization > 30 days, FH, vitamin def (iron, zinc), vaccinations (flue, DTP, MMR)
ii. Recurrent febrile seizure
1. Age of onset of 1st seizure, more than 1 prior febrile seizure
a. Age < 18 mo
b. Short interval btw fever onset and seizure (< 1 hr)
c. Lower peak fever >104
d. First degree relative
f. Diagnosis
i. Simple->no workup needed, LP if <12 mo
ii. Complex-> CBC with culture, UA, LP, EEG, MRI
g. Treatment
i. Simple Active: airway management, high flow O2, supportive, benzodiazepine, tylenol
1. Lowering temp with tylenol DOES NOT prevent seizure
2. Warn parents/pt that recurrence is likely
3. No imaging necessary
ii. Complex: benzodiazepine to abort
1. EEG if not sure if seizure, LP if thinking meningitis, MRI looking for something in the brain
2. Start antiepileptic drugs :phenobarbital and valpric acid
iii. Rectal/buccal diazepam are effective and can be given at home for seizure lasting longer than 5 minutes
iv. *Never give Aspirin->may cause rayes syndrome

4. Immunization guidelines
a. Hep B (3)
i. Birth, 1-2 mo, 6-18 mo
b. Rotavirus (3)
i. 2,4,6 month
ii. CI: hx of intacusseption
 c. DTaP (5+1)
i. 2,4,6, 15-18 months, 4-6 years…booster @ 11-12 (TdaP)
d. Hib (3 + 1)
i. 2,4,6…booster @ 12-15 months
ii. CI: <6 wk old
e. PCV13 (3 + 1)
i. 2,4,6…booster @12-15 months
ii. If high risk kids >2, they will also get PPSV23 8 weeks after completed series
f. IPV (3+1)
i. 2,4,6-18 months, 4-6 YO
g. Influenza
i. Annually starting at 6 months
h. MMR/varicella (1+1)
i. 12-15 months…booster @ 4-6 years
ii. MMR:
1. PPD test should be performed, the day of, or 4-6 weeks after the MMR vaccine as it reduces the
sensitivity
2. CI in neomycin allergy
i. Hep A (2)
i. 2 doses between 12-23 months w/ 6-18 mo gap in between dosed
j. HPV (3)
i. 3 doses 0, 2 ,6 months apart
ii. Female: 11-12 to 26 YO
iii. Male: 11-12 to 21 YO
k. Meningococcal (1)
i. 11-13 YO
*considerations:

*misconceptions

*note- avoid in mod to severe illness

5. Meningitis
Bacterial
a. Patho: may have history of sinusitis or pneumonia prior to meningitis.
b. Symptoms: Fever/chills, meningeal sx (HA, nuchal rigidity, photosensitivity, N/V)-> AMS, seizures.
i. Kernigs sign-can’t straighten leg with hip flexion (flex hip 90 deg, try to straighten leg; + if pain)
ii. Brudzinski sign-neck flexion produced knee/hip flexion
c. DX: LP CSF examination is definitive dx= 100-10,000 PMN (neutrophils), decreased glucose (<40), increased
total protein (>200), increased CSF pressure, turbid appearance (cloudy)
i. Do head CT if high risk (Think FAILS: focal neuro deficit (AMS), immunocompromised, lesions on spine,
seizures) BEFORE LP and give dose of ceftriaxone
ii. Don’t wait for LP to start empiric abx
iii. LP UNSAFE  blood culture then CT w/ abx prior to CT/LP  if CT normal can do f/u with LP
iv. LP SAFE  LP to obtain CSF culture and give abx immediately after
d. Etiology/TX
i. <1 month: GBS MC, L. monocytogens ampicillin (for listeria) + cefotaxime
ii. 1M-18y: N.meninigdis MC, S.pneumo, H.influenzae ceftriaxone + Vanco
iii. 18y-50y: S.pneumo MC, N meningitides, H.influenza Ceftriaxone + Vanco
iv. >50y: S.pneumo, Listeria monocytogens, gram neg rodsampicillin + ceftriaxone +/- Vanco
v. +/- steroids
e. Prophylaxis: ciprofloxacin 1 dose post exposure (Rifampin is alternative)
f. Give dexamethasone if step pneumo suspected or H. influenza in kids to reduce hearing loss, inflammation
g. Note: Also look out if hx of limes syphilis, listeria, RMF, TB, crypto which don’t show PNM on LP (“not bacterial”)
i. Cryptococcal->AIDs and CD4<200, seizures. May require serial taps to reduce pressure. DX with
cryptococcal antigen
ii. Lymes->targetoid lesions and endemic travel. DX with ab TX with ceftriaxone not doxy
iii. RMSF->campers, peripheral rash, DX with ab in CSF, tc with ceftriaxone
iv. TB->consider if pulmonary TB, tx with RIPE

Viral Meningitis
h. Etiology: Enterovirus MC (echovirus, coxackie), arbovirus (west nile), mumps, HSV 1 & 2, HIV
i. Symptoms: HA, fever, confusion, meningeal sx, NORMAL cerebral function
j. DX: CSF = lymphocytosis (mononuclear, NL glucose, mildly incr protein (<100), NL pressure, clear appearance
i. MRI shows diffuse enhancement of meninges; Frontal/temporal enhancement with HSV
k. TX: supportive (antipyretics, IV fluids, antiemetic’s)
l. Prog: Good, self-limited (7-10 days)
6. Normal growth and development
a. Primitive reflexes
Asymmetric tonic neck Laying supine, turn head to side  fencing posture with one arm 2-3 mo
reflex outstretched to that side, opp side flexes
Galants relfex Support baby prone, stroke back  spine curves to stimulated 2-3 mo
side
Rooting/sucking Stimulus near mouth  turning head towards + sucking 2-3 mo

Palmar/planter grasp Object placed in palp  flex fingers 2-3 mo

Moro Sudden head extension  symmetrical extension, then flexion of 3-4 mo/4-5
limbs
Placing/stepping Held vertically  lifts one foot, placing it on surface, then other 4-6 m

Positive supporting Held vertically  legs take body weight, push against (jump) 4-6

b. Mile stones

Birth Recognizes voices

2 months Raises head off chest, grasps toys, sucks finger, tracks object past midline, coos, turns
head towards sound, social smile

4-5 Rolls front to back, lifts body, holds head, bring hands to midline, belly laughs
*primitive reflexes disappear between 4-6 months

6-7 Rolls over front to back and back to front, Babbles consonants, stranger anxiety, transfers
hand-to-hand, Tripod, rakes/transfers, dada non specific

9-10 Crawls, sitting (8 mo), pull to stand (9 mo), cruising (10 mo), Sitting without support,
radial-palmer grasp

12 months Stands well, independent steps, fine pincer grasp, points to desired object, follow one
step command, one word (dad correctly)

15 months Walks well, uses spoon with spilling, drinks from cup, turns pages, follow one step
command without gesture, points to one body part, uses 3-5 words

18 months Runs well, pretend plays, imitates household task, points to three body parts, 10-25
words, spoon fork use

24 months Kicks balls, throws overhand, draws horizontal line, parallel play, follows 2-step
command, 2-word sentences, 50 + words, toilet training begins, uses stairs

36 months Toilet trained, goes upstairs alternating feet, pedals tricycle, copies circle, imaginative
play, 3-word sentences, handedness develops by 3

c. Blocks
i. 1 year = 3 block, 2 year = 6 blocks, 3 years=9 blocks
d. Shapes
i. 2 yrs = line, 3 yrs = circle, 4 yrs = square/cross (hopping), 5 yrs = triangle (skipping), 6 yrs = diamond
e. Apgar score

i. Note:
1. Taken at 1st minute and 5th minute after birth
2. Ideal score is 7 or greater; if <7 but >4 child may need extra support; 0-3 needs immediate
resuscitation
3. Low score 1 minute after may be due to high risk, premature, C-section, fast delivery, meds
given to mother
4. Low score at 5 minutes may be other issues (heart, lung, CNS)
f. Tanner stages

g. Pulsatile and seasonal (spring and summer)

h. Plot on growth charts
i. Must correct for twins, prematurity, congenital issues
i. Weight
i. Term babies lose up to 10% in first few days, return to birth wt in 2 weeks
ii. Breast fed gain weight quicker than formula fed
iii. Trends
1. ~ 30g/day until 3 mo
2. ~ 20g/day 3-6 mo
3. ~ 10g/day 6-12 mo
4. ~ 2kg/yr 2yr-puberty
5. DOUBLE birth weight by 4 mo, TRIPPLE it by 1 yr
j. Feeding
i. Adult diet by 2 YO
ii. encourage breast feeding
iii. Newborn drinks 1.5-3 oz every 2-3 hours, 2 month old drinks 4-5 onces every 3-4 hours, 4 months old
drinks 4-6 ounces , 6 month old drinks 6-8 ounces every 4-8 hours
iv. Solid foods: There is no known benefit to add complementary foods before the age of 4 months. If
delay in introduction-> delays oral motor function, child can be averse to solid foods, risk of atopic
disease
v. Toddler: avoid too much juices and sweats, consume zinc and iron, Whole cow’s milk recommended up
to 2 years of age
vi.
k. Height
i. 0 to 6 months – One inch (2.5 cm) per month
ii. 7 to 12 months – One-half inch (1.25 cm) per month
 iii. 12 to 24 months – Usually >4 inches (10 cm) per year
iv. 24 to 36 months – 3 inches (8 cm) per year
v. 36 to 48 months – 2.75 inches (7 cm) per year
vi. 4 to 10 years – 2 to 2.4 inches (5 to 6 cm) per year
l. Head circumference
i. 35 cm average at birth
ii. Increases 1 cm/mo during year one
iii. Mostly completed by 4 y/o
m. BMI
i. Start measuring at age 2 yo
n. Ideal body weight
i. For pts < 8
ii. Percent IBW
1. >120 – Obese
2. 110 to 120 – Overweight
3. 90 to 110 – Normal variation
4. 80 to 90 – Mild wasting
5. 70 to 80 – Moderate wasting
6. <70 – Severe wasting
o. Upper segment to lower segment ratio
i. Lower = top of symphysis pubis to plantar surface of foot
ii. Upper = height minus lower
p. Arm span to height
q. Failure to thrive
i. 1st babies will lose weight, then height, then HC
ii. Organic - Genetic (ie. CF), cardiac disease, pyloric stenosis, GERD
iii. Inorganic - formula, feeds, frequency

7. Seizures

a. Partial (focal) seizureconfined to small area of the brain

i. Simple partial
1. Consciousness fully maintained, NO LOC
2. EEG: focal discharge at onset of seizure
3. Symptoms: Focal, sensory, autonomic or motor sx
a. Indicated by jacksonian march - twitching of hand, then arm, then whole body
ii. Complex Partial
1. Consciousness impaired
2. EEG: interictal spikes with slow waves in temporal area
3. Symptoms: aura (patient aware of symptoms) ->impaired consciousness. (LOC). Automatisms;
lip smacking, manual picking, patting, coordinated motor movements
4. TX: partial seizures best treated with Carbamazepine, phenytoin
b. Generalized seizurediffuse brain involvement (best treated with valproate or lamotrigine)
i. Absence (Petit Mal)
1. Brief lapse of consciousness (aware of attacks), brief staring episodes, eyelid twitching, NO
post-ictal phase. LOC, no loss of tone.
2. EEG: bilateral symmetric 3Hz spikes & wave action or may be normal
3. Symptoms: can be clonic (jerking), tonic (stiffness), or atonic (loss of postural tone)
4. Epi: MC in childhood, ceasing in 20’s
5. TX: Ethosuxamide 1st line, valproic acid 2nd line, Lamotrigine
 ii. Tonic clonic (Grand Mal)
1. Phases:
a. Tonic phase: LOC->rigidity (60 sec)->clonic phase
b. Clonic phase: repetitive, rhythmic jerking (<2-3 min)->post ictal phase
c. Post ictal phase: flaccid coma/sleep (variable duration)
2. EEG: generalized high-amplitude rapid spiking, may be normal in between
3. Symptoms: may be incontinent, tongue biting, or aspiration. Auras are pre warning sign
4. TX: Valproic Acid (pancreatitis, hepatotoxicity), Phenytoin, Carbamazepine, Lamotrigine
iii. Myoclonus
1. Sudden, brief, sporadic, involuntary twitching with NO LOC. Give valproate
iv. Atonic:
1. Drop attacks-sudden loss of postural tone, NO LOC. Give valproate.
v. Status epilepticus
1. Repeated generalized seizure without recovery >30 min
2. TX: Lorazepam/Diazepam->Fosphenytoin->midazolam/propofol->phenobarbital. Thiamine +
ampule of D50
vi. DX: may require 24 hr video monitoring + EEG. Looking for spikes and waves indicative of organized
neuronal firing (abnormal for awake adults)
c. Epilepsy: recurrent seizures (two or more) which are not provoked by systemic or acute neurologic insults
i. TX: Levetiracetam (keppra). Can also use phenytoin, valproate…

d. VITAMINS work up

8. Teething
a. Symptoms: cranky, chewing on objects, excessive drooling, diarrhea
b. Facts: first teeth erupt are central incisors at 6-10 months. Primary dentition fully erupted by 30 months.
Permeant teeth by 6 YO
c. DX: clinical
d. TX: palliative-chewing on chilled teething ring, systemic analgesics? (OTC not recommended)

9. Turner syndrome (gonadal dysgenesis)

a. Patho: 45, XO karyotype (loss of part or all of x chrom in female)
b. Complications: bicuspid AV/coarctation of the aorta, ectopic kidney, horsehoe kidney, hypothyroid, hearing
loss, pul stenosis,
c. Symptoms: primary amenorrhea, short stature, infertility, shield chest, webbed neck, spaced nipples, scant
pubic hair, high palate, short 4th metacarpal, low post hairline, multiple pigmented nevi, ptosis, micrognathia
(undersized jaw)
d. DX: clinically, confirmed with karyotype. Prenatal US shows increased nuchal folds
e. TX: GH at 2-5 YO, estrogen 12-13 YO, TSH replacement, repair CoA, pyshc referral
Pediatric Orthopedics

1. Avascular necrosis of the proximal femur (Legg Calve Perthes Disease)

a. Patho: due to ischemia of femoral capital femoral epiphysis in children
b. Epi: MC in children 4-10y, 4 x MC in boys, around 6YO
c. Symptoms: painless limping x weeks (worse at end of day, with activity). Intermittent hip/thigh/knee/groin pain.
Restricted ROM (loss of abduction and internal rotation). Insidious onset and an antalgic gait (less time on
painful leg)
d. DX: XR- inc density of femoral head, widening of cartilage space. In advanced-> deformity, crescent sign
(microfractures with collapse of bone)
e. TX: PT and cast for all. Observation and bed rest if < 6 YO (self-limiting with revisualization within 2 years).
Recommend non weight baring initially with ortho f/u. NSAIDs for pain management. If > 6 YO or more
advanced->surgery
i. May need pelvic osteotomy in children >8 YO

2. Congenital hip dysplasia (DDH)

a. Risk: breech, female, large fetal size, first born, FH
b. Etiology: MC left hip
c. Symptoms: unequal thigh folds, shortening of leg, painless limp to effected side.
d. PE
i. Barlow’s (add/post): pressure to medial aspect of thigh as it is adducted thus slipping the hip posteriorly
and eliciting a palpable clunk as the hip dislocates
ii. Ortolani sign (abd/ant): a feeling of slipping as head relocates is a sign of instability
iii. Galeazzi test (one knee higher than the other when knees bent)
e. DX: Done during newborn/well-baby exam with Barlow’s/Orlani maneuvers with repeated evaluation at each
child well visit until child walks. Do US at 4-6 weeks to confirm. Can do XR if after first 6 wks
i. Limited hip abduction of less than 60 degrees while the knee is 90 digress flexed is most sensitive
f. TX: spontaneous correction by 2-6 weeks (physiologic laxity around time of birth which resolves), reversible if
corrected. Pavlik harness (keeps hips externally rotated). If failure of therapy-> open reduction
g. Complication: AVN of capital femoral epiphysis 2/2 to forced abduction/reduction

3. Juvenile rheumatoid arthritis

a. Patho: autoimmune mono or polyarthritis in children <16 YO that last for >6weeks
b. Cause: viral infection MC cause, if RF + can be due to lupus, liver dz, malignancy
c. Types
i. Pauci-Articular (oligoarticular) 50%
1. <5 joints in 1st 6 months, MC large (knee). Type 1-> iridocyclitis (anterior uveitis) + asymmetric
joint involvement. Type 11->increased incidence of ankylosing spondylitis
ii. Systemic/acute febrile (Stills disease) 20%
1. Daily arthritis, diurnal high fever, small and large joints. Salmon colored/pink migratory rash
with fever. NO iridocyclitis but + hepatosplenomegaly, hep, lymphadenopathy and serositis
association
iii. Polyarticular 30%
1. Arthritis >/= 5 joints (usually symmetric), similar to adult RA. Hip involvement common.
Increased risk of iridocyclitis, systemic symptoms less common
d. DX: really a dx of exclusion. clinical. ESR, CRP, + ANA in oligoarticular. 15% have + RA
e. TX: NSAIDs. Methotrexate. Frequent eye exams
4. Neoplasia of the musculoskeletal system
a. Osteosarcoma
i. Patho: Malignant tumor from osteoblasts, mc malignant bone neoplasm (although uncommon in
general)
ii. Epi: MC in metaphyseal plates, 10-20 YO male
iii. Present: bone pain that is dull and achy for months (ends of bones), worse at night and with activity, ST
mass, long bones MC (femur, prox tibia), gait disturbance, pathologic fracture
iv. Associations: retinoblastoma
v. DX: XR- Codman’s triangle (new bone reaction), sunburst pattern, mixed sclerotic and lytic lesions. CT
for pulmonary disease, MRI, RI surgical planning, bone bx for definitive dx required
vi. TX: amputation/limb salvage, resection, chemo, relatively resistant to radiation
vii. Prog: 3-10 year survival rate, pulmonary mets is COD
b. Ewing Sarcoma
i. Patho: From medullary tissue, caused by t (11:22) translocation
ii. Epi: MC 10 YO, then 10-20, Caucasian male
iii. Presentation: pain mid-shaft (diaphysis), MC flat and long bones, increased pain, FEVER, wt loss,
fatigue, swelling at site. Wakes child up at night. Tender to palpation
iv. DX: XR-periosteal elevation/reaction which produces reactive bone (onion skin, moth eaten,
radiolucent lytic bone lesion). CT for mets. MRI is BEST radiographic test. BX is BEST diagnostic step
v. TX: radio therapy (sensitive), chemo, surgical resection, bone transplant
c. Ostechodroma
i. Patho: BENIGN, cartilage capped protrusion of occeus tissue arising from bone surface, MC bone tumor
in kids
ii. Presentation: painless, hard mass, in distal metaphysis such as femur, prox humorus and tibia
iii. DX: XR-pedunculated or sessile mass in metaphyseal region
iv. TX: excision if symptomatic
v. Prog: malignant transformation very rare
d. Osteoid osteoma
i. Patho: BENIGN, originates from osteoblast, reactive lesion of the bone, mc male
ii. Present: MC in evening, relieved with ASA, MC in femur and tibia long bones
iii. DX: XR- osteosclerosis which surrounds small radiolucent nidus
iv. TX: tx pain with ASA, surgical excision of nidus
v. Prog: no cases of malignant transformation
 e. Osteoblastoma
i. Patho: BENGIGN, presents in 20s, MC in posterior column of spine
ii. Symptoms: involves the spine, dull aching, limp or neuro symptoms 2/2 to chord compression
iii. DX: XR, CT, MRI-similar to osteoid osteoma but larger (>2 cm)
iv. TX: curettage and bone grafting, radiation for spinal lesions that cannot be fully resected
v. Prog: can progress to neuro symptoms if not treated
f. Enchondroma
i. Patho: cartilaginous lesion (mult lesions=Olliers disease)
ii. Presentation: tubular bones of hands and feet, swollen bone
iii. DX:XR- radiolucent diaphysis or metaphyseal lesion, fingernail streaks in bone
iv. TX: excision
v. Prog: malignant transformation possible in childhood

5. Nursemaid elbow
a. Patho: lifting/swinging/pulling a child (MC 2-5 y) while the forearm is pronated and extended->radial head
wedges into stretched annular ligament
b. Symptoms: arm slightly flexed, refuses to use arm, tenderness to palpation
c. TX: reducation (pressure to radial head with supination and flexion). If child uses arm after 15 minutes, no XR
needed, if no use consider XR to r/o fracture or reattempt reduction
i. Hyperpronation method (best) - apply pressure to the radial head and hyperpronating the forearm
ii. Supination/flexion method - supinate and fully flex the elbow while applying pressure to the radial
head and pulling with gentle traction

6. Osgood-schlatter disease
a. Patho: osteochondritis of the patella tendon @ tibial tuberosity from overuse or small avulsions (2/2 to
quadriceps contraction on the patellar tendon insertion into the tibia)
b. Epi: MC cause of chronic knee pain in the young and active. MC males 10-15 with growth spirts. Teenage
athletes
c. Symptoms: activity related knee pain/swelling (running, jumping), painful lump below knee tenderness to the
anterior tibial tubercle
d. DX: clinical. XR shows prominence or heterotropic ossification at the tibial tuberosity
e. TX: RICE, NSAIDs, quadriceps stretching, resolves with time. If refractory->surgery once growth plate is closed

7. Scoliosis
a. Patho: lateral curvature of spine >10 degrees +/- associated with kyphosis or lordosis
b. Epi: MC begins 8-12 in girls
c. NOTE: if seen with café-au lait spots, skin tags, axillary freckles->think neurofibromatosis type 1
d. DX: Adams forward bending test (sensitive)  asymmetric shoulders. Confirm w XR  Cobb’s angle on
AP/lateral film
e. TX: observation in most cases. Brace if 20-40 degrees. Surgical correction if >40
f. Note: To determine if a scoliosis curve is likely to progress and need treatment, must assess growth trajectory,
including signs of puberty. The greatest risk of curve progression is during an adolescent’s growth spurt

8. Slipped capital femoral epiphysis

a. Patho: femoral head slips posterior and inferior at growth plate
b. Epi: MC in 7-16y obese, African American males during growth support (hormonal changes at puberty). If seen
before puberty think hormonal/systemic disorders like hypothyroidism
c. Symptoms: sudden hip, thigh, knee pain with limp, leg is externally rotated (adduction usually normal)
d. DX: XR- lateral and Launstein (frog) view, bilaterally. Trendelenburg test + when standing on effected leg-hips
tilt downwards towards effected leg +/- changes in the torso alignment.
e. TX: non weight-bearing with crutches->ORIF. +/- prophylactic pinning of opposite leg
Extra:
a. Presentation->work up->staging->bone bx
b. X-ray is first test, CT is good for cortical involvement and mets, MRI is modality of choice, and bone scan assesses
multiple lesion presence. Always evaluate rest of skeleton with bone or PET scan to r/o mult lesions. Bone bx prior to tx
c. If the fracture involves the growth plate, is external, or communicated/non-aligned->ORIF is needed, otherwise kid will
grow up with one leg shorter than the other
Pediatric Psychiatry

1. Anxiety Disorder
a. Panic attacks
i. Definition: Episodes of intense fear or discomfort that develops abruptly, peaking in 10 min and lasts
<60 min with >/= 4 of the following:
1. Dizziness, trembling, chocking, paresthesia’s, sweating, SOB, CP, chills/hot flashes, fear of dying
or losing control, palpitations, nausea, depersonalizations
ii. TX: benzos- lorazepam or alprazolam. Long term->SRRIs
b. Panic Disorder
i. Criteria:
1. recurrent, unexpected panic attacks (at least 2)
2. At least one of the following must occur for at least one month: panic attacks followed by
concerns for future attacks, worry about implications of attack, significant change in behavior
related to the attack
3. Exhibit at least 4 of 13 typical symptoms
4. +/- agoraphobia: anxiety about places or situations from which escape may be difficult
ii. TX: SSRIs 1st line (Paroxetine, Sertraline, Fluoxetine). CBT
c. Generalized anxiety disorder
i. Definition: excessive anxiety or worry a majority of days >/= 6 months periods about various aspects of
life. Not episodic. Associated with fatigue, restlessness, sleep disturbances, HA.
ii. TX: SSRI (paroxetine, escitalopram). Buspirone
d. Social Anxiety Disorder
i. Definition: persistent (>6 months) of intense fear of social or performance situations in which the
person is exposed to the scrutiny of others for fear of embarrassment
ii. TX: SSRI, beta blockers, psychotherapy
e. Specific Phobias
i. Definition: persistent (>6 months) intense fear of specific situation. Fear out of proportion to any real
danger. Everyday activities must be impaired by distress or avoidance
ii. TX: exposure/desensitization therapy is TOC. Childhood phobia may disappear or lessen with age
f. Separation Anxiety Disorder
i. developmentally inappropriate; excessive anxiety about being apart from home or individual
ii. normally begins at 7 months and decreases after 30 months
iii. Signs: recurrent excessive distress when separated; persistent worry about losing or harm befalling
major attachment figure, worry of event that will lead to separation, reluctance to go to school; afraid to
be alone, refuse to sleep alone, nightmares of separation, complains of physical symptoms when
separated
iv. risks factors: genetic/temperaments, insecure attachment patters, parental anxiety, parenting style
(controlling), negative life experiences
v. TX: Multimodal approach with therapy and possible medications with goal of a quick return to school
g. Selective Mutism
i. failure to speak in specific social situations; speaks in other situations; interferes with achievement or
communication, least 1 month

2. Attention-deficit/hyperactivity disorder
a. Definition: problems paying attention, difficulty controlling behaviors and hyperactivity that is not age
appropriate
b. DX:
i. symptoms of hyperactivity or inattentiveness leading to impairment with onset BEFORE age 12 and
present for at least 6 months
ii. Symptoms musts occur in at least TWO settings (school, home) with at least 6 of the following
1. Inattentiveness: easily distracted, difficulty focusing on one task, carless mistakes, forgets or
loses things, difficulty completing assignments, becoming bored with task after few minutes
 2. Hyperactivity: fidgets in seat, constantly in motion, talks excessively, impatient, dashes around
playing with everything, trouble sitting for long periods, difficulty doing quit tasks, restlessness,
blurts out comments, interrupts conversations
c. TX: Multimodal
i. Behavior modification
ii. Sympathomimetic medications pharm TOC: Methylphenidate (Ritalin),
amphetamine/dexamphetamine (Adderall)
1. S/E: insomnia, decreased appetite, weight loss, abdominal pain, nausea, HA, tics, drowsiness,
mood lability, no addiction shown, lowers seizure threshold
2. Concerns: stunts growth after 2-3 years use (1-2.5 cm shorter), HTN
iii. Nonstimulants: Atomoxetine (Strattera)
d. Guidelines:
i. (4-5 YO)= behavior therapy, Methylphenidate if no improvement, (6-11) =ADHD meds are 1st line +/-
behavior therapy (stimulant recommended over atomoxetine or clonidine); (12-18) =ADHD meds and
behavior therapy together

ii.

e. FDA: school age: 1st line is stimulants (methylphenidate compounds/Ritalin, dextroamphetamine, and mixed
amphetamine salts/Adderall; 2nd line is non stimulants (Alpha 2 Agonists-Atomoxetine/ Stattera)
f. Complications: Oppositional defiant disorder is the most common comorbid condition associated with ADHD
with a prevalence of up to 50%.
g. When starting meds:

3. Autism Spectrum Disorder

a. Epidemiology: highly genetic (associated in 10-15% cases of Fragile X, Rett’s and tuberous sclerosis)
i. Cadherin’s are an identified gene
b. DX criteria:
i. Persistent deficits in social interaction and communication
1. deficit in social-emotional reciprocity, difficulty in nonverbal communicative behaviors used for
social interaction, difficulty in developing and maintain relationships
ii. Restricted, repetitive and stereotyped patterns of behavior, interest, activities
1. repetitive speech or motor movements (line up toys), sameness/ routines or ritualized pattern,
fixated interests, hyper or hypo reactivity to sensory input
iii. Symptoms must be present in early developmental periods
iv. Symptoms cause clinically significant impairment in functioning
v. Disturbances are better explained by intellectual disability
c. Presentation on age:
i. 0-5= sensory dysregulation
ii. 6-15=present with ADHD
iii. 13-18=at risk for depression, anxiety, psychosis
iv. 19-35= at risk for drug abuse
v. >36= suffer from anxiety and mood dysregulation
d. Concerns: Due to high pain tolerance and inability to report symptoms-> increased untreated medical
conditions
e. Screening criteria: studies show infants at risk (siblings) have shown deficit in social responsiveness,
communication and play as young as 6-12 M->recommended that all 18 and 24 months olds be screened (most
no dx prior to age 4)
f. TX: Multi-modal approach (behavioral, educational, pharmacological)
i. Early psychosocial innervations can change the course, especially language (>20 hrs. weekly)
 ii. Appropriate educational interventions, multidisciplinary treatment approach, parent training and
education, Individual therapy, ABA therapy, Speech/OT/PT prn, social skills group therapy
iii. No curative medicine
iv. Neuroleptics have been used to decrease aggressively, stereotypic behaviors and impulsivity.
1. Typical: low dose Haldol; Atypicals: Risperdal, Zyprexa, Seroquel, Clozaril, Geodon, Abilify
v. Antidepressants: SSRI’s helpful with repetitive thoughts/behaviors, aggression and social relatedness
(Prozac, Zoloft, Paxil and Celexa)

4. Child Abuse and Neglect

a. Types:
i. Abuse: Active, intentional, doing something you SHOULDN’T be doing
ii. Neglect: Passive, not doing something you SHOULD be doing
b. Risk factors:

c. Toxic stress may result when children endure prolonged, severe trauma and adversity without the buffer of
supportive caregivers
d. Physical abuse- MC perpetrator is first degree caregiver and MC female (parent, guardian). Look for subdural
hematoma, hypema/retinal hemorrhages (shaken baby syndrome), cigarette burn, stocking glove pattern burn
e. Sexual abuse- perpetrator usually male and known to the victim (common to be a member of the family),
sometimes brother-sister incest
f. red flags-> delayed care for injury, inconsistent explanation, mult injuries at different healing stages, spiral bone
fractures, bruising patterns, cigarette burn, head injury
g. Symptoms:

h. Inc. risk of developing: PTSD, anxiety disorders, depressive disorders (MC), dissociative disorders, self-
destructive behaviors, and substance use disorders
i. Note: Report to CPS if suspect-certainty is NOT required. Most of the time the parent does not know they are
abusing the child…it is important to council and help parents cope with outside stressors that may be
contributing factors to being ‘bad parents’
5. Depressive Disorders
a. Major Depressive Disorder
i. Definition: Depressed mood or loss of pleasure with >/= 5 associated symptoms almost every day for
most of the days for at least 2 weeks
1. Associated symptoms: fatigue, insomnia, guilt, thoughts of death/suicide, agitation, weight
change, appetite change, dec concentration
2. not due to substance use, bereavement, medical condition
3. cause clinical distress or impairment in social, occupational, or other important areas
ii. Symptoms:
1. prepubertal=somatic complaints, agitation, separation anxiety, phobias, *child is irritable*
2. adolescent=antisocial, substance use, restlessness, aggression, grouchiness, problem with
family/friends, not being understood, F-inward sx, M-acting out
iii. subtypes
1. Season affective disorder. TX with SSRI
2. Atypical depression: experience mood reactivity in response to positive events. TX MOA
inhibitors
3. Melancholia: inability to find pleasure in things
4. Catatonic depression: major immobility, stupor, extreme withdraw
iv. Patho: alteration in neurotransmitters, neuroendocrine dysregulation (adrenal, thyroid, GH)
v. Screen: Patient Health Questionnaire (PHQ)-2 form for initial screen. If + use PHQ-9
vi. TX: psychotherapy. SSRI first line in mild to mod disease (for atleast 3-6 weeks). ECT if failed response
or severe symptoms
b. Persistent depressive disorder
i. Definition: chronic depressed mood >2 years in adults (>1 yr in child), usually milder then major
depression. Usually able to function
1. Not symptom free for more than 2 months at a time
2. Atleast 2 of the following: insomnia, hypersomnia, fatigue, low self-esteem,, eating habits
extreme, hopelessness, poor concentration
ii. Epi: MC begins in late teens, women
iii. Symptoms: loss of interest, social withdraw, pessimism, decreased productivity.
iv. TX: psychotherapy. SSRI first line medical tx
c. Adjustment Disorder
i. depression (within 3 months of stressor), anxiety, disturbance of conduct, or all

6. Disruptive, Impulse-control and conduct disorders

a. Disruptive Mood Dysregulation Disorder
i. severe and recurrent temper outbursts that are grossly out of proportion in intensity or duration to
the situation; average 3x/wk for 1 + year; Between outbursts the children display a persistently irritable
or angry mood most of the day; occurs in at least 2 settings for 12 months, onset before 10
b. OCD
i. Definition: Combination of thoughts (obsessions) + behaviors (compulsions)
ii. Epi: mean onset of 20
iii. Specifiers: Good/fair insight (recognizes OCD beliefs are not true), Poor insight (thinks they are probably
true), absent insight (completely convinced the beliefs are true)
iv. Symptoms: contamination (cleaning hands), pathologic doubt (forgetting to unplug iron), symmetry
precision (arrange objects), intrusive obsessive thoughts
v. TX: SSRI, TCA, SNRI
c. Body dysmorphic Disorder
i. Definition: preoccupation that > 1 body part is deformed or an over exaggeration of a minor flaw
ii. Epi: teenage females MC
iii. Symptoms: repetitive acts-mirror checks, skin picking, comparison to others, reassurance
iv. TX: psychotherapy, SSRI
d. Hoarding Disorder
i. Definition: difficulty with discarding or parting with possessions, perceived need to save items; results in
accumulation of possessions that conject living space; causes distress or impairment; not attributable to
other conditions
 e. Trichotillomania: recurrent, irresistible urges to pull out body hair.
f. Excoriation Disorder: repeated picking at one's own skin
g. Conduct disorder
i. Definition: persistent patterns of behavior that deviate sharply from the age appropriate norms and
violate the rights of others. Social and academic difficulty. Lack remorse. 3 behaviors over last year (1
within past 6 months)
1. serious violations of laws
2. aggressive/cruel to people/animals (physical/sexual)
3. deceitfulness
4. destruction of property
ii. Epi: MC in boys
iii. Risk: low IQ, poor supervision, erratic discipline, abuse, parental conflict, absent father, antisocial
parents, large family
iv. Prog: 40% develop antisocial personality disorder
v. TX: A multimodal treatment approach with behavior modification, family, and community involvement;
PMT, meds to target comorbid conditions (SSRIs, guanfacine, propranolol, mood stabilizers,
antipsychotics)
h. Oppositional defiant disorder
i. Definition: persistent pattern of negative, hostile defiant behavior towards adults. Does not involve
aggression or violence.
1. At least 6 months of the following 3 components:
a. angry/irritable (blames others for misbehaviors)
b. argumentative/defiant behavior
c. vindictiveness
2. Must involve one non-sibling
ii. TX: psychotherapy. No psychosis association (ADHA association), May progress to conduct disorder
(Behavior modification, conflict management training, and improving problem-solving skills, parent
management training, meds for comorbid conditions)

7. Feeding and eating disorder

a. Anorexia Nervosa
i. Definition: refusal to maintain a minimally normal body weight with morbid fear of fatness or weight
gaining
ii. Epi: MC mid-teens, 90% are women, frequently seen in athletes. High incidence with depression
iii. Symptoms: behaviors targeted at maintaining low weight (excess water intake, food obsessions)
1. Restrictive type: reduced calorie intake, dieting
2. Purging type: self-induced vomiting
iv. DX: BMI </=17.5 or body weight <85% of ideal weight
v. PE: emaciation, hypotension, bradycardia, lanugo, dry skin, amenorrhea, arrhythmias, osteoporosis
vi. Complication: MVP
vii. Labs: leukopenia, hypokalemia, inc BUN, hypothyroidism
viii. TX: hospitalization for <75% expected body weight. Psychotherapy. Supervised meals. If depressed->
SRRI or atypical antipsychotics (help with weight gain too)
b. Bulimia Nervosa
i. Definition: major difference from anorexia is patients with bulimia have normal weight or overweight
ii. Symptoms: Binge eating (occur at least weekly for 3 months)Compensatory behavior (self-induced
vomiting, reduced calorie intake)
iii. PE: teeth pitting or enamel erosion, parotid gland hypertrophy, met alkalosis
iv. TX: psychotherapy. Fluoxetine has been shown to reduce the binge-purge cycle (s/e cardiac esp if
electrolyte abnormalities)

8. Suicide
a. facts: MC firearm, suffocation, poisoning; 3rd LCOD 15-24 (70% 19-24)
i. Most completed suicides involve firearms. Most attempted suicides involve ingestions (MC:
antidepressants). All overdose patients: obtain acetaminophen level
ii. MVA MC COD 1-15 YO
 b. risks: biological-> familial and heritable, impulsive aggression, serotonin metabolism, suicidal ideation, previous
suicide behavior, availability of lethal means, sociodemographic and educational factors, family adversity,
negative life events, psychiatric problems, LBGT, substance abuse, psychosocial stressors
c. TX: Electroconvulsive Therapy may reduce suicidality, DBT, CBT-SP, CAMS, non-demand follow-up contact
d. Meds
i. Antidepressants (SSRIs 1st line) good for mod-severe depression
ii. Lithium-decrease suicidality with BPD
iii. Clozaril- decreases suicidality with schizophrenia
iv. Antipsychotics/anxiolytics effective for acute agitation
v. Ketamine may be effective for acute SI
vi. Treat withdrawal even nicotine with replacement

Random

SSRIS
 First line (do 2 trials for 6 weeks),
 Fluoxetine (Prozac) only FDA approved for MDD under age 18 (8 YO +)
 Escitalopram (Lexapro) 12-17 approved
 Others: Sertraline (Zoloft), Paroxetine (Paxil), Citalopram (Celexa) Nefazadone
 No prior labs needed, dosing same as adult except start lower, increase suicidal thoughts (blackbox warning)
 General med rule: continue meds for 6-12 months, then taper over at least 6 weeks; if 2-3 episodes of MDD
then TX for 1-3 years

SNRI’s
 Duloxetine/Cymbalta
 Venlafaxine/Effexor (help anxiety, increased irritability)
 Desvenlafaxine

Bupropion (Wellbutrin)
 Also for ADHD/substance
 C/I: anxiety/eating disorder

Mirtazapine (Remeron) - sedation

Augmentation strategies
 Aripiprazole and other atypical antipsychotics, Lithium, Thyroid Supplementation
Pediatric Pulmonology

1. Acute bronchiolitis
a. Patho: lower resp tract infection of small airways->proliferation/necrosis of bronchiolar epithelium produces
obstruction with sloughed epithelium->mucus plugging and edema->peripheral airway narrowing and variable
obstruction
i. RSV MC cause, adenovirus, influenza
b. Risk: infants <2y MC (esp <2 mo), premature (<37 weeks), cigarette exposure <6 mo,
c. Complications: otitis media with S.pneumo MC acute exacerbation (asthma in older)
i. If Sp02<90%, premature, age<3 months, cardiopulmonary abnormality, immunodeficient->contact
isolation, 02, IV fluids
d. Symptoms: dyspnea, wheezing, fever, URI 1-2 days->respiratory distress. Winter months common
e. DX: Can be clinical. CXR shows peribronchial cuffing and hyperinflation. Pulse Ox BEST predictor of dz in kids
(<96%=admit). Definitive->Nasal washing using monoclonal Ab testing (rapid antigen test from nasopharyngeal
swab)
f. TX: humidified O2 mainstay, IV fluids. +/- SABA or nebulized racemic epi (trial of beta-agonist therapy no longer
recommended). NO steroids unless hx of underlying airway disease
i. Give Ribavirin if severe lung or heart disease or immunocompromised
g. Prevention: Palivizumab prophylaxis (a monoclonal ab) in high risk groups. Hand washing.

2. Asthma
a. Triggers: smoke, exercise, mild, pet dander, dust mites, viral illness, cockroaches, GERD
b. Prevention: avoid triggers. Remove pets, cigarette smoke (paramount!), mold, carpet, dust mites
c. TX:
i. For those 5 and up
1 - SABA PRN
2 - Add low dose ICS
3 - Add LABA OR LTRA OR increase to medium dose ICS
4 - Increase to medium dose ICS AND add LABA (whichever wasn't done in 3)
5 - Increase to high dose ICS
ii. For those under 5
1 - SABA PRN
2 - Add low dose ICS
3 - Increase to medium dose ICS
4 - Add either LABA or LTRA
5 - Increase to high dose ICS
d. DX: Hospital admission based on need for supplemental 02 and peak flow prior to/after bronchodilator therapy
i. Broncho provocation (when presenting normal) via methacholine challenge tests (>20% dec in FEV1),
Broncho dilator test when presenting with symptoms (>12% inc in FEV1) or Exercise challenge-f/u with
PFT (>15% dec in FEV1).
ii. PEFR best way to assess asthma exacerbation and response in ED, pulse ox <90% indicates respiratory
distress.
iii. Allergen skin test to assess triggers.
iv. Charcot-leyden crystals on sputum.
e. Acute exacerbation
i. Signs: breathless at rest, hunched forward, speaks in words, agitated, PF<60%, failure to respond to
initial TX
ii. TX: Duoneb (albuterol/ipratropium) every 20 min for 1 hr + oxygen + systemic corticosteroids. May
require escalating therapy such as Mg, subQ epi, intubation
f. Action plan: (green zone) all clear/breathing good, no symptoms and/or peak flow 80-100%; (yellow zone)
caution/slow down, some symptoms and or peak flow 50-80%; (red zone) medical alert/stop, severe symptoms
and/or peak flow <50%
3. Croup (laryngotracheobronchitis)
a. Patho: inflammation MC 2nd to acute viral infection of the upper airway->subglottic larynx/trachea swelling-
>stridor/barking-seal-like/hoarseness.
i. Parainfluenza MC cause, adenovirus, RSV, diphtheria
b. Epi: MC 6mo-6 YO in fall/winter
c. Symptoms: seal like cough, stridor (inspiratory), hoarseness, dyspnea (worse at night), URI symptoms prodrome
*(unlike epiglottitis),
d. DX: clinical, frontal AP cervical XR shows Steeple signs (subglottic narrowing of trachea)
e. TX:
i. Mild (no stridor @ rest)  cool humidified air mist, hydration, +/- dexamethasone. O2 if sat <92%. Send
home
ii. Mod (stridor at rest)  dexamethasone + supportive +/- racemic epinephrine. Should observe 3-4 hrs
iii. Severe (Stridor at rest with marked retraction)-> dexamethasone + nebulized epi and hospitilzation

4. Cystic fibrosis
a. Patho: autosomal recessive disorder defect in CFTR->prevents chloride transport (water transport out of cell)->
Buildup of thick, viscous mucus in lungs, pancreases, liver, intestines, repro system
b. Risk: white, European, survival median age is 36.8
c. Symptoms: young with bronchiectasis, growth delay (FTT), pancreatic insufficiency and infertility.
i. Meconium ileus at birth
ii. Pancreatic (dec fat absorption): steatorrhea, pale, foul smelling stools. Vit ADEK deficiency, failure to
thrive seen in kids
iii. Pulmonary: recurrent respiratory infections (pseudomonas MC and staph aureus)
 d. DX: Most often dx on prenatal screening with CVS (some escape-immigrants). If + screen or symptoms-> sweat
chloride test (>60 mmol/L x 2 occasions after Pilacropine to induce sweating, >40 in infants), CXR shows
bronchiectasis and hyperinflation, PFTS are obstructive, DNA analysis if sweat neg
i. Elevated fecal elastase is another supporting test, as it indicates malabsorption
e. TX: airway clearance (bronchodilators, mucolytic, abx), pancreatic enzyme replacement and ADEK vit
supplementation, pneumococcal vaccine. Do genetic counseling in parents
i. DNase (dornasa alfa) is a mucolytic that can thin sputum in cystic fibrosis
f. Note: Cystic fibrosis is the most common risk factor in developed countries for developing an infection with
nontuberculous mycobacterial disease

5. Foreign body
a. Patho: MC on right side. Supine position->superior right lower lobe. Sitting/standing-> mc in posterobasal
segment of the right lower lobe. Laying on right side->mc in right middle lobe or posterior segment of right
upper lobe
b. Symptoms: sudden onset of dyspnea (esp in unsupervised child <3 YO), coughing, choking, wheezing,
hemoptysis. Gastric aspirations may lead to ARDS (Extrathoracic->inspiratory stridor. Intrathoracic-> expiratory
stridor)
c. DX: AP/lateral xray. If in trachea you will have – coin sign on AP and + coin sign on lateral film. EXPIRATORY
CXR may show regional hyperinflation 2/2 to air trapping
d. DX/TX: rigid bronchoscopy if in lung, laryngoscopy if high up, endoscopy if in esophagus.
e. Risk foods: peanuts, M&Ms

6. Hyaline membrane disease (IRDS – infant respiratory distress syndrome)

a. Patho: insufficient surfactant production and lung structural immaturity  atelectasis and perfusion without
ventilation *MC LCOD in 1st month of life*
b. Risk: white, male, C-section delivery (stress causes cortisol production), perinatal infections, mult births
(premature!), maternal DM (insulin delays surfactant)
c. Symptoms: presents shortly after postpartum with respiratory distress (tachypnea, tachycardia, chest wall
retractions, expiratory grunting, nasal flaring, cyanosis) 2-3 days
d. DX: XR shows bilateral diffuse reticular ground glass opacities and air bronchodiagrams with poor expansion.
ABG shows hypoxia with normal C02
e. TX: exogenous surfactant given to open alveoli (via ET). CPAP
f. Prevention: steroid given to mature lungs if premature delivery expected (24-26 weeks)
g. Prog: normal return to function within 1 mo, 90% survival
h. Note: Surfactant begins to be expressed in the fetal lung at 20 weeks gestation and gradually increases until 33-
36 weeks gestation. Phosphatidylglycerol-measured as a marker for fetal lung maturity and more mature
surfactant levels

7. Pneumonia

1-6 Months Treatment

Chlamydia trachmatis, pertussis-rare Macrolide, admit if pertussis

Viral (RSV, influenza, adenovirus) Supportive

S. aureus/bacterial Ceftriaxone (also given in other ages if not fully immunized)

6 months-5 years

Viral RSV (etc) Supportive

Strep pneumo Amoxicillin or Augmentin. PCN allergy  3rd gen ceph (cefdinir). Can use
macrolide or clindamycin. High resistant area  levofloxacin or lenazolid
 Mycoplasma or Chlamydia Macrolide or levofloxacin

>5YO

Typical bacteria (strep pneumo) Amoxicillin, levo, clinda, erythro, azithro, clarithro

Mycoplasma or chlamydophilia Azithromycin, clarithromycin, doxy

 Admission criteria: If 1-6 months, <90% on RA, respiratory distress, toxic appearing, failure of outpatient therapy,
inability to feed  admit to hospital for empiric therapy
 Tachypnea: <2 mo = >60 RR. 2-12 mo = >50 RR. 12-5y = >40 RR. >5 YO = >20 RR
 Inpatient: ampicillin or ceftriaxone. Add vanco if MRSA suspected
 Severe pneumonia: Ceftriaxone + azithromycin
 ICU admission pneumonia: Vanco + ceftriaxone + azithromycin
 Nosocomial pneumonia: Gentamicin + zosyn OR meropenem OR clindamycin OR ceftazidime
 Aspiration pneumonia: amp/sulbactam + clindamycin (if MRSA expected)
 Most pneumonia in toddler is viral

8. RSV
a. Patho: paramyxovirdae family, high incidence in infants 1-6 mo
b. Risk: down syndrome, attend daycare, underlying CLD, asthma, immunocompromised
c. Symptoms: LRTI/bronchiolitis, wheezing, apnea, mild systemic symptoms
d. DX: clinical. CXR- diffuse interstitial infiltrates to segmental or lobar consolidation. PCR
e. TX: supportive (humidified air), suctioning, hydration, supplemental O2. Nebulized ribavirin in high risk (not in
pregnancy).
i. Albuterol, steroids, and xray should not be administered to children with a diagnosis of RSV bronchiolitis
f. Complications: sinusitis, AOM
Pediatric Urology

1. Cryptorchidism
a. Patho: undescended testicle, most descend spontaneously. MC right side
b. Risk: premature infants, low birth weights
c. Symptoms: empty, small scrotom, inguinal fullness, 10% bilateral
d. Complication: testicular CA (both testis), subfertility, testicular torsion, inguinal hernia
e. TX: orchioplexy (as early as 6 mo of age). Observation if < 6 mo old as most descend by 3 months (rarely
descend AFTER 6 mo). hCG or GRH>stimulates testosterone and hormonal testicular distention. Orchiectomy
recommended if detected at puberty to reduce CA risk

2. Cystitis
a. Age
i. <30 day old:
1. Amp & gent (same as sepsis tx-don’t use cephalosporin <30 days old  may cause kernicterus)
2. Prophylaxis if freq UTIs (3 febrile UTIs in 6 mo, 4 total in 1 yr) with Bactrim or nitrofurantoin
3. Duration: 7-14 days if <2 or hx of UTI
ii. >1 mo
1. 3rd gen cephalosporin: ceftriaxone, cefixime
2. *Admit if <2 mo old*
3. Inpatient: ampicillin and gentamicin
4. Duration: 7-14 days
iii. Children (2+) and adolescents
1. (uncomplicated) x 5 days
a. Cefexime, cephalexin, Augmentin, Bactrim
b. Based on coverage-> PO Bactrim x 3 days or nitro x 5 days or quinolone
(S.saprophyticus), Augmentin, 3rd gen cephalosporin (E.coli), Enterococcus
(amoxacillin)
2. (complicated) x 7-14 days
a. Ceftriaxone, gentamicin, cefotaxime
iv. Pyelonephritis in children
1. Outpatient: Fluoroquinolone (Cipro PO) x 7d, Bactrim x 14 d  admit all pedi pts with pyelo (?)
2. Inpatient: 2nd/3rd gen ceph, unasyn, amp/gent
3. Duration: 7-14 days
b. Management
i. Initiate antimicrobial therapy for acute cystitis pending cx results for:
1. Febrile children, immunocompromised, ill-appearing, have indwelling catheter, underlying GU
abnormalities or previous h/o UTI
2. Afebrile, immunocompetent, well-appearing, w/o catheter, underlying UG abnormality, or h/o
UTI if evidence of bacteriuria (w/ or w/o pyuria) on dipstick or micro
c. Symptoms (neonates): Fever, poor weight gain, jaundice, vomiting, loose stools, poor feeding. (preterm) The
clinical manifestations of UTI in preterm infants are similar to those of term infants, with the addition of apnea
and hypoxia
d. DX: urine culture from cath or suprapubic aspiration

3. Enuresis
a. Patho: episodes of urinary incontinence while sleeping in children >/= 5 years old in absence of infection
b. Types:
i. Primary: Primary nocturnal (bedwetting)
ii. Secondary: previously dry, emotionally upset, family stress
c. TX: behavioral (avoid caffeine fluid restriction, motivational therapy, bladder training). Enuresis alarm (if fail
behavioral therapy-most effective long term, cont until minimum of 2 weeks of dry nights). Desmopressin
(better for short term use-use liberal amount of salt with it). TCA such as Imipramine ( if all else fails->detrusor
muscle relaxation, dec REM, ADH sec)
4. Glomerulonephritis
a. Patho: HTN, hematuria (rbc casts), dependent edema (proteinuria) and azotemia
i. immunologic INFLAMMATION of glomeruli causing protein AND RBC leakage into urine
b. Etiology:
i. IgA nephropathy (Berger’s disease) -focal
1. Etiology: MC cause in adults, young males within 24-28 hours post viral URI or GI infection (due
to IgA release)
2. DX: IgA mesangial deposits
3. TX:ACE inhibitors +/- steroids
ii. Post infectious/Post strep-diffuse
1. Etiology: MC after GABS, 10-14 days after impetigo, or pharyngeal infection.
2. Symptoms: 2-14 y boy with facial edema after strep with scanty, cola, colored dark urine
3. DX: antistreptolysin titers. Low C3. Bx (seldom done) showing hypercellularity, lymphocytes,
immune humps of IgG/IgM/C3
4. TX: supportive, +/- abx
iii. Membranoproliferative/Mesangiocapillary-diffuse
1. Etiology: SLE, viral hep (HCV)
2. DX: ANA, dsDNA, Sxs. Tram tracks Immune complement deposition on bx.
3. Symptoms: mixed nephrotic/nephritic picture
iv. Rapidly progressive glomerulonephritis
1. Patho: Crescent formation on bx due to fibrin and plasma protein deposition collapsing the
crescent shape of Bowman’s capsule
2. Prog: poorESRD in weeks/months
3. TX: steroids + cyclophosphamide
4. Any AGN can have RPG but 2 only present with RPG
a. Goodpastures Disease
i. Patho: ab vs collagen of basement membrane in kidney/lung->kidney
failure/hematuria + hemoptysis
ii. Etiology: post URI common
iii. DX: Linear IgG deposits on bx, Anti GBM ab
iv. TX: steroids + cyclophosphamide + plasmaphereses
b. Vasculitis
i. Patho: lack of immune deposits, effects sinus/lung/kidney
ii. Etiology:
1. Microscopic polyangitis: arterioles, venules, capillaries. No
necrotic/granulomatous
a. P-ANCA +
2. Wegeners/granulomatosis with polyangitis: necrotizing vasculitis
a. C-ANCA + w/ necrotizing granulomas on bx
c. Symptoms: Hematuria +/- gross (cola colored urine), peripheral/periorbital edema, HTN, fever, abdominal pain,
flank pain, if AKI->oliguria (<200ml)
d. DX:
i. UA-> RBC casts, dysmorphic rbc, proteinuria (usually <3g/d), high specific gravity (>1.20)
ii. Inc BUN/Cr of varying degrees
iii. Renal bx-gold standard (not needed if post strep suspected) hyper cellular (inc WBC and mesangial
cells), immune complex deposition, crescent shaped in RPG

5. Hydrocele
a. Patho: accumulation of fluid in tunica vaginalis
b. Etiology: Congenital in infants (close within 1st year), adults acquire via injury, infection, inflammation
c. Types:
i. communicating: result as a failure of closure of the processus vaginalis
ii. non-communicating: caused by processus vaginalis being obliterated during development resulting in
no connection to peritoneum
 iii. common in newborns, resolve spontaneously by age 1
iv. Older children/adolescents: noncommunicating can be caused by epididymitis, orchitis, torsion, etc.
d. Signs: painless, fluctuates in size, increased size while upright
i. communicating may increase in size during the day or w/ valsalva
ii. noncommunicating- not reducible and does not change size/shape with crying/straining
e. DX: U/S to rule out CA, + transilluminate
f. TX: Watch/wait, scrotal support. If painful or large->hydrocelectomy. Surgical repair if-> indicated for newborns
w/ hydroceles that persist beyond 1 year old, communicating hydroceles or idiopathic hydroceles that are
symptomatic/compromise skin integrity

6. Hypospadias
a. Patho: abnormal urethral placement (proximal and ventral)
b. Note: epispadia is dorsal displacement

7. Paraphimosis
a. Patho: foreskin becomes trapped behind the corona of glans and forms tight band constricting penile tissue-
>impairs blood flow->gangrene (emergency)
b. Symptoms: enlarged, painful glans with constricting band of foreskin behind it
c. TX: manual reduction (reduce edema with cool compresses or pressure dressing and then attempt reduction).
Pharmologic therapy (granulated sugar, injection of hyaluronidase). Incision (dorsal slit)

8. Phimosis
a. Patho: inability to retract foreskin over gland. Not emergent
b. Tx: circumcision
i. Application of corticosteroid cream on the foreskin thrice a day for a month may loosen the phimotic
ring. However, if ballooning of the foreskin is observed or if phimosis persists even after ten years of
age, circumcision is warranted

9. Testicular torsion
a. Patho: spermatic cord twists and cuts off blood supply due to congenital malformation (bell clapper deformity)
b. Epidemiology: teenagers 10-20 y
c. Symptoms: abrupt onset of scrotal, inguinal or lower abdominal pain (<6hrs) +/- N/V
d. PE: swollen, tender, retracted testicle, neg Prehn’s sign, absent cremesteric reflex, +/- blue dot sign
e. DX:US best initial (avascular testicle), sx exploration emergently
f. TX: detorsion and orchioplexy within 6 hours and in obvious cases; orchiectomy if not salvageable

10. Vesicourethral reflux

a. Definition: retrograde passage of urine from the bladder into the ureter/upper urinary tract
b. NOTE: predisposes pts to hydronephrosis or pyelonephritis by transport of bacteria from the bladder to the
kidney and recurrent UTI → may lead to scarring, HTN, and ESRD
c. Types:
i. Primary VUR (MC): d/t incompetent or inadequate closure of the ureterovesical junction (UVJ), possibly
d/t congenitally short intravesical ureter
1. Spontaneous resolution of low-grade VUR occurs with patient growth
ii. Secondary: Results from abnormally high voiding pressure in the bladder that results in failure of the
closure in the UVJ during bladder contraction
1. Assoc w/ anatomic (posterior urethral valves) or functional bladder obstruction
d. Epidemiology
i. Primary: MC urologic finding in children, 1% of newborns. Common in white girls, usually dx after a UTI
e. Clinical Presentation
i. Prenatal: hydronephrosis on prenatal US (renal pelvic diameter >/= 4 mm in 2nd trimester and >/=
7mm in 3rd trimester)
ii. Postnatal: dx of VUR made after dx of febrile UTI
iii. Chronic: Multiple episodes of UTI throughout childhood, Proteinuria, elevated BP
f. Diagnosis:
 i. Diagnosis based on demonstration of urine reflux from bladder to upper urinary tract via contrast
voiding cystourethrogram* (VCUG) or radionuclide cystogram (RNC)
1. Indications: After the first UTI in all < 5 YO, Any kid with febrile UTI, Boys with UTI, Children
with prenatal identification of hydronephrosis should be evaluated postnatally; however US
during the first 3 days of life may have high false neg
ii. Grading:
1. Grade I: reflux only fills ureter w/o dilation
2. Grade II: reflux fills the ureter and the collecting system w/o dilation
3. Grade III: reflux fills and mildly dilates the ureter and the collecting system w/ mild blunting of
the calyces
4. Grade IV: reflux fills and grossly dilates the ureter and the collecting system with blunting of the
calyces, some tortuosity of the ureter is also present
5. Grade V: massive reflux grossly dilates the collecting system; all the calyces are blunted w/ loss
of papillary impression, and intrarenal reflux may be present; there is significant ureteral
dilation and tortuosity
g. Prognosis
i. There is spontaneous resolution in majority of cases of primary VUR if low grade, when age of dx is
below 2 years old, and there is only unilateral involvement
h. Treatment
i. General: spontaneous resolution is common in young children, less common as puberty approaches
ii. Grades I & II
1. Surveillance if toilet-trained, verbal children
2. Abx prophylaxis if not toilet trained or with BBD
3. Surgical correction not recommended as initial therapy
iii. Grades III-V
1. Abx prophylaxis
2. Detection and tx of BBD
3. Indications for surgery:
a. Grade IV/V persisting past 2-3 years of age
b. Children who failed medical therapy w/ breakthrough infections
c. Children w/ significant S/E’s from continuous prophylactic abx
d. Non-compliance w/ a long-term medical regimen
iv. Antibiotics
1. Neonates and infants < 2 months: amoxicillin
2. Older: trimethoprim-sulfamethoxazole, nitrofurantoin, and PCNs