MIDTERM Flashcards
lead screening
-CDC recommends blood lead screening at 12 + 24 months
-screen in temper tantrum
-Lead intoxication (plumbism) can cause developmental and behavioral abnormalities
-RF: older homes w/ cracked lead-based paint, industrial exposure, use of foreign remedies, and use of pottery with lead paint glaze
-affects the CNS
-vague sx:
-Early: Weakness, irritability, wt loss, vomiting, personality changes, ataxia, constipation, h/a, and colicky abdominal pain
-Late: Developmental delays, convulsions, and coma assoc with increased ICP
-If lead +, investigation if:
-levels of 20 mcg/dL on 1x test OR
-persistent 15 mcg/dL over 3mo (decontamination techniques used once source identified)
-Tx:
-Succimer- oral chelator recommended in asymptomatic with levels > 45 mcg/dL
-IM dimercaprol/BAL and IV calcium sodium edetate in symptomatic with encephalopathy or levels > 70 mcg/dL
sleep safety
-Sudden infant death syndrome (SIDS)- sudden death of infant < 1yo that is unexplained after thorough case investigation
-Sudden unexpected infant death syndrome (SUID)- sudden and unexpected infant death (explained or unexplained) –> preferred term
-Includes deaths due to infection, ingestions, metabolic diseases, cardiac arrhythmias, and trauma
-peaks between 2-4 months
-Most occur at night
-RF: Socioeconomically disadvantaged (continued prone positioning, sharing beds), preterm, low birth wt, recent infection, young maternal age, high maternal parity, maternal tobacco or drug use, and crowded living conditions
-MC findings in SUID: Intrathoracic petechiae, mild inflammation/congestion of respiratory tract, findings consistent with chronic hypoxia prior to death
-Tx + prevention:
-Back to Sleep initiative -> 60% decline in SIDS since 1990
-Supine positioning
-Sleep in parents’ room, but on a separate surface for 1st 6mo
-Remove soft objects/loose bedding, stuffed animals, or wedge positioners
-Breastfeeding is recommended
-Pacifier at naptime and bedtime
-no smoking during pregnancy and after birth
-Avoid car seats, swings, and baby slings for sleep
-Avoid use of adult beds and bed rails (increases risk of suffocation)
colic
-Episodes of uncontrollable crying in healthy infant
-Paroxysmal, characterized by facial grimacing, leg flexion, and passing flatus
-Wessel rule of 3s:
-Crying for > 3 hours/day
-At least 3 days/week
-> 3 weeks
-Etiology: Unknown
-Cow’s milk intolerance
-Change in fecal flora
-Increase in serotonin secretion
-Poor feeding technique
-Maternal smoking may be assoc
-Tx:
-Dr. Harvey Karp’s “5 Ss”:
-Swaddling
-Side/stomach holding
-Soothing noises
-Swinging/slow rhythmic movement
-Sucking on pacifier
-Educating on hunger cues, avoid excessive caffeine and alcohol in nursing mothers, ensuring adequate bottle/nipple flow, and cautioning overfeeding
-Effectiveness of dietary changes, herbal supplements, and/or meds very limited
-No evidence of long-term effects for patient or parents
-Most serious complication -> nonaccidental trauma
teething
-can mimic ear infection
-Remedies for pain:
-OTC teething gels or liquids that contain benzocaine
-Systemic analgesics
-Chewing on teething object (distraction)
-Eruption Cysts: Localized, red/purple, round, raised, and smooth lesion, resolved with eruption of tooth (NORMAL)
-All children 1yo+ should have dental exam by dentist at least annually and cleaning q 6mo
-Preventative: Brushing, flossing, concentrated fluoride topical tx (dental varnish) and acrylic sealants on molars
-Recommended PCPs apply dental fluoride varnish to infants and children q 3-6mo between 9mo-5yo
-Fluoridation of water or fluoride supplements if no fluoridation are important in prevention of caries
car seat safety
-infants + toddlers (<2yo)- rear facing
-toddlers + preschool (2-6)- forward facing/harness
-school age (6-8)- booster
-4ft 9in or 8-12yo -> seat belts
tanner stages (female)
-growth spirt is 1yr after thelarche (tanner stage 3)
-menarche at tanner stage 4
-Stage 1- elevation of papilla only
-Stage 2- breast bud -> elevation of papilla and breast
-Stage 3- increase breast + areola
-Stage 4- increase areola + papilla
-Stage 5- areola recession
-Stage 1- none
-Stage 2- straight, along labia
-Stage 3- dark, course, curly
-Stage 4- adult, no thighs
-Stage 5- adult, thighs
anorexia
-1.5% in teenage girls
-F:M- 20:1, familial pattern
-Dx Criteria:
-Restriction of energy intake relative to requirements leading to low wt for age, sex, physical health, and developmental trajectory
-Strong fear of gaining wt or becoming fat, even though underwt
-Disturbance in body wt or shape is experienced, undue influence of body wt or shape on self-evaluation, or denial of seriousness of low body wt
-1st event - behavioral change in eating or exercise
-oversized or excessively tight clothing, fine hair on face and trunk, rough/scaly skin, bradycardia, hypothermia, decreased BMI, erosion of tooth enamel (if emetic episodes with the binge-purge type versus restricting type), and acrocyanosis of hand/feet
-Tx and Prognosis:
-Multi-disciplinary approach with family-based therapy
-voluntary freeding of regular foods, nutritional formula orally, or NG tube
-When 80% of normal body wt -> pt given freedom to gain wt at personal pace
-3-5% mortality, development of bulimic sx (30%), and persistent anorexia nervosa syndrome (20%)
bulimia
-5% in female college students (overwt, hx of dieting)
-F:M ratio 10:1
-Dx Criteria:
-Recurrent episodes of binge-eating, characterized by both:
-Eating a larger amount of food than most people would eat in a discrete period of time
-lack of control during episode
-Recurrent inappropriate compensatory behavior to prevent wt gain (vomiting; laxatives, diuretics, excessive exercise; fasting)
-Binge eating and behaviors occur at least 1x week for 3mo
-Complications: Metabolic disturbances from excessive vomiting
-Tx and Prognosis:
-Nutritional, educational, and self-monitoring techniques to increase awareness of maladaptive behavior, followed by efforts to change the eating behavior
-May respond to anti-depressants
-Attempted suicide and completed suicide (5%)
HEADDSS
-Home
-Education
-Alcohol
-Drugs
-Diet
-Sex
-Suicide
-15-17yo is high risk behavior
birth injuries
-Caput Succedaneum:
-Diffuse, edematous, dark swelling of soft tissue of scalp
-boggy
-extends across midline and suture lines
-Often following prolonged labor
-over the periosteum -> free flowing
-Cephalohematoma:
-Subperiosteal hemorrhage
-does not cross suture lines
-May organize, calcify, and form a central depression
-tx-
-observe- they will absorb
birth injury: brachial plexus
-Phrenic nerve palsy: C3-5- diaphragmatic paralysis/respiratory distress
-Erb-Duchenne paralysis: C5-6 injury
-Cant abduct arm at shoulder, externally rotate arm, or supinate forearm
-Klumpke paralysis: C7-C8, T1–
-Paralyzed hand with ipsilateral Horner syndrome, claw hand
-Tx: Supportive, active/passive ROM exercises, nerve grafting
jaundice
-1st day: PATHOLOGIC -> can be unconjugated or conjugated (MC)
-usually hemolysis, internal hemorrhage, or infection
-2-3 days after birth- PHYSIOLOGIC (dx of exclusion) -> Increased RBC mass, shortened RBC lifespan, hepatic immaturity
-indirect, unconjugated
-Peak, indirect bilirubin level of < 12 mg/dL on day 3 of life
-> 2wks: PATHOLOGIC -> direct hyperbilirubinemia
-Physical signs: Observed when bilirubin reaches 5-10 mg/dL
-Labs: Total bilirubin (possible breakdown), blood typing, Coombs test, CBC, blood smear, and reticulocyte count
-Breast-feeding jaundice (1st few days) -> decreased fluid intake
-Breast Milk Jaundice (1wk-2wk) -> milk may contain inhibitor of bilirubin conjugation or may increase enterohepatic recirculation of bilirubin
-kernicterus spectrum disorder (bilirubin encephalopathy):
-Earliest sx (4 days of life): Lethargy, hypotonia, irritability, poor Moro response, poor feeding
-Late sx: Bulging fontanel, pulmonary hemorrhage, fever, hypertonicity, paralysis of upward gaze, seizures
-Crigler-Najjar Syndrome: Serious, rare, autosomal recessive, permanent deficiency of glucoronosyl transferase (conjugation enzyme)
-Gilbert Disease: Mutation of glucoronosyl transferase
jaundice tx
-INDIRECT HYPERBILIRUBINEMIA:
-Phototherapy: Blue/white lights reduce bilirubin
-Exchange transfusion
-Level of 20 mg/dL of indirect-reacting bilirubin (infants > 2000 grams)
-Umbilical venous catheter placed in IVC/umbilical vein/portal system
-immediate exchange transfusion if kernicterus spectrum disorder (bilirubin encephalopathy) -> >25 mg/dL
-DIRECT/CONJUGATED:
-always pathologic
-treat the cause -> does NOT respond to phototherapy or exchange transfusion
respiratory distress syndrome (hyaline membrane disease)
-after onset of breathing
-assoc with insufficiency of surfactant -> prevents atelectasis
-Surfactant contributes to lung recoil
-ALWAYS THINK THIS FIRST WHEN THERE IS RESPIRATORY DISTRESS
-RF: Prematurity, low GA, hx of preterms with RDS, maternal DM, hypothermia, fetal distress, asphyxia, males, 2nd born twin, C-section
-Initial sx: Cyanosis, tachypnea, nasal flaring, intercostal/sternal retractions, and GRUNTING (BAD); over 72 hrs - increased distress, hypoxemia
-CXR: Ground-glass haze surrounding air-filled bronchi or white-out (severe)
-Uncomplicated cases -> spontaneous improvement –> diuresis and marked improvement of edema
-Severe cases (edema, apnea, respiratory failure) –> assisted ventilation
respiratory distress syndrome (Hyaline Membrane disease): complications
-PDA
-pulmonary air leaks from ventilation -> distention -> rupture -> interstitial emphysema -> PTX!
-retinopathy of prematurity (retrolental fibroplasia)- MCC blinding in VLBW -> vasoconstriction -> vaso-obliteration
-bronchopulmonary dysplasia (chronic lung ds):
-due to prolonged ventilation and O2 therapy
-failure to improve >2wks, continued need for ventilation/O2 @ 36wks
-hypercapnia with compensatory metabolic alkalosis, pulmonary HTN, poor growth, R-sided HF
-CXR: Lung opacification -> cyst development = Sponge-like appearance
-Tx:
-ventilation for several months
-Tracheotomy may be indicated (prevent subglottic stenosis)
-Dexamethasone
PE of newborn neck
-Short and symmetric
-Midline clefts (thyroglossal duct cysts), lateral masses (branchial clefts), cystic hygromas, hemangiomas
-Neonatal torticollis!!: Shortening of SCM muscle with fibrous tumor over muscle produces head tilt/abnormal facies -> goes away with PT usually
-vision loss in eye thats not working as much
-Edema/webbing of neck suggest Turner syndrome
-Palpate clavicles for fractures
congenital toxoplasmosis
-TRIAD:
-1. Hydrocephalus
-2. chorioretinitis
-3. diffuse intracerebral/cortical calcifications
-small, early-onset jaundice, hepatosplenomegaly, and generalized maculopapular rash
-seizures are common
-Dx- Serologic testing
-Tx- Pyrimethamine (supplement with folic acid) + sulfadiazine, up to 1 year
congenital rubella
-TRIAD:
-B/L cataracts
-sensorineural hearing loss
-cardiac defects- PDA, pulmonary artery stenosis
-eyes: Cataracts, retinopathy, glaucoma
-Neurologic: Behavioral disorders, meningoencephalitis, developmental delay
-Dx: Serologic testing; isolation from blood, urine, CSF, throat
congenital CMV
-MC congenital infection and leading cause of sensorineural hearing loss, intellectual disability, retinal disease, and cerebral palsy
-Microcephaly, thrombocytopenia, hepatosplenomegaly, hepatitis, intracranial calcifications, chorioretinitis, and hearing abnormalities
-Dx: Detection of virus in urine or saliva
-Tx: Ganciclovir has shown positive effect on hearing loss
congenital herpes simplex
-Sx develop 5-10 days of life: Disseminated infection (liver, lungs, possibly CNS)
-Dx: Sampling from skin vesicle, NP, eyes, urine, blood, CSF, stool, rectum (PCR)
-Treatment: Acyclovir (parenteral)
congenital syphilis
-Hepatosplenomegaly, snuffles, lymphadenopathy, mucocutaneous lesions, osteochondritis, rash, hemolytic anemia, and thrombocytopenia
-Later sx in untreated:
-!Hutchinson triad! - Interstitial keratitis, CN VIII deafness, Hutchinson teeth
-Bowing of the shins, frontal bossing, mulberry molars, saddle nose, rhagades (skin cracks), and Clutton joints
-CXR- >90% abnormal long bones consistent with osteochondritis/perichondritis
-Dx:
-Dark-field exam of direct fluorescent antibody staining of organisms obtained by scraping of a skin or mucous membrane lesion
-Serologic testing (VDRL/RPR)
-CSF should be examined as well
-Increased WBC count + protein concentration suggest neurosyphilis
-+ CSF VDRL is dx
-Tx:
-Penicillin (parenteral) x 10-14 days
-repeat titers at 3, 6, 12, months (neurosyphilis q 6 months x 3 years)
congenital infection: zika, G/C, herpes
-HERPES:
-Sx- 5-10 days of life: Disseminated infection (liver, lungs, possibly CNS)
-Dx: Sampling from skin vesicle, NP, eyes, urine, blood, CSF, stool, rectum (PCR)
-TX: Acyclovir (parenteral)
-ZIKA:
-arthropod-borne via mosquitos
-transmitted to fetal brain -> craniofacial abnormalities, pulmonary hypoplasia, contractures
-microcephaly, cerebellar hypoplasia, ventriculomegaly, lessencephaly
-GONORRHEA:
-MC infection of eyes- ophthalmia neonatorum (1st 5 days)
-hyperacute onset of mucopurulent conjunctivitis
-TX: IM ceftriaxone x 1
-CHLAMYDIA:
-MC site is nasopharynx; conjunctivitis, PNA
-conjunctivitis- 1-2wks, mucopurulent
-Dx- culture discharge, Giemsa staining of conjunctival scraping is dx, PCR
-Tx- Azithromycin (PO) x 3days or erythromycin x 14 days
down syndrome
-1:700 newborns
-facial features and generalized hypotonia
-Newborn: feeding problems, constipation, prolonged physiologic jaundice, and transient blood count abnormalities
-Childhood: thyroid dysfunction, visual issues, hearing loss, OSA, celiac disease, and atlanto-occiptal instability
-Increased incidence of transient myeloproliferative disorder and leukemia!!
-Facies: Upslanting palpebral fissures, flat nasal bridge, epicanthal folds, midface hypoplasia, flattened occiput
-Minor limb abnormalities
-Generalized HYPOTONIA!!
-up to 50% have CHD (septal defects)- VSD
-GI: Esophageal/duodenal atresias
sex chromosome: turner syndrome (monosomy x)
-1:2500 females
-95% are miscarried
-Caused by missing X chromosome or structurally abnormal X chromosome (only a single functional copy of X chromosome) in females
-Short, webbed neck; edema of hands/feet, triangular facies
-Older females: Short stature, shield chest with wide-set nipples, mixed conductive/SN hearing loss, horseshoe kidneys, streak ovaries, amenorrhea, absence of development of secondary sex characteristics, infertility
-Cardiac anomalies: Coarctation of the aorta, bicuspid aortic valve (newborn), aortic root dilatation (adults)
-Learning disabilities common, secondary to difficulties in perceptual motor integration
-Tx:
-Hormonal therapy (GH, estrogen/progesterone)
-surgical intervention (cardiac anomalies)
-speech therapy/academic support
klinefelter syndrome (XXY)
-1:1000 in males
-rarely causes spontaneous abortions
-After puberty: Small testes, gynecomastia, diminished facial/body hair, tall/eunuchoid build, decreased muscle mass
-IQ borderline-normal
-Extra X chromosome > decreased testicular growth > low testosterone > delayed/absent/incomplete puberty, azoospermia, and infertility
-Tx: Testosterone replacement
measles (rubeola)
-Highly contagious (droplet and airborne transmission)
-caused by single-stranded RNA paramyxovirus
-4 phases: Incubation (8-12 days from exposure to onset), prodromal (catarrhal), exanthematous (rash), and recovery
-3 day prodromal period: Cough, coryza, conjunctivitis and pathognomonic Koplik spots! (gray-white, sand-grain-sized dots on buccal mucosa, opposite lower molars)
-Conjunctiva with possible Stimson line! (transverse line of inflammation along the eyelid margin)
-Exanthematous phase: Sx + FEVER
-Macular rash, spreading from HEAD TO TOE over 24 hours; rash fades in the same pattern
-Generalized lymphadenopathy (cervical nodes most prominent)
-AOM, PNA, and diarrhea common in infants
-Dx:
-Serologic testing for IgM antibodies (1-2 days into rash, persist for 1-2 mo)
-+/- genetic testing -> RT-PCR
-Tx:
-Supportive care– fluids, antipyretics
-routine vitamin A x 2 days to children with acute measles
rubella (german/3-day measles)
-Caused by single-stranded RNA togavirus, humans only host
-Incubation 16-18 days, mild catarrhal symptoms
-Retroauricular, posterior cervical, and posterior occipital lymphadenopathy with erythematous, maculopapular, discrete rash
-Rash spreads from head to toe, lasts for 3 days
-Rose-colored spots (FORCHHEIMER SPOTS) on soft palate may appear before rash
-Other sx: Pharyngitis, conjunctivitis, anorexia, headache, malaise, LOW GRADE fever, polyarthritis, parasthesias, tendonitis
-Dx:
-Serologic testing for IgM antibodies (+ 5 days after onset) or by 4-fold or greater increase in specific IgG antibodies in acute/convalescent sera
-Treatment: Supportive
erythema infectiosum (5th ds)
-Caused by single-stranded DNA virus, parvovirus B19!!
-Viral affinity for RBC progenitor cells -> aplastic crisis in pts with hemolytic anemias (SCD, spherocytosis, and thalassemia)!!!
-Incubation 4-14 days
-Begins with mild illness -> fever, malaise, myalgias, and headache -> rash 7-10 days later
-3 stages of rash:
-1. Initially: “Slapped cheek” rash
with circumoral pallor
-2. 1-4 days later: Erythematous, symmetric, maculopapular, truncal rash
-3. Central clearing of rash takes place, distinct LACY!, RETICULATED! rash
-Rash may be pruritic, does not desquamate
-possible myalgia, significant athralgias/ARTHRITIS, headache, pharyngitis, coryza, and GI upset
-May cause hepatitis, myocarditis, and papular-purpuric gloves and socks syndrome
-Transient aplastic crisis (SCD): Fever, lethargy, malaise, pallor, headache, GI symptoms, respiratory symptoms
-Extremely low reticulocyte count, low hemoglobin, transient neutropenia/thrombocytopenia
-Dx:
-Hematologic abnormalities: Reticulocytopenia x 7-10 days, mild anemia, thrombocytopenia, lymphopenia, and neutropenia
-Detected by PCR and electron microscopy of erythroid precursors in bone marrow
-Serologic testing (IgM antibodies) is diagnostic (detects infection within prior 2-4 months)
-Tx: Supportive care, transfusion (aplastic crisis), IVIG for immunocompromised
roseola infantum (exanthem subitum, 6th disease)
-Caused by double-stranded DNA virus, human herpesvirus type 6 (HHV-6) in most cases (HHV-7 in 10-30% of cases)
-Major cause of acute febrile illnesses in infants
-up to 20% of ER visits for 6-18mo
-HIGH FEVER!!! (> 40C) with abrupt onset, lasts 3-5 days -> maculopapular, rose-colored rash (lasts 1-3 days)
-URI symptoms, erythematous TMs, and cough
-Dx: PCR for detection of HHV-6 in blood (does not differentiate latent, reactivation, or primary infections)
-Tx: Supportive
varicella zoster
-Caused by double-stranded DNA virus, varicella-zoster virus (VZV)
-direct contact, droplet, and air
-Incubation 14-16 days
-Prodromal sx- fever, malaise, and anorexia may precede rash by 1 day
-Rash progression:
-Small red papules -> nonumbilicated, oval, tear-drop-like vesicles on an erythematous base -> vesicles ulcerate, crust -> heal
-New crops appear for 3-4 days
-begins on trunk -> head, face, and extremities (rare)
-All forms of lesions are present at same time
-Marked pruritis
-Pre-eruption phase: Intense, localized, burning pain and tenderness (acute neuritis) along a dermatome, accompanied by malaise and fever
-Rash progression:
-Several days later, eruption of papules -> vesiculation (in dermatomal distribution/unilateral) -> crusting/healing
-Thoracic and lumbar MC
-CN V: Corneal/intraoral lesions
-CN VII: Ramsay Hunt Syndrome –facial paralysis and ear canal vesicles
-Postherpetic neuralgia: Pain persisting > 1 month is uncommon
-Dx- PCR of vesicular fluid is method of choice
-Tx:
-Varicella- Anti-pyretics, cool baths, and careful hygiene
-Acyclovir (all age groups), valacyclovir (> 2yo)
-NOT recommended in otherwise healthy children
->Early (within 24hrs of rash) in immunocompromised -> effective in preventing PNA, encephalitis, and death
-Zoster:
-Acyclovir, valacyclovir, famciclovir (adults)
coxsackie (hand-foot-mouth ds)
-Caused by coxsackieviruses, especially types A5, A10, and A16
-Mild fever, sore throat, and malaise
-Rash:
-Vesicles/red papules found on pharyngeal pillars, tongue, oral mucosa, hands (palms), and feet (soles)
-Lesions may last 1-2 weeks
-soft palate tiny red spots
-nails are peeling 1-2 months after
-swab for strep jic
-Treatment: Supportive
impetigo
-Erosions covered by honey-colored crusts
-Staphy and group A streptococci
-Tx: Topical (mupirocin, polymyxin, gentamycin, erythromycin) and/or PO -> if widespread (B-lactamase- resistant PCN, cephalosporins, clindamycin, amoxicillin-clavulanate) x 7-10 days
-Bullous impetigo: Border filled with clear fluid; tx with PO abx x 7-10 days
-Ecthyma: Firm, dry crust, surrounded by erythema that exudes purulent material (deeper form of impetigo affecting the superficial dermis); tx with systemic PCN
cellulitis
-Erythematous, hot, tender, ill-defined, edematous plaques accompanied by regional lymphadenopathy
-Invasion of microorganisms into lower dermis/beyond
-MCC- GABHS (Group A beta-hemolytic streptococcal) and coagulase-positive staphylococci
-Tx- systemic antibiotic
folliculitis
-Pustule at follicular opening
-MC- Staph and strep
-Tx: Warm, wet compresses x 24 hrs, topical keratolytics, topical/PO antibiotics
abscess
-Erythematous, firm, acutely tender nodule with ill-defined borders
-MC- Staph
-paronychia
-Tx: I&D alone/with adjuvant antibiotics
-bactrim
bacterial conjunctivitis
-MCC: Haemophilus species, S. pneumoniae, M. catarrhalis, and S. aureus
-Injected conjunctiva with significant discharge (purulent), typically unilateral > bilateral
-very contagious
-Tx:
-Topical antibiotics: Polymyxin/trimethoprim sulfate or fluoroquinolones
-Systemic therapy for conjunctivitis associated with C. trachomatis, N. gonorrhoeae and N. meningitidis
viral conjunctivitis
-MCC is adenovirus
-Injected conjunctiva with watery discharge
-typically unilateral > bilateral
-Enlarged preauricular lymphadenopathy can be present
-red w/ no purulent discharge
-Tx:
-Supportive
-Contagious 10-21 days from day of onset or as long as the eyes are red/tearing persists
-Herpes conjunctivitis: Topical versus PO antivirals
-when can you go back to school -> until you stop seeing discharge and at least 24hrs on the antibiotic
allergic conjunctivitis
-Itchy, watery eyes with injected conjunctiva, usually bilateral!
-Allergic shiners may be present -> nasal congestion causes venous congestion
-may be a hx of asthma or other allergies
-chemosis if severe- bubbling, swelling of conjunctiva
-Tx:
-Topical solutions that combine antihistamine and mast cell stabilizer
-Systemic anti-histamines
-Limitation of exposure to allergen
-if not old enough for drops -> cool packs
corneal abrasion
-Sudden, severe eye pain
-Decreased vision, tearing, conjunctival injection, poor cooperation with ocular exam
-Dx:
-Fluorescein dye > illumination with Wood lamp
-Evert upper/lower eyelids to evaluate for FBs
-Tx:
-Ophthalmic ointment, follow-up until healing complete
-preventative antibiotics
-refer to specialist 2-3 days later to make sure healing
-if the pt cant tolerate drops for staining -> empiric tx and f/u with specialist who can sedate and view the eye
blunt ocular trauma
-Blunt trauma can lead to orbital fx, retrobulbar hemorrhage can lead to orbital compartment syndrome -> permanent vision loss
-Orbital blowout fx: Diplopia, pain with eye movements, restriction of EOM
-CT scan! useful in dx extent of injuries
-Orbital compartment syndrome: Severe eyelid edema and proptosis (can progress to this)
-Neuroimaging will show retrobulbar hemorrhage and proptosis
-Tx:
-OBF: Nonurgent repair to prevent enophthalmos, advise not to blow nose (orbital emphysema/proptosis)
-OCS: Emergent lateral eyelid canthotomy and cantholysis to decompress orbit
eye foreign body
-discomfort, tearing, red eye
-Pain with blinking suggests FB trapped under eyelid/corneal surface
-every time you blink can be scratching the cornea
-Tx:
-Eyelid eversion!
-Removal with irrigation or cotton applicator
-Referral to specialist for failed attempt/corneal FB
-Topical antibiotics typically prescribed for several days following FB removal
-corneal FB / rust ring -> specialist
pre-septal vs orbital cellulitis
-PRE-SEPTAL:
-from local exogenous source (abrasion/insect bite), other infections (hordeolum, dacryocystitis), or after hematogenous spread
-May progress to orbital cellulitis
-Red, swollen eyelids; pain; mild fever
-NORMAL- Vision, eye movements, and eye
-TX: PO antibiotics
-ORBITAL:
-Serious complications: Subperiosteal abscess, meningitis, septicemia, and optic neuropathy
-MC- from paranasal sinus infection
-Proptosis!, eye movement restriction, decreased vision
-Eye red and chemotic
-decrease visual acuity
-CT w/ contrast- establish extent and eval for subperiosteal abscess
-Complications: Permanent vision loss (compressive optic neuropathy), corneal exposure/drying/scarring (proptosis), cavernous sinus thrombosis, intracranial extension, blindness, death
-Tx:
-Initially, broad-spectrum antibiotics
-Surgical drainage of abscesses/sinuses
acute otitis media
-MC reason for antibiotics
-S. pneumoniae > H. influenzae > M. catarrhalis > S. pyogenes
-2 critical findings: Bulging TM AND a MEE
-Otoscopic findings: Bulging TM, impaired visibility of ossicular landmarks, yellow or white effusion, opacified/inflamed TM, squamous exudate/bullae on TM
-Season (winter > summer)
-Ages 1-3
-Eustachian tube dysfunction
-Infants and young children more prone due to shorter, more compliant, horizontal ET
-Trisomy 21, cleft palate risk factors
-RF: Bacterial colonization of nasopharynx: S. pneumoniae, H. influenzae, M. catarrhalis
-Smoke exposure, poor immune, daycare, genetics
-Bottle feeding: aspiration into middle ear
-Tx:
-Pain control (1-3 days before antibiotic relieves pain)
-Wait and see approach:
-Observe episode w/o tx
-Option for healthy children (> 2 years) with mild-moderate OM and no underlying conditions
-Decision with parents to begin antibiotics if worsening or lack of improvement within 48-72 hrs
-Antibiotic therapy: (know this)
-1st line: High dose amoxicillin (80-90 mg/kg divided BID)
-Augmentin if child has had amoxicillin within last 30 days or clinically failing x 48-72 hours on amoxicillin
-Cephalosporins (cefuroxime, cefpodoxime, cefdinir) for those with rash to PCN – risk of cross-sensitivity is less than 0.1%
-Macrolide (azithromycin) only if history of type 1 hypersensitivity to PCN -> Resistance of S. pneumoniae and H. influenzae (macrolide efflux pump)
-Second-line antibiotics indicated when child experiences symptomatic infection within 1 month of finishing amoxicillin
acute otitis externa
-Cellulitis of soft tissues of external auditory canal -> extend to surrounding structures -> pinna, tragus, and lymph nodes
-Humidity, moisture, heat known to contribute
-Trauma (breaks skin-cerumen barrier) -> first step in infection -> swab use, earbuds, scratching, ear plugs
-MC organisms: S. aureus, S. epidermidis, P. aeruginosa
-fungal in 2-10%
-Acute onset of pain, aural fullness, decreased hearing, and pruritis (peak within 3 days)
-touching tragus/pinna -> considerable pain
-Discharge may be clear/purulent
-EAC narrowed/swollen (may be difficult to visualize entire TM)
-Complications:
-Cellulitis of neck and face
-Malignant OE: Spread of infection to skull base with resultant osteomyelitis
-Tx:
-Pain control
-removal of debris from canal
-topical antimicrobial therapy
-avoidance of causative factors
-1st line- Fluoroquinolone ear drops; combo with a steroid may be necessary (ciprofloxacin/dexamethasone) -> Ensure no TM perforation before STEROIDS!
-PO antibiotics for any invasive infection signs (fever, cellulitis, cervical lymphadenopathy)
middle ear effusion
-fluid in middle ear w/o signs or sx of acute inflammation
-TM may be opacified/thickened, fluid can be clear/amber/or opaque, typically in neutral/retracted position
-Pneumatic otoscopy and/or tympanometry for confirmation
-Management:
-Abx, anti-histamines, and steroids NOT shown to be useful in tx
-Audiology eval after 3mo of continuous B/L effusion
-Hearing loss/speech delay -> referral to ENT for possible T-tube placement
-Uncomplicated -> observed 3mo with f/u q 3-6mo to eval for effusion clearance
-T-tube indications:
-Hearing loss > 40 dB, TM retraction pockets, ossicular erosion, adhesive atelectasis, and cholesteatoma
tympanic membrane perforation
-AOM may result in rupture of TM
-Discharge from ear seen with rapid relief of pain
-Tx:
-Ototopical antibiotics x 10-14 days with ENT f/u for exam/hearing eval
-Failure to heal may require surgery (typically deferred until age 7, when ET has reached adult orientation)
mastoiditis
-Infection from middle ear spreads to mastoid of temporal bone
-Inflammation of periosteum to bony destruction of mastoid air cells with abscess development
-any age, most < 2yo
-Clinical dx!
-Postauricular pain, fever, and outwardly displaced pinna
-Exam: Mastoid appears indurated, red, swollen, fluctuant with severe tenderness (earliest sx)
-AOM -> almost always present
-Imaging Studies:
-CT scan -> determine extent
-Progressed ds: Coalescence of mastoid air cells with bone destruction
-Complications:
-Meningitis (high fever, stiff neck, severe headache)
-Brain abscess (fever, headache, changes in sensorium)
-Facial palsy, sigmoid sinus thrombosis, epidural abscess, cavernous sinus thrombosis, thrombophlebitis
ear foreign bodies/cerumen impaction
-removed if easily visualized and with appropriate instrumentation
-ENT referral for large FBs, rounded/globular objects, deep objects
-Vegetable matter -> NEVER irrigated (may swell)
-Button-battery -> emergent referral
-Cerumen impactions removed if symptomatic and obstructing visualization of TM
acute pharyngotonsillitis: viral pharyngitis: Infectious Mononucleosis (Epstein-Barr Virus)
-Infectious Mononucleosis (Epstein-Barr Virus)
-MC > 5yo
-Exudative tonsillitis!!
-generalized cervical adenitis
-fever
-Dx:
-palpable spleen or axillary lymphadenopathy increases likelihood of dx
-> 10% atypical lymphocytes on peripheral blood smear or + Monospot -> supports dx (though false neg in kids < 5yo)
-!!Epstein-Barr virus serology showing elevated IgM antibody is definitive
-Tx:
-Supportive
-avoid contact sports
-4-6-week f/u (LFTs)
-Amoxicillin is contraindicated –> precipitates rash
acute pharyngotonsillitis: bacterial pharyngitis
-20-30% w/ pharyngitis have group A streptococcal (GAS)
-Other causes: Mycoplasma pneumoniae, Chlamydia pneumoniae, groups C/G streptococci, and Arcanobacterium hemolyticum
-MC 5-15 yo -> winter/early spring
-Sudden onset sore throat, fever, tender cervical adenopathy, palatal petechiae!, beefy-red uvula, and a tonsillar exudate
-Headache, stomachache, nausea/vomiting
-Scarlet fever!: 1-2 days into sx -> sandpapery rash (diffuse, finely papular, erythematous, blanchable) with strawberry tongue
-Modified Centor Score
-Def dx with throat culture or rapid antigen test -> RAT specific but only 85%-95% sensitive
-KNOW THE CHART
Acute pharyngotonsillitis: diptheria
-Acute infection of URT or skin
-caused by exotoxin-producing Corynebacterium diphtheriae
-Gram-positive, club-shaped rods on gram stain
-Toxin absorbed into mucous membranes -> destruction of epithelium -> inflammatory response -> embedded in fibrin with WBCs/RBCs -> grayish pseudomembrane forms over tonsil, pharynx, larynx
-Pharyngeal diphtheria:
-Mild sore throat, moderate fever, and malaise -> rapid decompensation
-Pharyngeal membrane forms (tenacious, gray, border of erythema/edema) -> may spread to nasopharynx or trachea -> obstruction
-Cervical lymph node swelling -> “bull neck”
-Dx: Culture of C. diphtheriae from infected tissue(s)
-Tx:
-Report to CDC to acquire anti-toxin (give within 48 hrs of sx)
-Antibiotics (erythromycin IM/PO or procaine PCN G IM, q12hrs) x 14 days
-Vaccination during convalescence, observation in hospital setting 10-14 days (isolate for at least 1-7 days, until respiratory secretions are noncontagious)
strep complications (untreated)
-Acute rheumatic fever
-Glomerulonephritis
-Suppurative complications: Cervical adenitis, peritonsillar abscess, AOM, cellulitis, septicemia
-Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS)
-Sudden onset of OCD and/or tics (or worsening of such symptoms) following a strep infection
croup
-MCC- parainfluenza virus serotypes!!!!!!!
-6mo – 5yo -> fall and early winter
-Edema in subglottic space -> signs of upper airway obstruction (inflammation of entire airway is typically present)
-Prodrome of URT sx, followed by barking cough, laryngitis, and stridor
-Mild: Stridor only with agitation
-Worsening obstruction: Stridor at rest, retractions, air hunger, cyanosis, hypoxemia
-Imaging: Not indicated (maybe in atypical presentations to r/o other causes)
-Tx:
-!!!Mild- Supportive, hydration; with or w/o dexamethasone
-expose child to cold moist air
-Dexamethasone: 0.15-0.6 mg/kg PO/IV x 1 dose
-Adjuvant tx: Prednisolone (1 mg/kg) QD x 3 days and/or inhaled budesonide
-!!!!Severe/stridor @ rest: Nebulized racemic epinephrine (diluted in sterile saline!)
-give dexamethasone too (prevents rebound)
-Sx resolution within 3-4 hrs of glucocorticoids/nebulized epinephrine -> safely discharged w/o fear of rebound
-If recurrent nebulized epinephrine tx required -> admission for observation, supportive care, and repeat steroid dosing/neb tx PRN
-Impending respiratory failure -> intubation with ET tube, with extubation within 2-3 days
epiglottitis
-MC- Haemophilus influenzae!!!!!!!; streptococcal species in immunized pts
-Sudden onset of high fever, dysphagia, drooling, muffled voice, inspiratory retractions, cyanosis, and soft stridor
-Pts sit in “sniffing dog” position (neck hyperextended, chin stretched forward)
-can progress to total airway obstruction -> respiratory arrest
-Def dx: Direct inspection of epiglottis (OR during intubation) -> cherry-red and swollen epiglottis
-!!!Imaging: Lateral neck radiograph -> “thumbprint” sign caused by swollen epiglottis
-Tx:
-ET intubation to establish airway
-Blood and epiglottis cultures performed
-IV antibiotics (ceftriaxone or equivalent cephalosporin) x 2-3 days, followed by PO abx x 10 days
-Extubation within 1-2 days, when reduction in size of epiglottis is evident
pertussis
-Caused by Bordetella pertussis!!!!!!(only infects humans, transmitted via coughing)
-Incubation 7-10 days -> most contagious 1st 2 wks of cough
-Peaks among <6mo of age (too young for complete immunization + most likely to have severe complications)
-Catarrhal stage: 1-2 weeks
-Non-specific signs (low-grade fever, nasal congestion)
-Paroxysmal stage: 3-4 weeks
-Coughing occurs in paroxysms during expiration (to dislodge plugs of necrotic bronchial epithelial tissues and thick mucus)
-Forceful inhalation against narrowed glottis that follows = “whoop”
-Convalescent stage: 1-2 weeks
-Gradual resolution of sx
-Dx:
-Isolation of B. pertussis or PCR
-Culture from NP swabs or aspirates
-Lymphocytosis in 75-85% but not dx
-Imaging: Segmental lung atelectasis, perihilar infiltrates
-Tx:
-Macrolides (azithromycin, clarithromycin, erythromycin)!
-Complications/Prognosis:
-MC is PNA (primary or secondary)
-Other complications: Atelectasis, free air (from paroxysms), epistaxis, hernias, retinal/subconjunctival hemorrhage, OM, sinusitis
asthma
-80% develop sx < 5yo
-40% who have wheezing w/ viral infections in 1st few years -> continuing asthma
-Strongest predisposing factor is atopy (personal or familial)
-Shedding of airway epithelium, edema, mucus plug formation, mast cell activation, and collagen deposition beneath basement membrane
-Air wall remodeling/irreversible changes
-Dx- clinical
-Auscultation: Prolonged expiratory phase with wheezing
-Increased severity: High-pitched wheeze with diminished breath sounds
-Severe obstruction: Nothing
-Flaring of nostrils, intercostal and suprasternal retractions, use of accessory muscles
-Cyanosis
-Tachycardia/pulsus paradoxus
-Agitation/lethargy may be signs of impending respiratory failure
acyanotic vs cyanotic defects
-left to right shunts- acyanotic
-right to left shunts- cyanotic
VSD
-MC
-Small VSD: asymptomatic; high-frequency, loud murmur
-Moderate-large- HF
-Auscultation: Pansystolic murmur at LLSB
-Large shunts increase flow over mitral valve causing a mid-diastolic murmur at apex
-Splitting of S2 and intensity of P2 depend on PA pressure
-Imaging:
-ECG: LAE/LVH
-CXR: Cardiomegaly, LVH, increase PA size/blood flow
-PHTN -> RVH
-Echo: Location/size of defect + hemodynamic information (magnitude of shunt and R/PA pressure)
-Tx:
-1/3rd close spontaneously
-Small: Close spontaneously; if not -> surgical closure
-Initial for moderate-severe: Diuretics + digoxin/afterload reducers -> if still poor growth/PHTN -> surgical closure (closure device)
ASD
-asymptomatic, even if large
-RV impulse at LLSB palpable
-Auscultation: Soft (grade I/II) systolic ejection murmur in region of RV outflow tract and a fixed split S2 (due to overload of RV with prolonged ejection into pulmonary circuit)
-Larger shunt: Mid-diastolic murmur at LLSB from increased volume
across tricuspid valve
-Imaging:
-ECG- RV enlargement
-CXR- cardiomegaly, RAE, prominent pulmonary artery
-Echo- location/size and magnitude of shunt
-Tx: Significant shunt still at 3yo -> closure (cath lab – closure device)
patent ductus arteriosus
-Small- asymptomatic
-moderate-large- HF
-Widened pulse pressure
-Auscultation: Continuous, machine-like murmur at L infraclavicular area, radiating along pulmonary arteries
-Larger shunts: Increased flow across MV -> mid-diastolic murmur at apex and hyperdynamic precordium
-Splitting of S2/intensity of P2 depend on PA pressure
-Imaging:
-ECG- LVH -> RVH if PHTN present
-CXR- full pulmonary artery silhouette and increased pulmonary vascularity
-Echo- size/anatomy of PDA and magnitude of shunt and PA pressure
-Tx:
-Moderate-large/symptomatic: Indomethacin!!!!!!, diuretics, eventual closure (cath lab with coil embolization or PDA closure device)
tetralogy of fallot
-MC cyanotic
-4 structural defects:
-1. VSD
-2. Overriding aorta (over VSD)
-3. Pulmonary stenosis
-4. RVH
-Pulmonary stenosis murmur -> initial finding
-R-L shunting increases
-Single S2 and right ventricular impulse at L sternal border
-Hypoxic/Tet spells
-Infant: Restless, agitated, inconsolable crying
-Toddler: Squatting -> increase venous return
-Hyperpnea with gradually increasing cyanosis
-blue mucous membranes -> BAD
-Severe spells: Prolonged unconsciousness and convulsions, hemiparesis, or death
-Imaging:
-ECG: RAD, RVH
-CXR: Boot-shaped heart (small main pulmonary artery and upturned apex from RVH)
-Echo: Anatomy of pulmonary stenosis, coronary anomalies
-Tx:
-Progressive pulmonary stenosis/cyanosis
-Hypoxic spells: Oxygen, knee-chest position, ketamine/phenylephrine (increased SVR)
-Indication for surgical repair
-Complete surgical repair with VSD closure and removal/patching of pulmonary stenosis
transposition of the great arteries
-Cyanosis, tachypnea, single S2
-Imaging:
-ECG: RAD/RVH
-CXR: Increased pulmonary vascularity, “egg on a string” cardiac shadow (narrow superior mediastinum)
-Echo: transposition, sites/amounts of mixing, assoc lesions
-Tx:
-Prostaglandin E1 -> maintain patency/relax pulmonary vasculature
-Balloon atrial septostomy
-Arterial switch (complete surgical repair)
tricuspid atresia
-Severely cyanotic, single S2
-Imaging:
-ECG: LVH
-CXR: Normal/slightly enlarged cardiac silhouette with decreased pulmonary blood flow
-Echo: Anatomy, lesions, source of pulmonary blood flow
-Tx:
-Prostaglandin E1 (maintains pulmonary blood flow until surgery)
-Surgery in stages: (dont need to know)
-Blalock-Taussig procedure
-Glenn procedure
-Fontan procedure
truncus arteriosus
-HF as pulmonary vascular resistance decreases
-Tachypnea, difficulty feeding, poor growth
-Bounding peripheral pulses
-Auscultation: Possible systolic murmur with click at L sternal border, single S2 (single valve)
-Imaging:
-ECG/CXR: LVH + RVH, cardiomegaly, increased pulmonary vasculature
-Echo: Anatomy, truncal valve function, and origin of PAs
-Tx:
-Medical management: Anti-congestive medications
-Surgical repair: VSD closure with placement of conduit between RV and PAs
total anomalous pulmonary venous return
-Most important determinant is presence or absence of obstruction to pulmonary venous drainage
-pulmonary veins empty into RA instead of LA
-Absence of obstruction:
-Minimal cyanosis/asymptomatic
-Hyperactive RV impulse, widely split S2 (increased RV volume) and a systolic ejection murmur at LUSB
-Mid-diastolic murmur at LLSB from increased flow across the tricuspid valve
-Presence of obstruction:
-Cyanosis, marked dyspnea/tachypnea, and signs of R sided HF
-Imaging:
-Absence of obstruction:
-ECG: RV overload
-CXR: Cardiomegaly with increased pulmonary blood flow
-Presence of obstruction:
-ECG: RAD/RVH (from increased pulmonary congestion)
-CXR: Heart normal/mildly enlarged with varying degrees of pulmonary edema
-Echo: Extent of volume overloaded R side of heart, R-L atrial level shunting, and common pulmonary vein site of drainage/degree of obstruction
-Tx:
-Surgery: Common pulmonary vein opened into the LA, ligation of any vein/channel that had been draining the common vein
hypoplastic left heart syndrome
-Ductus arteriosus constriction -> S&S of HF from excessive pulmonary blood flow/obstruction of systemic blood flow
-Diffusely weak/absent pulses, usually no heart murmur, S2 single/loud
-Low CO -> grayish color to cool, mottled skin
-Imaging:
-ECG: RVH with decreased LV forces
-CXR: Cardiomegaly (R-sided enlargement) and pulmonary venous congestion/edema
-Echo: Small L heart, degree of mitral/aortic valve stenosis, hypoplastic ascending aorta, adequacy of L-R atrial flow and R-L ductal flow
-Tx:
-Medical: PGE1, correction of acidosis, BP support as needed
-Surgery is staged (newborn, 4-6 months, 2-3 years)
-Heart transplant for failed surgical palliation or if systemic RV fails
coarctation of the aorta
-Infants:
-Hypoplastic aortic arch, abnormal aortic valves, and VSDs
-Sx develop when ductus closes (2 wks)
-Poor feeding, respiratory distress, and shock possibly sooner
-Femoral pulses are weaker compared to R radial pulse
-BP in LE < UE
-Older children:
-Leg discomfort with exercise, headache, epistaxis
-Decreased/absent LE pulses, HTN of UE
-Auscultation: L interscapular area of back, continuous (if collateral vessels have formed)
-Systolic ejection murmur with click if abnormal aortic valve (50% of time) is present
-Imaging
-Infants:
-ECG/CXR: RVH, marked cardiomegaly, pulmonary edema
-Older children:
-ECG/CXR: LVH, mildly enlarged heart; rib notching (from collateral vessels)
-Echo: Site/degree of coarctation, presence of LVH, aortic valve morphology/function
-Tx:
-Infant with cardiac decompensation: IV prostaglandin (chemically opens ductus – closure would otherwise worsen coarctation), inotropic agents, diuretics, supportive care
-Balloon angioplasty < surgical repair
rheumatic fever
-Group A B-hemolytic streptococcal infection
-Carditis
-Pancardiac inflammation
-Mitral valve MC affected -> insufficiency
-Aortic valve 2nd MC affected
-Early decrescendo diastolic murmur consistent with aortic insufficiency
-Polyarthritis (80% of pts)
-Large joints MC -> typically migratory
-Joint swelling/limitation of movement
-Sydenham Chorea
-emotional lability, ataxia/slurring of speech, Muscular weakness
-up to 3mo, may not be apparent for months to years after acute episode of rheumatic fever
-Erythema Marginatum: Macular, serpiginous, erythematous rash with sharply demarcated border on trunk/extremities
-Subcutaneous Nodules (severe cases)
-Occur over joints, scalp, and spinal column
-Few mm – 2 cm in diameter, nontender, free mobile
-Jones- 2 major or 1 major + 2 minor PLUS evidence of streptococcal injection
-Acute Treatment:
-Anti-Infective tx:
-Benzathine PCN: Single IM injection
-Alternative: PCN V or amoxicillin
-Allergic to PCN? Narrow-spectrum cephalosporins, clindamycin, azithromycin, or clarithromycin
-Anti-inflammatories:
-Aspirin
-Tx for HF as indicated, activity limitations
-Tx after acute episode:
-Prevention
-Regular, long-acting IM injections of benzathine PCN q 4 weeks x 5-10 years of therapy (or d/c at 21yo whichever is longer)
-Alternatives: PCN V, sulfadiazine, erythromycin less effective
-Residual Valvular Damage: Replacement, if indicated
endocardial cushion / AV septal defect
-May be complete, partial, or transitional
-Complete: ASD, posterior/inlet VSD, common AV valve
-Partial/transitional: 2, separate AV valves
-May have AV valve insufficiency at either level
-common with downs syndrome
-Sx of HF by 6-8 wks of life (decreased PVR)
-PHTN present due to increased pulmonary blood flow, and pulmonary vascular obstructive ds may develop early
-Murmurs vary
-Imaging:
-ECG: LAD and combined atrial enlargement/ventricular hypertrophy
-CXR: Cardiomegaly with enlargement of all chambers and presence of increased vascularity
-Echo is dx
hypertension
-start checking at 3yo
-Treatment (primary HTN)
-1st line: Lifestyle changes with diet and exercise!!!!!!!!!!!!!!
-Anti-HTN agents: ACEIs, ARBs, CCBs, diuretics
-Maximizing monotherapy prior to introducing a second agent remains official guideline
syncope
-Hx:
-Age, time of day, state of hydration/nutrition, environmental conditions, activity/body position, frequency/duration of episodes, aura/prodrome/symptoms prior to episode
-Additional: Meds, hx of viral illness, medical hx (neuro disorders, TBI, neurosurgical interventions), family hx (cardiac, exertional, sudden death in children, seizures), witnesses
-NO loss of urine, NO AMS
-Physical:
-General: Hydration, nutritional status, thyroid disease manifestations
-Orthostatic VS
-Decrease in systolic BP of 20 mmHg or diastolic of 10 mmHg after 3 minutes of standing when compared to BP in supine or sitting position
-Pulse strength, rate, and differences between U/L extremities
-Heart murmurs > echocardiogram
-Phenotype of inherited genetic disorders
-ECG: HR, QT interval, T-wave abnormalities, ventricular arrythmias, AV conduction disturbances, or Brugada syndrome (predisposes to VT)
-Tx:
-adequate intravascular volume
-Clear urine 5x daily
-Increase salt
-Leg pumping, leg crossing, and squatting with presyncopal sx
-Regular aerobic exercise
-Meds (limited studies)
iron deficiency anemia
-ID- Insufficient iron to maintain normal functions such that iron stores are reduced
-IDA- Hmg > 2 SDs below normal for age and gender, 2ndary to ID
-Normal term infants born with sufficient iron to prevent ID x 4mo
-Premature, LBW, neonatal anemia, perinatal blood loss, hemorrhage –> reduce iron stores
-Breast milk is low in iron relative to cow’s milk and fortified formulas
-Exclusively breast-fed -> 1 mg/kg/day of supplemental iron x 6mo
-Pallor, fatigue, irritability
-Hx of pica is common
-Assoc with increased lead absorption – neurotoxicity
-screening for anemia @ 12mo with hmg concentration and review of RF
-RF: Low socioeconomic status, premature/LBW, exclusively breast-fed > 4 mo w/o iron supp, lead exposure, weaning to whole milk or complementary foods low in iron, feeding/growth problems, inadequate nutrition
-Hmg < 11 = high-risk ID –> iron eval (iron saturation, ferritin, CRP, reticulocyte hemoglobin concentration)
-Tx:
-Hmg 10-11 at screening: Closely monitored/empirical tx with iron supplementation and a re-check in 1 mo
-If ID/IDA: PO iron 3 mg/kg/day x 3 mo
-supplementation -> increased reticulocyte hmg x 48 hrs; maximal between 5-7 days
-Rise in hmg of 1 or more g/dL after 1mo is a good response
-Therapy continued x 3 months to replenish stores of iron
-Parenteral iron for those with CKD and erythrocyte stimulants maybe celiac or IBD as well
idiopathic thrombocytopenic purpura (ITP)
-MC bleeding disorder of kids
-Often after viruses (rubella, varicella, measles, parvovirus, influenza, EBV, or HIV)
-Thrombocytopenia from clearance of circulating IgM/IgG-coated platelets by reticuloendothelial system
-Most pts recover spontaneously x several mo
-Acute petechiae and ecchymosis
-Epistaxis and gingival bleeding are common
-Dx Blood:
-Platelets markedly reduced (< 50,000 and often < 10,000)
-Large platelets on blood smear (accelerated new platelet production)
-WBC/diff and Hb usually normal
-PT and aPTT normal
-Bone marrow: Megakaryocyte hyperplasia with normal erythroid and myeloid cellularity
-Complications:
-Severe hemorrhage and bleeding
-RF: Platelets < 10,000/uL and mean platelet volume < 8 fL
-Tx:
-Observation in absence of bleeding, regardless of platelet count
-Avoid NSAIDs, physical activities
-Corticosteroids
-Severe acute bleeding- intravenous immunoglobulin (IVIG) is tx of choice (alt or adjunct to corticosteroids)
-Anti-Rh(D) IG: Only effective for Rh (+) pts
-Splenectomy:
-Considered if persists x 12mo and failure of preferred/alt 2nd-line tx
-Thrombopoietin receptor agonists (eltrombopag, romiplostim); FDA-approved for > 12mo
-Typically postponed to > 5yo if possible
-Complete response in 70%, partial in 20%
-Prognosis:
-80% remission
-Tx with combination steroid and IVIG better remission rates at 12 and 24mo than either alone
immunoglobulin A vasculitis/Henoch Schonlein Purpura (HSP)
-MC type of small vessel vasculitis in kids
-URI precedes dx in 2/3
-Antigens from GABHS, viruses, drugs, foods, and insect bites
-Small vessels of skin, GI tract, and kidneys MC affected
-Skin: Urticarial -> maculopapular -> symmetrical, palpable, purpuric rash on legs, buttocks, and elbows
-Migratory polyarthralgia or polyarthritis (ankles/knees)
-Intermittent, sharp abdominal pain (50%)
-Renal involvement in 2nd-3rd weeks with nephritic or nephrotic picture, often high BP (25-50%)
-Intussusception, hemorrhage/edema of small intestine, testicular torsion, neurologic symptoms also assoc
-Dx:
-Platelets normal/elevated,
-hemostasis and platelet function are normal
-UA with hematuria, sometimes proteinuria
-Stool with occult blood possible
-ASO titer elevated and throat culture + for group A B-hemolytic streptococci
-Serum IgA may be elevated
-Tx/Prognosis:
-Supportive, NSAIDs, corticosteroids
-If ASO titer elevated or + strep culture –> PCN
-Good prognosis: Recurrence of symptoms in 25-50%, progressive renal failure in < 5%
Acute lymphoblastic Leukemia (ALL)
-MC malignancy of kids (25% of cancer dx < 15yo)
-Peak age- 4yo; 85% dx 2-10yo
-Trisomy 21– 10-20x risk
-Uncontrolled proliferation of immature lymphocytes
-> 25% malignant hematopoietic cells (blasts) in bone marrow aspirate
-> 70% w/ aggressive combo chemotherapy and early pre-symptomatic tx to CNS are cured
-decreased production of RBCs, WBCs, or platelets, and leukemic infiltration of extramedullary sites
-Intermittent fevers, bruising/pallor, bone pain (pelvis, back, legs)
-PE- normal to highly abnormal
-Pallor, petechiae, purpura
-Hepatomegaly/splenomegaly (> 60%)
-Lymphadenopathy, testicular enlargement, SVC syndrome (adenopathy), tachypnea/orthopnea/respiratory distress (mediastinal mass), CN palsies (leukemic infiltration), leukemic infiltration/hemorrhages of optic fundi, flow murmur/tachycardia (anemia)
-Labs:
-CBC w/ diff- most useful
-decrease in at least 1 cell type (neutropenia, thrombocytopenia, or anemia) - 95%
-WBC low/normal (50%), with neutropenia (< 1000)
-Peripheral smear: RBC abnormalities (teardrop shapes)
-Uric acid/LDH elevated as a result of cell breakdown
-Bone marrow bx: Infiltration of leukemic blasts replacing normal marrow
-Imaging:
-CXR: Mediastinal widening/mass, tracheal compression due to lymphadenopathy or thymic infiltration
-AUS: Kidney enlargement, intra-abdominal adenopathy
-Plain films of long bones/spine: Demineralization, periosteal elevation, growth arrest lines, compression of vertebral bodies
-Tx:
-Induction (1st month)– > 95% remission
-Consolidation
-Intensification
-Maintenance
-Tumor lysis syndrome- anticipate
-Hyperkalemia, hyperuricemia, and hyperphosphotemia
-Maintaining urine output with IV fluids + PO allopurinol
-Hyperleukocytosis (with hyperviscosity and respiratory distress, AMS): Leukopheresis
-During tx, fever/neutropenia requires prompt assessment -> blood cx/tx with empiric broad-spectrum abx
-Prophylaxis for PCP (trimethoprim-sulfamethaxzole)
-Prognosis- Most important features: WBC count and age
-1-9yo w/ WBC count < 50,000– survival rate > 90% range
-Ages > 10 - ~ 88%
acute myeloid leukemia (AML)
-25% of all leukemias kids -> but 1/3 of deaths
-RF: Congenital, acquired (ionizing radiation, cytotoxic CTX agents, benzenes)
-Aggressive induction therapy -> 75-85% remission
-Anemia (44%), thrombocytopenia (33%), and neutropenia (69%)
-Hyperleukocytosis: Venous stasis, sludging of blasts in small vessels (hypoxia, hemorrhage, infarction)
-CNS leukemia present in 5-15% of pts at dx (higher than ALL)
-auer rods
hodgkin lymphoma
-Better response to tx than adults
-5-10 year survival rate of > 90%
-15% in children < 16yo (3% < 5yo)
-M>F
-Painless cervical lymphadenopathy
-Firm, rubbery texture; not fixed to surrounding tissues; variable growth rate
-Bx: No identifiable infection in region by enlarged node, > 2 cm, supraclavicular/abnormal CXR, increase in size after 2wks or failing to resolve within 4-8wks
-Constitutional symptoms (33%): Fever, wt loss of 10% in prior 6mo, drenching night sweats (Ann Arbor staging)
-Asymptomatic mediastinal disease (adenopathy, mass) in 50%: Sx with compression of vital structures
-Labs: CBC usually normal (although anemia, neutrophilia, eosinophilia, and thrombocytosis may be present), ESR and other acute phase reactants often elevated
-Staging:
-Ann Arbor classification (determines tx and prognosis)
-CT of neck, chest, abdomen, and pelvis, as well as PET scan (with or w/o bone marrow bx)
-Pathologic Findings:
-Reed-Sternberg cell (germinal-center B cells with malignant transformation)
-20% in developed countries are + for EBV
-Tx/Prognosis:
-Based on stage, presence of B symptoms, tumor bulk, and # of involved nodal regions
-CTX and/or immunotherapy alone – less often by radiation therapy
-5-year survival rate- 90-95% in Stages I and II (slightly lower in Stages III and IV)
-2/3rds of all relapses within 2 years after dx, relapse rarely beyond 4 years
non-hodgkin lymphoma
-5-10% of malignancies in < 15yo
-Incidence increases with age
-3:1 male predominance
-in Africa ~50% due to EBV and assoc w/ Burkitt lymphoma
-congenital or acquired immune deficiencies -> 100-10K x greater risk
-rapidly proliferating, high-grade, diffuse malignancies -> very responsive to tx though
-Arise at any site of lymphoid tissue as well as extra-lymphatic sites (bone, bone marrow, CNS, skin, and testes)
-S&S determined by location of lesions and degree of dissemination
-Dx:
-Bx of involved tissue with histology immunophenotyping, and cytogenetic studies
-CBC, LFTs, and biochemical profile -> Elevated LDH reflects tumor burden
-CXR, CT scan- neck/abdomen/pelvis, PET scan
-Bone marrow and CSF exams
-Tx/Prognosis
-Management of life-threatening problems at presentation is critical -> Acute TLS, SVC syndrome, airway compromise, cardiac tamponade
-Systemic CTX
-Intensive intrathecal CTX for CNS prophylaxis x 3-9mo
-LL: Tx protocols for ALL x 2 years
-BL/BLL, LCBL, ALCL: Alkylating agents/methotrexate
-Prognosis based on extent of ds at dx
-90% with localized disease – long-term, disease-free survival
-Disease on both sides of diaphragm, CNS involvement, or BM involvement – 70-80% failure-free survival rate
-Relapses early – may have chance for cure with HSCT
brain tumors
-MC solid tumors of childhood
-misdx or dx late
-Infratentorial tumors (<2):
-Sx: Vomiting, unsteadiness, lethargy, irritability
-Signs: Macrocephaly, ataxia, hyperreflexia, cranial nerve palsies
-Supratentorial tumors (older kids):
-Headache, visual symptoms, seizures, and focal neurologic deficits (personality changes)
-Cerebellar/posterior fossa tumors: Morning vomiting
-Brainstem tumors: Facial and extraocular muscle palsies, ataxia, hemiparesis, hydrocephalus
-Dx:
-MRI- study of choice (with and w/o contrast)
-Imaging of entire neuraxis and CSF cytologic exam for medulloblastoma, ependymoma, and pineal region tumors
-MRI of spine for midline tumors of 4th ventricle/cerebellum
-Lumbar CSF»_space;» ventricular CSF
-Biomarkers (hcg and a-fetoprotein) helpful in dx and f/u
-2 categories (based on cell origin):
-1. Glial tumors: Astrocytomas, ependymomas
-2. Embryonal tumors: Medulloblastomas, atypical teratoid/rhabdoid (AT/RT) tumors
-Astrocytoma !!!
-MC brain tumor of childhood
-Low-grade may be curable by complete surgical excision alone
-CTX effective alone in 40-50% of low-grade cases (multiple courses)
-Tx:
-Supportive care: Dexamethasone, anti-convulsants (levetiracetam)
-Specific therapy
-Maximal safe surgical resection is preferred initial approach
-Radiation use varies
-CTX effective in tx low-grade and malignant astrocytomas and medulloblastomas
-Older children with malignant gliomas: Combination of above
-Prognosis:
-Low-grade astrocytomas: 5 and 10-year survival rates 60-90%
-Low-stage medulloblastoma: 10-year survival rate ~ 40-60%
-High-risk: 5-year survival rate ~ 25-40%
-Glioblastoma: Cure rates poor (survival rates < 10%)
neuroblastoma
-from neural crest tissue of sympathetic ganglia or adrenal medulla
-Small cells with scant cytoplasm and hyperchromatic nuclei (rosette pattern) -> differentiate from other “small, round, blue cell” malignancies
-MC solid neoplasm outside CNS
-50% dx < 2yo and 90% < 5yo
-Constitutional: Fever, wt loss, irritability
-PE: Firm, fixed, irregularly shaped, midline abdominal mass
-wherever there is sympathetic nervous tissue (location determines varied exam findings)
-Common metastatic sites: Bone, bone marrow, lymph nodes, liver, and subcutaneous tissue
-Skull/retrobulbar area: Periorbital ecchymosis, proptosis
-Liver: Massive hepatomegaly
-Skin: Bluish/purplish subcutaneous nodules (“blueberry muffin baby”)
-Paraneoplastic: Opsoclonus-myoclonus ataxia (“dancing eyes/dancing feet”)
-Rapid, chaotic eye movements, myoclonic jerking of limbs and trunk, ataxia, and behavioral disturbances
-Labs: Anemia (60%), urinary catecholamines (VMA/HVA) elevated (90%)
-Imaging:
-X-rays- stippled calcifications
-CT- extent of primary tumor, effects on surrounding structures, and presence of metastatic ds
-MRI- spinal cord involvement
-PET- bone metastases
-Staging:
-International Neuroblastoma Staging System/Risk Group
-Bx of tumor and bone marrow
-Tumors classified as favorable or unfavorable based on histologic characteristics and pt of dx (younger age -> more favorable dx)
-Tx based on classification
-Low-risk: Surgical resection of >50% of tumor is usually sufficient for cure; survival rates 98%
-Intermediate-risk: Surgery + CTX; survival rates 90-95%
-High-risk: Intensive, multimodal therapy including CTX, surgery, HSCT, irradiation, biologic therapy, and immunotherapy; 5-year overall survival rate 73%
nephroblastoma (wilms tumor)
-2nd MC abdominal tumor in kids (after neuroblastoma
-sporadic
-MC between 2-5yo, unusual after 6 yo
-Increasing size of abdomen or an asymptomatic abdominal mass
-Mass is smooth, firm, well-demarcated, rarely crossing midline
-Labs- CBC normal, possible anemia; UA blood/leukocytes
-Imaging/Staging:
-US/CT- mass -> Liver, chest for metastases
-IVC evaluated via Doppler flow
-Staging at time of surgery
-Tx:
-Surgical exploration of abdomen
-Following excision, stage assigned, -> defines tx (CTX)
-Higher stages require irradiation to tumor bed/sites of metastases
-Overall cure rate of 90% (varies based on stage)
osteosarcoma
-relationship between rapid bone growth and malignant transformation
-Metaphyses of long bones primarily affected
-Distal femur > proximal tibia > proximal humerus > mid-proximal femur
-Pain with or w/o assoc soft tissue mass; systemic sx rare
-Labs: Possible elevation in serum alk phosphatase or LDH levels
-Imaging:
-Permeative (“moth-eaten”) destruction of normal bony trabecular pattern with indistinct margins
-Periosteal new bone formation and lifting of bony cortex may create a Codman triangle
-Soft tissue mass + calcifications in radial/sunburst pattern
-MRI > CT scan in defining primary tumor
-CT scan chest/bone scan for metastases
-MC sites of metastases: Lungs and other bony sites
-Bx of tissue for def dx
-Tx:
-Surgery + CTX (prior to definitive surgery)
-Resection of tumor
-Postsurgical CTX x 1 year -> Highly radioresistant
-Localized ds – 70-75% long term survival rate
ewing sarcoma
-2nd decade of life
-white males
-Small, round, blue cell malignancy
-Pain with or w/o swelling and erythema
-Fevers, wt loss
-Elevated LDH possible
-Imaging/Staging:
-Similar to osteosarcoma, but involves diaphyses of long bones
-MRI of primary lesion
-CT scan for staging (chest) -> MC sites of metastases: Lung, bone, BM
-Bone scan, BM bx also essential
-Further electron microscopy, immunocytochemistry, and/or cytogenetic analysis may be necessary
-Tx:
-CTX followed by surgery, radiation
-CTX continued x 6mo following local control
-Localized ds – 70-75% long-term survival rate
rhabdomyosarcoma
-MC soft tissue sarcoma of childhood (10%)
-Peak- 2-5yo, M > F,
-70% dx < 10yo
-anywhere in body
-Classified into subtypes based on features: embryonal RMS and alveolar RMS
-Embryonal RMS (70%): GU tract, head/neck; young children
-Alveolar RMS: Trunk and extremities; older children/adolescents
-Sx- Vary based on site affected
-Staging:
-CT and/or MRI scan
-CT of chest as well – Lungs MC site of metastasis
-Bone scan and bone marrow bx
-Tx: (dont need to know)
-Tumor excised if feasible (CTX prior if not)
-Radiation for localized tumor control
-CTX for all pts following resection
-Low-risk – FFS 90%, intermediate-risk – FFS 60-70%, high-risk – FFS < 20%
-MRI is best imaging for osteosarcoma
-tanner stage?
-rheumatic fever
