Transcript Document 7160635

GENERAL PEDIATRICS
LMCC Review
Presented by Marc E. Zucker MD, FRCPC
Division of Pediatric Medicine
CHEO
March 22, 2010
Feeding & Growth
Breastfeeding
CPS recommends exclusive breastfeeding
for babies up to 6 months (when possible)
 Breast milk has a caloric content of
~20 Kcal/oz (0.67 Kcal/ml)
 Babies need 100-130 Kcal/Kg/day in 1st 3
months
 Feeding/growth spurts occur at 8-12 days,
3-4 wks, 3 mo, variably after that
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Nutritionally, how does breast
milk compare to cow’s milk?
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Lower protein content - decreased solute load
Greater whey:casein (70/30 vs 18/82, formula
60/40)
CHO - both are lactose based (6.5% vs 4.5%)
Fat - 30-50% vs 3.5-4%
Vitamins - richer in A,C,E, lower in D & K
Minerals - lower Fe but better absorbed
Breast Feeding Benefits for
Baby
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Immunological benefit
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secretory IgA, lactoferrin, lysozyme as GI
defence
Lower rate OM, LRTI, gastro, possibly UTIs,
Hib
Less allergenic
Less constipating
Better jaw/mandible development
Attachment and ?Improved cognitive
functioning
Breast Feeding Benefits for Mother
Postpartum weight loss & uterine involution
 Delayed return of fertility
 Bonding
 Pre-menopausal breast & ovarian Ca
reduced
 Economical benefit
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“Disadvantages” To Breast
Feeding
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Takes 3-7 days for milk supply to come in
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Jaundice is more common
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ineffective latch/sore nipples/engorgement
Infections
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Breastmilk jaundice
“Mom/baby team”
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risk of dehydration/ “breastfeeding jaundice”
thrush , mastitis/abscess
Reduced levels vitamin D & K
Vitamin D Supplementation
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Rickets is still a problem in Canada!
400 IU per day
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All Breastfed infants
Pregnant and nursing mothers in northern
Canada
Formula Fed infants living in northern Canada
800 IU per day - < 2 yrs breastfed babies
with a risk factor
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Home above 55 degree latitude, darker skin, sun
avoidance
Community with high prevalence Vit D deficiency
Vitamin D is found in milk, margarine,
salmon, tuna, liver, kidney & from the sun
Contraindications to
Breast Feeding
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Maternal infections
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HIV, AIDS, active TB, malaria, herpes on breast,
hepatitis
Maternal sepsis
Psychotropic meds or others crossing
Chemo/radiation
Alcohol/drug abuse
Infant Galactosemia (lactose)
*May breastfeed even with VZV
Cow’s Milk Formula

Always Fe fortified
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Many choices!
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Specialty formulas
soy, lactose free, increased calories
 Protein hydrolysate formulas
(eg.Alimentum, Nutramigen, Progestemil)
 Amino-acid based formulas (Neocate)
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Introduction of Solids
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cereals 4-6 months
vegetables
fruits
meats
Rest gradually in this
order
cow’s milk should be postponed until at least
10-12 months of age (renal load)
2% or 1% milk should be postponed until
after second birthday (inadequate fat content)
Infant Growth: Rules of Thumb
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Weight gain:
Regain birth weight by 10-14 days (max 10%
loss)
 Double birth weight by 5 months
 Triple birth weight by 1 year
 Quadruple birth weight by 2 years
 Increase by 5 lbs/year for rest of childhood
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Growth - Height
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Average length at birth 50 cm (20 inches)
Increases by 50% by 1 yr
Doubles by 4 yrs
Triples by 13 yrs
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Ave growth 5-6 cm / yr (4 yrs-puberty)
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Growth- Body Mass Index (BMI)
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BMI helps to quantify the weight to height
relationship
BMI = weight(kg)/height (m)2
BMI of 20-25 is acceptable
BMI > 30 indicates obesity
BMI < 18 suggest severe anorexia or
Failure to thrive
Growth- Head Circumference
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2 cm/month 1-3 months
1cm/month 3-6 months
0.5cm/month 6-12 months
Most of growth is in first yr!
12 cm in first yr, 2 cm in 2nd yr, 6-8 cm rest of life
Growth Monitoring

Routinely recommended
 Height, weight, head circumference
 Plot on appropriate chart considering ethnicity, genetic
syndromes (eg. Tri 21, Turner’s), and prematurity
 Prematurity, correct hc (18 mo), wt (24 mo),
ht (40 mo)
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Only way to detect FTT
 Also detects chronic illness, feeding difficulties
What is Failure to Thrive?
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US National Center for Health Statistics defines
FTT for children < 2 yrs of age as:
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Weight <3rd-5th centile for age on more than one
occasion
Weight <80% of ideal body weight for age
Weight crosses 2 major centile curves
downwards on a standardized growth curve
Exceptions: genetic/familial short stature,
constitutional growth delay, SGA infants &
preterm infants
Caloric needs
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0-10 kg: 100 kcal/kg/day
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10-20 kg: 1000 + 50 kcal/kg/day
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>20 kg: 1500 + 20 kcal/kg/day
FTT- Infant Growth

Caveats to normal growth velocity:
>50% of babies shift their growth parameters
upwards between birth and 3 months
 Nearly 30% of well babies shift their
parameters downwards between 3 and 18
months
 Exclusively breastfed babies plot higher for wt
at 0-6 months and lower at 6-12 months5
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Growth Velocity
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Average age to “settle” on a growth curve is 13
months6
Downward shift seen with constitutional growth delay
 downward shift between 6 & 24 months
 may have decreased weight for height
 re-establish normal growth velocities by 3 yrs
*Genetically Programmed curve is established by 18-24
months
FTT- Assessment
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Grading of malnutrition:
Grade
Wt for Age
(%)
0-Normal
>90
1-Mild
75-90
2-Moderate
60-74
3-Severe
<60
Wt for Ht
(%)
>90
81-90
70-80
<70
FTT- Assessment
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“Organic” vs. “non-organic”
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Historical way of viewing FTT
Refers to presence/absence of diagnosis of
major disease process or organ dysfunction
“Non-organic” accounts for >80%
Now felt to be more of a continuum
Multifactorial process
FTT- Assessment
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Under-nutrition results from:
1)
2)
3)
4)
Decreased caloric intake
Inadequate caloric absorption
Increased caloric losses
Increased caloric requirements
FTT- Differential Diagnosis
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Decreased caloric intake:
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Inadvertent (decreased breast milk, improper formula
preparation)
Neglect or abuse
Behavioural (ex. Food refusal)
Pain (GERD, injury to mouth or esophagus)
Fatigue /anorexia (anemia, cardiac dz, resp dz, RTA)
Impaired swallowing (neurologic dz)
Craniofacial abnormalities (cleft lip/palate, choanal
atresia)
Toxin (lead)
FTT- Differential Diagnosis
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Inadequate Caloric Absorption & Increased Caloric Losses
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GI
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Pancreatic insufficiency (CF)
Liver disease (biliary atresia, chronic cholestasis)
Generalized malabsorption (CF, Celiac, short gut)
Diarrheal state (infectious, post-infectious)
Persistent vomiting (pyloric stenosis, GERD)
Inflammatory disorders (IBD)
Allergic gastroenteropathy
Protein-losing enteropathy
FTT- Differential Diagnosis
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Increased Caloric Losses cont’d
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Renal
Protein loss
 Carbohydrate loss
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Inability to use nutrients
Diabetes Mellitus
 Metabolic dz
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FTT- Investigations
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Careful and complete history taking and physical
examination are ESSENTIAL
Unless an illness other than primary undernutrition is suspected on Hx or P/E the yield of
lab investigations is almost nil!
Lab testing helps with diagnosis in 1.4%
FTT- Investigations
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Non-specific “screening”
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Markers of nutritional status
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CBCD, ESR, lytes, BUN, Cr, venous gas
Urine R&M, C&S
Total protein, albumin, glu, Ca, PO4, Iron studies
Zinc, vitamin levels
Dependent on specific aspects of Hx & P/E
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Liver function tests
Thyroid studies
Stool OB, reducing substances, culture, O&P, trypsin
Sweat test, immunoglobulins & celiac screen, viral
serology (incl HIV), TB testing, immune w/up,
metabolic w/up, CXR, ECG, milk scan
FTT- Management
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Admit if :
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Suspect enviro. deprivation/neglect/abuse
Suspect chronic dz which needs stabilizing
Severe under-nutrition (consider if moderate)
 ie. <60% of median weight for age
Failed out-patient management
With hospitalization:
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greater likelihood of catch-up growth
no change in developmental outcomes
FTT- Management
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Inter-disciplinary approach!!
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Treat any underlying illness and provide
nutritional support:
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Increase caloric intake
1.5-2 X RDA
 (120 kcal/kg/day x ideal wt)/current wt
 Estimate 150-200 kcal/kg/day
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FTT- Management
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Mild under-nutrition
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Ensure frequent feedings (q 3 hrs)
Increase formula concentration (eg. 24 kcal/oz)
Add calorie-rich foods to diet (butter, PB, oils)
Provide dietary counseling
Prescribe multivitamin with zinc and iron
Follow-up frequently (?public health nurse)
Expect catch-up growth at 2-3x regular rate in first
month
FTT- Management
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Moderate under-nutrition
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Determine caloric intake
Consider whether investigations are necessary
Increase caloric intake (150-200 kcal/kg/day)
Ensure adequate protein (3-4 g/kg/day)
Consider meal supplements (eg. Pediasure)
Add Multivitamin
Consider therapeutic doses of iron
Monitor weight gain
FTT- Management
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Severe under-nutrition
Admit
 Initiate re-feeding slowly
 Consider using elemental formula
 Consider diluting formula
 May need ng continuous feeds or tpn
 Follow fluid and lytes status closely
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FTT- Long-term implications
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Persistent growth deficits
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Cognitive impairment
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Behaviour problems
IMMUNIZATIONS
Immunization Schedule
(Recommended by the Canadian Immunization Guide)
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Age
2 mos
4 mos
6 mos
12 mos
18 mos
4-6 year
q10 years
Vaccine
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DaPTP-HIB, Prevnar, Menj
DaPTP-HIB, Prevnar,Menj
DaPTP-HIB, Prevnar,Menj
MMR, Varicella, Prevnar
DaPTP-HIB, MMR
DaPTP
dTaP/dT
Contraindications to Vaccines
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Strict
- anaphylaxic or anaphylactic shock
- encephalopathy
Precautions
- febrile reaction > 40.5
- shock collapse or hypotonia
- hyporesponsive collapse
- seizures
Contraindications to vaccines
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Anaphylaxis to eggs:
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Severe immune deficiency:
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All live vaccines (MMR, VZV, OPV, BCG, Yellow
fever, Oral cholera, Oral typhoid)
Pregnancy:
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Influenza and yellow fever
MMR and Varicella
Anaphylaxis to neomycin:
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MMR and IPV
Immunization Reactions
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DaPTP/Hib
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reactions occur within 72 hrs
MMR
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reactions occur 5-12 days
Delayed Immunization
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Age 1-6 years
0 mos:DPTP-Hib,
MMR,HepB, P,V,MC
2 mos:
Pentacel,MMR,HepB,
Prevnar
4 mos: DPTP
12 mos:DPTP
4-6 yrs: DPTP
14-16 yrs: dTaP
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> 7 Years Old
0 mos: TdaP,Polio,
MMR,V,Menj,HepB
2 mos: TdaP, Polio,
HepB,MMR, V
6-12 mos:
TdaP+Polio,HepB
TdaP (no polio) q10
yrs thereafter
Other Immunizations
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Hepatitis A & B
Influenza
HPV
Rotavirus
INFECTIOUS DISEASE
Fever
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Temp > 38.3 Celsius rectal
Occult bacteremia: most in 3-24 mos
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3-5% febrile are bacteremic
most common org. is Strep. Pneumo **
0-1 mos: FSWU
1-3 mos:
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toxic = FSWU
non-toxic and low risk (WBC 5-15,
bands <5%, urine neg, well-looking,
reliable family): investigate and follow
Otitis Media
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Incidence:
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Peak:
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15% to 20%
6 to 36 months
4 to 6 years
decreases > 6 years old
Etiology: S. pneumoniae, M. catarrhalis,
non-type H. Flu, GAS & viral
Otitis Media
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Risk Factors
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mid-face hypoplasia (Down Syndrome)
daycare attendance
Inuit/Aboriginal
low SES
2nd hand smoke
Otitis Media
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Treatment:
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1st line: Amoxil
2nd line: High dose Amoxil, Clavulin,
Macrolides, Cephalosporin
T-Tubes if recurrent or persistent effusion
Complications:
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hearing loss
chronic effusion
mastoiditis
meningitis
Sinusitis
Mainly ethmoid sinus
 Predisposed by viral URTI, allergy,
asthma, periodontal disease
 Same bugs as OM +/- anaerobes
 Presents with fever, purulent nasal
discharge (> 10 days), periorbital
tenderness, halitosis
 Treat with same Abx as OM, may
need longer course (3 weeks)
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Meningitis
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Newborn period (LEG)
Listeria
 E. Coli
 Group B strep
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2 months - 12 years (SHIN)
Strep pneumonia, N. meningitides
 Less common Hib with immunization
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Meningitis
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in abnormal hosts or anatomic defects:
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increased Pseudomonas, Staph, Salmonella,
Serratia
Complications
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SIADH
seizures
subdural effusions
transient joint effusions (Ag-Ab reaction)
hearing loss
Urinary Tract Infection
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Newborn M › F (2)
Children F › M (10)
Schoolgirls - 5%
Recurrence - 80%
Vesicoureteral reflux - 35%
Renal scarring - 50%
All children ‹ 3 yrs
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U/S
VCUG
Urinary Tract Infections
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UTI
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Pyelonephritis
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KEEPPSS
Klebsiella, E. Coli, Enterococcus, Proteus,
Pseudomonas, Staph, Strep
ampicillin + gentamycin IV initially
then Amoxil or Septra po
VUR
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prophylactic Septra or nitrofurantoin (or Amoxil)
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Higher grades may require surgery
Osteomyelitis
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Organism
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neonate: Staph, GBS, E.Coli
> 3mos.: Staph, Hib, Strep,Pseudomonas
SS disease: Salmonella
Diagnosis
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bone scan
x-ray 10-12 days
Septic Arthritis
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Monoarticular (trauma)
Organism
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neonate
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group B strep, staph, E.Coli
>3 mos
Staph aureus
 Strep, Hib
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most common site is knee (40%)
Fever and Rash
Measles (First Disease)
Paramyxovirus
 Stages
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incubation: 8-13 days
prodrome: 4 C’s then fever with rash
skin rash (erythematous, maculopapular, starts at
hairline and spreads to face, trunk and
extremities)
Complications
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pneumonia
encephalitis
SSPE
Scarlet Fever (Second Disease)
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Fever, pharyngitis, exanthem (starts in
axilla, groin, neck, blanches,circumoral
pallor, Pastias lines)
Age › 3 yrs; recurrence
Group A strep:  erythrogenic toxin (2-5
days postStrep throat or GN)
Treatment with Penicillin
Complications
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cellulitis
Rheumatic fever
Rubella (Third Disease)
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Togavirus
Congenital
Postnatal
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mild disease
suboccipital nodes
maculopapular pink rash, starts on face, neck
to extremities, spreads quicker than measles
Roseola Infantum
(Fourth Disease)
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HHV6
High fever  rash maculopapular with
cessation of fever
High WBC  low WBC
Febrile convulsions
Erythema Infectiosum
(Fifth Disease)
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Parvovirus B19
No prodrome: red flushed face/slapped
cheek, maculopapular rash with lacelike
appearance
Complications
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miscarriage/SA
aplastic crises
ALTE/SIDS
Apparent Life Threatening Event:
Definition
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Clinical symptoms frightening to caregiver
Combo of apnea, colour change, tone
change, choking, gagging
Apnea: 20 seconds of breathing cessation
or shorter if associated with tone change,
colour change, CV change
ALTE
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Detailed Hx and Px
Talk to person witnessing event
Significant event?
ALTE
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Differential
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Neuro- seizure
GI- reflux
Pulmonary- aspiration, apnea
CV- arrhythmia
Infection- sepsis, pertussis, RSV
Metabolic
Abuse
ALTE
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Investigations
Labwork +/- infectious workup
EEG
ECG/Echo
UGI/pH probe
CT head
Monitor
SIDS
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Unexpected death by Hx and Postmortem
most common cause of death 1mo-1yr
peak 2-4 months, 95% <6 months old
SIDS
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Infant Risk Factors:
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prematurity
age, sex
prone sleeping
bottle fed
smoke environ.
Thermal stress
ethnicity
prior illness
winter months
low birthweight
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Maternal Risk
Factors
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low age
low SES
low education
smoker
drug use
poor nutrition
Gastroenterology/
Pediatric Surgery
Colic
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Unexplained irritability/crying
2-3 wks to 3 mos
At least 3 hrs/day
> 3 days/week
> 3 weeks duration
? Secondary to immature gut development
Colic
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++Gas/legs drawn up; otherwise well
No proven treatment - rhythmic
motion/sounds
Ovol/Tylenol- no proven benefit
Parental support and reassurance
Abdominal Pain
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Acute: Ddx includes gastro, hernia, UTI,
appendicitis, intussusception, malrotation,
volvulus, HSP, SC Crisis, pneumonia,
mesenteric adenitis,
Chronic: > 3 episodes affecting activities > 3
months
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Organic (<10%): constipation, IBD, mass, PUD,
GU, lactose intolerance
Functional (90%): 8-10 yo peak, girls
predominate, vague crampy periumbilical pain
with no awakening, ppting or alleviating factors.
Normal growth.
Gastroesophageal Reflux
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Incompetence of lower esophageal
sphincter
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improves by one year of age in most infants
Complications
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apnea in infants
aspiration pneumonia
chronic cough/wheeze
esophagitis- dysphagia,hemetemesis, Fe
deficiency anemia
Gastroesophageal Reflux
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Diagnosis
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pH probe
Ba swallow
nuclear scan
endoscopy
Gastroesophageal Reflux
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Treatment
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chalasia routine - attention to burping, small
frequent feeds, 300 prone
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thickening feeds
Medications:
H2 blockers or PPI if esophagitis or gastritis
present
 Domperidone for decreased gastric emptying
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Pyloric Stenosis
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boy > girl
3 weeks - 3 months
projectile vomiting (nonbilious)
hungry infant feeds vigorously
Pyloric Stenosis
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O/E:- dehydration, lethargy, weight loss,
peristaltic waves L R, palpable “olive”
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Lab- hypochloremic alkalosis
Investigation- U/S, UGI
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Rx: rehydrate and restore electrolyte
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balance
- myotomy of pyloric muscle
Intussusception
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3 months - 3 years (up to 6 years)
5% anatomic abnormality found
Meckel’s polyp
 duplication
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more frequent ileocolic or ileoileocolic
Intussusception
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Clinical
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severe paroxysmal pain
lethargy  shock
sausage shaped mass RUQ
vomiting
currant jelly stool
Intussusception
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Lab
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x-ray
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barium enema
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density or gasless right side
coil-spring sign
Treatment
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reduction by barium enema
surgical reduction
Meckel Diverticulum
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2% population
year peak incidence
2 feet from ileocecal junction
35% ectopic gastric or pancreatic tissue
painless rectal bleeding (typically bright red)
99Tc scan confirms diagnosis
treatment: excision
Constipation
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Def’n: passage of bulky or hard stool at
infrequent intervals
Retention of stool in rectum leads to
encopresis in up to 60%
Most causes are not organic but due to
voluntary or involuntary retentive behavior
Constipation DDx
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Dietary
Behavioral
Obstruction
Dehydration
Structural defects (fissures)
Metabolic (hypothyroid,hypoparaT,
hyperCa)
Neuromuscular ( MMC, MD, spinal cord)
Hirshsprungs
Constipation- Treatment
Dietary: increased fluid/fibre
 Stool softeners or laxatives

Lactulose
 Lansoyl
 PEG powder

Bowel evacuation (enemas)
 Bowel/toileting regimen

Hirshsprung’s Disease




Absence of ganglion cells in the bowel
wall
Most common cause of neonatal GI
obstruction
Aganglionic segment
NB: failure to pass meconium within 48 hrs
Hirshsprung’s Disease

Constipation







onset after 2 yr
encopresis
large caliber stool
normal growth
normal nutrition
normal anal tone
stool in ampulla

Hirshsprung’s







onset at birth
no encopresis
small stools
assoc. FTT/poor
nutrition
abdominal distension
normal anal tone
ampulla empty
Hirshsprung’s Disease
Diagnosis:
 rectal biopsy
 shows absence of ganglion cells
 rectal manometry
 barium enema ->transition zone
Treatment:


resection aganglionic bowel
colostomy, then pull through at
6 to 12 months of age
Umbilical hernia





Defect of central fascia beneath umbilicus
Most common condition of abdominal wall
Almost never incarcerate
Strong family history and
racial propensity
Medical risk factors:


Congenital hypothyroidism
Prematurity
Umbilical hernia

DDx:



Small omphalocele (looks like fixed hernia)
Supra-umbilical hernia
Refer to surgery if:




Ring defect > 1.5 - 2 cm in diameter
“elephant’s trunk” appearance
Incarceration
Not closing by 2 years of age
UROLOGY /
NEPHROLOGY
Cryptorchidism




3.4% of NB, 0.7% of children > 1 year of age
Bilateral in 20%
Consequences- tumour, infertility, torsion,hernia
Differential diagnosis




Ectopic testes
Retractile testes
Absent testes
surgical correction <2 year of age
Hypospadius




Sibling risk - 10%
Undescended testes - 10-15%
Not associated with UT anomalies
Do not circumcise
Enuresis






Nocturnal , Diurnal, both
Primary vs. Secondary
10% 5yr old, 5% 10 yr old, 1% 18 yr old
Male > Female
Familial
maturational defect in bladder control
Enuresis

Treatment




Rule out underlying cause (UTI, constipation,
IDDM)
Motivational maneuvers- star charts
Alarm
Medication- DDAVP, TCA
Proteinuria


Def”n: >150mg/24 hr (>4mg/m2/hr)
Nonpathologic:



Postural- incr. in upright position 10x
 Collection done in supine and upright
positions
Febrile
Exercise
Proteinuria

Tubular:



Hereditary- cystinosis, Wilson dis., RTA
Acquired- antibiotics, ATN, cystic diseases,
heavy metal
Glomerular:


Nephrotic syndrome
Glomerulonephritis, tumour, drug, congenital
Nephrotic Syndrome



Minimal change disease the most common
(76%)
Membranous (8%), Focal Segmental (7%)
Diagnosis




proteinuria(>40 mg/m2/hr)
hypoalbuminemia
hyperlipidemia
edema
Nephrotic Syndrome

Treatment


Renal biopsy




prednisone
Unusual age (<1yr, adol.)
Steroid resistant/ frequent relapse
HTN, decreased renal function
Complications



hypercoagulability
infections
Drug side effect- steroids, immunosuppressants

Marked eyelid edema in a
2-year-old boy with
minimal change disease
and nephrotic syndrome.
Eyelid edema in any
child should prompt the
performance of
urinalysis, rather than the
presumption of allergy.

Severe scrotal edema in a
6-year-old boy with
nephrotic syndrome.
Hematuria


Microscopic (> 5 rbc/hpf) vs. Macroscopic
Approach based on anatomy:




Kidney
Ureter
Bladder
Urethra
Hematuria


Glomerular
Tubulointerstitial





Hematologic causes


platelets, SS disease, renal vein thombosis
Anatomic abnormalities


ATN
Infections
Hypercalciuria
Drugs
Tumour, trauma, cysts, vascular
Exercise
Hematuria: Work-up

STEP 1:



STEP 2:


CBC, urine culture, Cr, C3, U/S
24 hr urine- Cr, protein, calcium
ASOT/antiDNase-B, T/S, ANA, coags, urine RBC
morphology, SS screen, VCUG (if infection/lower
tract suspect)
STEP 3:

biopsy
Glomerulonephritis



Proteinuria, hematuria, hypertension, edema
Etiology: Acute post Strep GN, IgA Nephropathy,
HSP, SLE Nephritis, RPGN, MPGN
Acute Post Strep GN:




school-aged, mean age 7, 2:1(M:F), 1-2 wks between
infection and presentation, dark urine, edema
Dx: UA, ASOT, anti DNAase B, low C3 (and in 6-8 wks)
Management: fluid/Na restriction, diuretics +/- antiHTN
98% recover completely, sx resolve in 3-4 wks
Hemolytic Uremic Syndrome




Diarrheal and non-diarrheal causes
E. Coli 0157:H7 verotoxin
Present with diarrhea followed by bloody
diarrhea
5-7 days later- Triad



microangiopathic hemolytic anemia
thrombocytopenia
renal failure
Hemolytic Uremic Syndrome

Treatment





supportive
lasix infusion
Dialysis
No role for antibiotics, steroids
Prognosis:


10-30% morbidity
5-10% mortality
RHEUMATOLOGY
Henoch Schonlein Purpura




Immune-mediated systemic vasculitis of small
vessels
Often preceding URTI
Ages 4-10yr; recurs in 1/3
Classically involves,




skin
GI
joints (75% have arthralgias)
kidney (20% develop gross hematuria)
HSP - Skin




Palpable nonthrombocytopenic
purpura
May be presenting sign in only 50%
of patients.
Purpura involves dependent areas of
the body.
Edema of the hands, feet, and scalp
often an early finding (20-40%)
Slide 1
HSP - Gastrointestinal

45 to 85% of children with HSP



major hemorrhage (5%)
intussusception (2%)
occult bleeding (33%)
HSP

Treatment





Steroids used if severe/life-threatening GI
involvement
Doesn’t affect renal outcome
Must monitor for renal involvement- may
occur late
Watch for recurrence
education
Kawasaki Disease
Criteria
 F ever for 5 days
 Plus 4 of 5:





E xanthem
E xtremities
L ymph nodes (>1.5 cm)
M ucosal changes
C onjunctivits
“feel my conjunctivitis”
Kawasaki Disease

CVS



coronary aneurysms- 20% of cases
Risk < 5% if treated
Phases



Acute- febrile 1-10 days
Subacute (peeling, afebrile, high
platelets/ESR) 10-21 days
Convalescent (normalize plt/ESR) >21 days
Kawasaki Disease
Associated Features





Uveitis
Hydropic gallbladder
Carditis
Pancreatitis
arthritis



Sterile pyuria
(urethritis)
Diarrhea
Aseptic meningitis
Kawasaki Disease

Treatment



IVIG
Aspirin- high followed by low dose
Echo at baseline and at 6-8 weeks for
coronary aneurysms
ONCOLOGY
Acute Lymphocytic Leukemia



Most prevalent malignancy under 15 yoimmature lymphoid cells accumulate in the
BM (lymphoblasts)
80% of all cases of acute leukemias : peak
2-6yo
Poor prognosis if < 2yrs or > 10yrs, WBC
> 50,000, CNS or testicular involvement at
diagnosis, T-Cell or B-Cell, Pseudodiploidy
(presence of translocations within leukemic
cells), and hypodiploidy (< 46 chr. in
leukemic cells), L3 morphology of blasts
ALL- Clinical Features




Bone marrow failure: anemia, low plts,
neutropenia
Lymphadenopathy
Hepatosplenomegaly
Bone pain
Acute Lymphocytic Leukemia

Relapse 30 - 40%




bone marrow
CNS
testes
Long term problems



secondary tumours
infertility
learning disability
Neuroblastoma









Malignancy of neural crest cells
Most common neoplasm in infants
Most in first 4 yrs (mean=2yo)
Most common site of primary tumor is abdomen (abd.
mass ,abd. pain ,HTN )
Thoracic tumors: resp. distress
H & N-Horner syn.
Constitutional s/sx
Metastases common to bone, BM, liver lung (50%)
High catecholamines in 90%
Wilms’ Tumor




5-6% of childhood Ca: 75% before 5yo
Palpable abdominal mass, HTN, hematuria
Bilateral in 5%
Association with aniridia,
hemihypertrophy, and Beckwith
Wiedmann Syndrome in 12-15%
Retinoblastoma

Bilateral (40%)



hereditary - AD
osteogeneic carcinoma
Unilateral (60%)

sporadic
Slide 3
Brain Tumors

Second most common tumor-most common
solid tumor



cerebellum 40%, brainstem and 4th ventricle
15%, suprasellar 15%
Presentation depends on location
Common signs: vomiting, papilledema,
lethargy, headache, personality change,
ataxia, loss of vision, seizures, focal
neurologic signs, nystagmus
HEMATOLOGY
Anemia

Low Retics (underproduction)


MCV- Low- iron, thal,lead, chronic
- Normal- renal, thyroid, infection
- High- B12, folate, fanconi
High Retics (increased loss)

Blood Loss

Hemolysis- intrinsic
- extrinsic
Iron Deficiency Anemia




Decrease in RBC Hb due to inadequate Fe stores
Etiology: poor dietary intake, early transition to
cow’s milk, high requirements with growth
spurts, cow’s milk intolerance, chronic GI blood
loss
Diagnosis: microcytic anemia, low serum iron,
ferritin,
S/sx: irritability, anorexia, lethargy, pale,
tachycardia, systolic murmur
Slide 1
.
Spherocytosis








Autosomal Dominant, northern European
abnormal membrane protein- Spectrin
leads to hemolysis- less flexible
newborn- jaundice < 24 hr
disease can be mild, moderate or severe
mild- mod. Anemia, reticulocytosis and
splenomegaly
Dx- osmotic fragility test
Rx.- support, splenectomy
From CD Atlas, MCCQE Toronto Notes, 2003
G6PD






Most common RBC enzyme defect
X-linked, African, Mediterranean
susceptible to oxidation stress--> Hgb precip.-->
membrane damage
Precipitating agents
infection, vit. C, fava bean, benzene,
Medications (nitrofurantoin, antimalarial,
sulfa, nalidixic acid, vit. K analog)
intermittent hemolysis, chronic hemolysis,
incidental with anemia and retics
smear- bite cells
Sickle Cell Disease



Newborn asymptomatic
 first sign (6 mos) - hand-foot syndrome
Crises
 sequestration
 vaso-occlusive
 aplastic(Parvovirus)
 hyperhemolytic
 infections
Prevent infections (considered asplenic)
From CD Atlas, MCCQE Toronto Notes, 2003
Slide 2
Classic Hemophilia

Factor VIII deficiency:


X-linked ie asymptomatic female carriers
transmit to sons
Symptoms:





excessive bruising with ambulation
intramuscular hematomas from minor trauma
hemarthrosis: often spontaneous
hematuria
risk for intracranial hemorrhage & bleeding into the
neck
Classic Hemophilia
Severity depends on level FVIII in plasma
mild 6% to 30%
 moderate 1% to 5%
 severe < 1%



Pts with mild FVIII deficiency experience
only prolonged bleeding following tooth
extraction, surgery or bleeding
Lab: PT normal, PTT greatly prolonged
Classic Hemophilia

Treatment:
- prevention of trauma
- FVIII concentrates
- strict avoidance of drugs that affect
platelet function
Immune Thrombocytopenic
Purpura (ITP)





Thrombocytopenia mediated by auto antibodies
causing destruction
Peak age 2-6yo: associated with antecedent viral
infection
Most resolve in 4-6wks: 20% duration > 6mos
Clinical Features: purpura, petechiae, bleeding
from mouth, gums, kidney, GIT, no
hepatosplenomegaly
Treatment- IVIG, steroids
Slide 5
CHILD ABUSE
Child Abuse







Physical - 80%
Sexual - 15%
Physical and emotional neglect
Munchausen by proxy
2nd cause of death in 1-6mos
1/3:1/3:1/3- <1yo:1-6yo:>6yo
Premature and developmentally impaired have
3x risk
Red Flags





Recurrent injury/ingestion
Injury poorly explained/ out of proportion
High risk injuries: scald, cigarette,spiral fracture, retinal
hemorrhage
Injury pattern/site
High risk environment
 preterm, neurologic impairment
 single parent
 family stress
 psychiatric illness
Slide 4
Slide 1
Slide 2
Slide 6
Slide 7
Slide 3
ADOLESCENCE
Adolescence- HEEADSS







Home
Education
Eating
Activities
Drugs
Sexuality
Suicide
Adolescent Suicide
Warning Signs





Depression
Psychosomatic complaints
Acting out
Previous attempt
Family history
ORTHOPEDICS
Growing Pains





3 - 6 years
Night time: poorly localized
Pain in shins, calves, thighs
Heat, massage, Tylenol
Normal physical exam
Congenital Dislocation Hip
(Developmental Dislocation Hip)


Age: 2 months to 2 years
Signs:





limitation of abduction
tight adductors
shortening of leg
asymmetric skin folds
+ Galeazzi sign (one knee lower than other)
Congenital Dislocation Hip
Assess stability: Ortolani(reduce) &
Barlow(dislocate) signs
Treatment:



triple diaper first for mild cases of
subluxation (x 6 to 8 weeks)
< 6 to 8 months, Pavlik harness
> 8 months, traction
 closed reduction  spica cast
Slide 2
Metatarsus Adductus




Forefoot faces in rather than lining up with
2nd metatarsal
May be secondary to intrauterine
positioning
Early treatment is stretching
If rigid may require casting to correct
Legg Calve Perthes Disease





Avascular necrosis femoral head
males > females
5 to 9 year old:sx: painful hip, limp,
referred pain
X-ray:  lucency, widening of the distance
and eventual distortion of the femoral head
Treatment: casts to keep hip in abduction &
medial rotation surgery
Slipped Capital Femoral
Epiphysis


Most common in obese boys in adolescence
femoral epiphysis slips posteromedially off the
metaphysis
unilateral or bilateral
 gradual or sudden causes pain & limitation of motion
 abduction & internal rotation are limited
 Klein’s line on xray
Treatment: pinning to prevent further slipping

Osgood-Schlatter’s Disease




Common cause of knee pain
Mostly in athletic or overweight kids
Pain arises in tibial tuberosity (at site of
attachment of patellar tendon)after exercise
or kneeling
Treatment mainly supportive: includes
reduced physical activity +/- bracing
DERMATOLOGY
Slide 3
Pityriasis rosea




Prodrome rare: fever, malaise, arthralgia,
pharyngitis
Herald patch: solitary 1-10cm annular papular
lesion anywhere on body
5-10 days later, widespread symmetrical
eruption involving trunk & proximal limbs
< 1cm slightly raised pink/brown papules
eruption, fine scale, especially at periphery
Pityriasis Rosea





Christmas tree pattern on back
Duration: 2 to 12 weeks
Mild to severe pruritus
? Viral trigger
Treatment:


antipruritic/antihistamine
lubricating lotion or topical cortosteroid if
moderate to severe pruritus
Impetigo





+ Prevalent during hot, humid months
+ Common in infants & children
Initiated by infection with Grp.A hem.strep
Bullous impetigo 2o to Staph Aureus Grp.2
phase type
Erythematous macule...vesicles & pustules
Impetigo
Bullae with erythematous halo...honey
coloured crusts (non bullous form),
superficial & rupture easily (bullous type
 Spread by contact to other parts of body
Treatment:




local measures...personal hygiene
compresses to remove crusts
systemic antibiotic
Atopic Dermatitis

Inflammatory skin disorder

erythema...edema...intense pruritus...
exudation, crusting & scaling

> risk to develop allergies & asthma
Atopic Dermatitis
Infancy:
 1st 2 to 3 months
 weepy patches on
cheeks, neck,
wrists, hands &
extensor aspect
extremities
Childhood:
 involvement of flexural
areas, especially
popliteal & antecubital
fossae
 also, neck, wrist, behind
ears, > with age; >
drying & thickening of
skin
Atopic Dermatitis
Other signs:
“Mask of atopic dermatitis”
 Hyperpigmentation of skin
 Lichenification
Atopic Dermatitis

Itch - scratch - itch cycle Rx:




antihistamines
topical corticosteroids
topical immune modulators (Protopic)
hydrating lotions
Slide 2
Slide 1
Seborrheic Dermatitis





Begins on scalp as “cradle cap”
Involvement behind ears, sides of nose &
eyebrows
Greasy, brownish scales
Shorter course than atopic dermatitis
Responds more rapidly to treatment than
atopic dermatitis
Treatment: General Guidelines






Keep bathing at minimum
Use of non-soap cleansers
Cotton garments/avoid wool
Keep nails cut short
Avoid environmental triggers
Treat superinfections with systemic
antibiotics

Staphylococcal diaper
dermatitis. There are
numerous thin-walled
pustules surrounded by
erythematous halos, as
well as multiple areas in
which pustules have
ruptured, leaving a
collarette of scale around
a denuded erythematous
base.

Irritant or ammoniacal
diaper dermatitis. Note
the involvement of the
convex surfaces and the
sparing of the
intertriginous creases.

Candidal diaper
dermatitis. The eruption
is bright red with
numerous pinpoint
satellite papules and
pustules. Intertriginous
areas are prominently
involved.

Psoriatic diaper
dermatitis. This child had
a persistent diaper rash
that did not respond to
routine therapy. Note that
scaling is not as intense
as in psoriatic lesions
seen elsewhere on the
body.
Erythema Multiforme

Erythema multiforme (EM
minor). A, The characteristic
target lesions are symmetrically
distributed. B, In these typical
target lesions with central dusky
areas, the peripheral rims are
beginning to vesiculate. C, In this
case, the peripheral rims have
become frankly bullous. (C,
Courtesy of Michael Sherlock,
MD, Lutherville, Md.)
Stevens-Johnson Syndrome

Stevens-Johnson syndrome (EM
major). A, Severe bullous and
erosive lesions cover the face,
neck, upper trunk, and proximal
extremities. Note the ocular and
oral involvement. B, Typical
bullae, target lesions, and erosions
of the lips are seen in this boy. C,
This child has numerous vesicles
and bullae of the oral mucosa
along with formation of a shaggy
white membrane consisting of
sloughed debris. (C, Courtesy of
Michael Sherlock, MD,
Lutherville, Md.)
Milia




White-yellow papules
Epidermal inclusion cysts
Face, gingivae, palate
 Ebstein pearls
Neonates:
 Occur spontaneously
 Resolve spontaneously


(weeks-months)
Older children:
 Occur at site of trauma


(blisters, abrasions)
May not resolve spontaneously
Erythema Toxicum Neonatorum








White papule/pustule (1-2mm)
surrounded by red wheal
Localized or generalized
Palms and soles spared
Usually starts ~ day 2
New lesions continue to
appear as rash waxes and
wanes up to 10 days
Less common & delayed
presentation in prems
Eosinophils on scraping
BENIGN & SELF-LIMITING
CLASS OF 2010
FACULTY OF MEDICINE
UNIVERSITY OF OTTAWA
GOOD LUCK!