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GENERAL PEDIATRICS LMCC Review
Presented by Marc E. Zucker MD, FRCPC Division of Pediatric Medicine CHEO March 22, 2010
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Feeding & Growth
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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 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?
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 % vs 3.5-4% Vitamins - richer in A,C,E, lower in D & K Minerals - lower Fe but better absorbed
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Breast Feeding Benefits for Baby
Immunological benefit 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
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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
Takes 3-7 days for milk supply to come in risk of dehydration/ “breastfeeding jaundice” Jaundice is more common Breastmilk jaundice “Mom/baby team” ineffective latch/sore nipples/engorgement Infections thrush , mastitis/abscess Reduced levels vitamin D & K
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Vitamin D Supplementation
Rickets is still a problem in Canada! 400 IU per day 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 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
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Contraindications to Breast Feeding
Maternal infections 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
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Cow’s Milk Formula Always Fe fortified Many choices!
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
cereals 4-6 months vegetables fruits meats cow’s milk should be postponed until at least months of age (renal load) 2% or 1% milk should be postponed until after second birthday (inadequate fat content) Rest gradually in this order
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Infant Growth: Rules of Thumb
Weight gain: Regain birth weight by 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 Average length at birth 50 cm (20 inches)
Increases by 50% by 1 yr Doubles by 4 yrs Triples by 13 yrs Ave growth 5-6 cm / yr (4 yrs-puberty)
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Growth- Body Mass Index (BMI)
BMI helps to quantify the weight to height relationship BMI = weight(kg)/height (m)2 BMI of is acceptable BMI > 30 indicates obesity BMI < 18 suggest severe anorexia or Failure to thrive
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Growth- Head Circumference
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
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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) Only way to detect FTT Also detects chronic illness, feeding difficulties
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What is Failure to Thrive?
US National Center for Health Statistics defines FTT for children < 2 yrs of age as: 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
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Caloric needs 0-10 kg: 100 kcal/kg/day 10-20 kg: 1000 + 50 kcal/kg/day
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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 Pattern over time more important than any one specific measurement “late bloomers”
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Growth Velocity 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 months
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FTT- Assessment Grade Wt for Age (%) Wt for Ht (%) 0-Normal >90
Grading of malnutrition: Grade Wt for Age (%) Wt for Ht (%) 0-Normal >90 1-Mild 75-90 81-90 2-Moderate 60-74 70-80 3-Severe <60 <70 This is referred to as Gomez criteria. But remember that the grade does not correlate with the risk of short or long-term sequelae. It does correlate with risk of mortality in developing countries (with higher mortality in the moderate & severe range).
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FTT- Assessment “Organic” vs. “non-organic”
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 Not mutually exclusive: Major medical illness may contribute to chaotic feeding environment and mild GERD along with inadequate education about normal caloric needs for an infant may be causing FTT.
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FTT- Assessment Under-nutrition results from:
1) Decreased caloric intake 2) Inadequate caloric absorption 3) Increased caloric losses 4) Increased caloric requirements
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FTT- Differential Diagnosis
Decreased caloric intake: 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) Abuse causes decreased intake because it causes anorexia Behavioural – historically blamed on mother “maternal deprivation syndrome”. We now know that it is a dynamic process of infant’s ability to elicit effective parenting, parents’ ability to provide appropriate care, and interaction of environment (chaotic etc.). Can become a downward spiral of poor feeding interaction, food refusal, and increasing malnutrition.
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FTT- Differential Diagnosis
Inadequate Caloric Absorption & Increased Caloric Losses GI 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
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FTT- Differential Diagnosis
Increased Caloric Losses cont’d Renal Protein loss Carbohydrate loss Inability to use nutrients Diabetes Mellitus Metabolic dz
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FTT- Investigations Careful and complete history taking and physical examination are ESSENTIAL Unless an illness other than primary under-nutrition is suspected on Hx or P/E the yield of lab investigations is almost nil! Lab testing helps with diagnosis in 1.4%
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FTT- Investigations Non-specific “screening”
CBCD, ESR, lytes, BUN, Cr, venous gas Urine R&M, C&S Markers of nutritional status Total protein, albumin, glu, Ca, PO4, Iron studies Zinc, vitamin levels Dependent on specific aspects of Hx & P/E 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
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FTT- Management Admit if : With hospitalization:
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: greater likelihood of catch-up growth no change in developmental outcomes No wt gain for 2 weeks or inadequate wt gain over 4 weeks = failed out pt management
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FTT- Management Inter-disciplinary approach!!
Treat any underlying illness and provide nutritional support: Increase caloric intake 1.5-2 X RDA (120 kcal/kg/day x ideal wt)/current wt Estimate kcal/kg/day
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FTT- Management Mild under-nutrition
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 Increase formula concentration by adding 10 gm (2 tsp) polycose to 4 oz formula
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FTT- Management Moderate under-nutrition Determine caloric intake
Consider whether investigations are necessary Increase caloric intake ( 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
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FTT- Management 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
Persistent growth deficits Cognitive impairment Behaviour problems
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IMMUNIZATIONS
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Immunization Schedule (Recommended by the Canadian Immunization Guide)
Age 2 mos 4 mos 6 mos 12 mos 18 mos 4-6 year q10 years Vaccine DaPTP-HIB, Prevnar, Menj DaPTP-HIB, Prevnar,Menj MMR, Varicella, Prevnar DaPTP-HIB, MMR DaPTP dTaP/dT
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Contraindications to Vaccines
Strict - anaphylaxic or anaphylactic shock - encephalopathy Precautions - febrile reaction > 40.5 - shock collapse or hypotonia - hyporesponsive collapse - seizures
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Contraindications to vaccines
Anaphylaxis to eggs: Influenza and yellow fever Severe immune deficiency: All live vaccines (MMR, VZV, OPV, BCG, Yellow fever, Oral cholera, Oral typhoid) Pregnancy: MMR and Varicella Anaphylaxis to neomycin: MMR and IPV
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Immunization Reactions
DaPTP/Hib reactions occur within 72 hrs MMR reactions occur 5-12 days
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Delayed Immunization > 7 Years Old
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 > 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
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Other Immunizations Hepatitis A & B Influenza HPV Rotavirus
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INFECTIOUS DISEASE
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Fever Temp > 38.3 Celsius rectal
Occult bacteremia: most in 3-24 mos 3-5% febrile are bacteremic most common org. is Strep. Pneumo ** 0-1 mos: FSWU 1-3 mos: toxic = FSWU non-toxic and low risk (WBC 5-15, bands <5%, urine neg, well-looking, reliable family): investigate and follow
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Otitis Media Incidence: Peak:
15% to 20% Peak: 6 to 36 months 4 to 6 years decreases > 6 years old Etiology: S. pneumoniae, M. catarrhalis, non-type H. Flu, GAS & viral
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Otitis Media Risk Factors mid-face hypoplasia (Down Syndrome)
daycare attendance Inuit/Aboriginal low SES 2nd hand smoke
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Otitis Media Treatment: Complications: 1st line: Amoxil
2nd line: High dose Amoxil, Clavulin, Macrolides, Cephalosporin T-Tubes if recurrent or persistent effusion Complications: hearing loss chronic effusion mastoiditis meningitis
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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 Newborn period (LEG) 2 months - 12 years (SHIN) Listeria
E. Coli Group B strep 2 months - 12 years (SHIN) Strep pneumonia, N. meningitides Less common Hib with immunization
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Meningitis Complications in abnormal hosts or anatomic defects: SIADH
increased Pseudomonas, Staph, Salmonella, Serratia Complications SIADH seizures subdural effusions transient joint effusions (Ag-Ab reaction) hearing loss
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Urinary Tract Infection
Newborn M › F (2) Children F › M (10) Schoolgirls - 5% Recurrence - 80% Vesicoureteral reflux - 35% Renal scarring - 50% All children ‹ 3 yrs U/S VCUG
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Urinary Tract Infections
UTI KEEPPSS Klebsiella, E. Coli, Enterococcus, Proteus, Pseudomonas, Staph, Strep Pyelonephritis ampicillin + gentamycin IV initially then Amoxil or Septra po VUR prophylactic Septra or nitrofurantoin (or Amoxil) Higher grades may require surgery
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Osteomyelitis Organism Diagnosis neonate: Staph, GBS, E.Coli
> 3mos.: Staph, Hib, Strep,Pseudomonas SS disease: Salmonella Diagnosis bone scan x-ray days
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Septic Arthritis Monoarticular (trauma) Organism neonate >3 mos
group B strep, staph, E.Coli >3 mos Staph aureus Strep, Hib most common site is knee (40%)
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Fever and Rash
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Measles (First Disease)
Paramyxovirus Stages 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 pneumonia encephalitis SSPE
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Scarlet Fever (Second Disease)
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 cellulitis Rheumatic fever
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Rubella (Third Disease)
Togavirus Congenital Postnatal mild disease suboccipital nodes maculopapular pink rash, starts on face, neck to extremities, spreads quicker than measles
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Roseola Infantum (Fourth Disease)
HHV6 High fever rash maculopapular with cessation of fever High WBC low WBC Febrile convulsions
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Erythema Infectiosum (Fifth Disease)
Parvovirus B19 No prodrome: red flushed face/slapped cheek, maculopapular rash with lacelike appearance Complications miscarriage/SA aplastic crises
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ALTE/SIDS
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Apparent Life Threatening Event: Definition
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
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ALTE Detailed Hx and Px Talk to person witnessing event
Significant event?
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ALTE Differential Neuro- seizure GI- reflux
Pulmonary- aspiration, apnea CV- arrhythmia Infection- sepsis, pertussis, RSV Metabolic Abuse
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ALTE Investigations Labwork +/- infectious workup EEG ECG/Echo
UGI/pH probe CT head Monitor
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SIDS Unexpected death by Hx and Postmortem
most common cause of death 1mo-1yr peak 2-4 months, 95% <6 months old
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SIDS Maternal Risk Factors Infant Risk Factors: low age low SES
prematurity age, sex prone sleeping bottle fed smoke environ. Thermal stress ethnicity prior illness winter months low birthweight Maternal Risk Factors low age low SES low education smoker drug use poor nutrition
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Gastroenterology/ Pediatric Surgery
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Colic 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
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Colic ++Gas/legs drawn up; otherwise well
No proven treatment - rhythmic motion/sounds Ovol/Tylenol- no proven benefit Parental support and reassurance
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Abdominal Pain Acute: Ddx includes gastro, hernia, UTI, appendicitis, intussusception, malrotation, volvulus, HSP, SC Crisis, pneumonia, mesenteric adenitis, Chronic: > 3 episodes affecting activities > 3 months Organic (<10%): constipation, IBD, mass, PUD, GU, lactose intolerance Functional (90%): yo peak, girls predominate, vague crampy periumbilical pain with no awakening, ppting or alleviating factors. Normal growth.
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Gastroesophageal Reflux
Incompetence of lower esophageal sphincter improves by one year of age in most infants Complications apnea in infants aspiration pneumonia chronic cough/wheeze esophagitis- dysphagia,hemetemesis, Fe deficiency anemia
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Gastroesophageal Reflux
Diagnosis pH probe Ba swallow nuclear scan endoscopy
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Gastroesophageal Reflux
Treatment chalasia routine - attention to burping, small frequent feeds, 300 prone thickening feeds Medications: H2 blockers or PPI if esophagitis or gastritis present Domperidone for decreased gastric emptying
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Pyloric Stenosis boy > girl 3 weeks - 3 months
projectile vomiting (nonbilious) hungry infant feeds vigorously
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Pyloric Stenosis Lab- hypochloremic alkalosis Investigation- U/S, UGI
O/E:- dehydration, lethargy, weight loss, peristaltic waves L R, palpable “olive” Lab- hypochloremic alkalosis Investigation- U/S, UGI Rx: rehydrate and restore electrolyte balance - myotomy of pyloric muscle
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Intussusception 3 months - 3 years (up to 6 years)
5% anatomic abnormality found Meckel’s polyp duplication more frequent ileocolic or ileoileocolic
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Intussusception Clinical severe paroxysmal pain lethargy shock
sausage shaped mass RUQ vomiting currant jelly stool
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Intussusception Lab Treatment x-ray barium enema
density or gasless right side barium enema coil-spring sign Treatment reduction by barium enema surgical reduction
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Meckel Diverticulum 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
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Constipation 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
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Constipation DDx Dietary Behavioral Obstruction Dehydration
Structural defects (fissures) Metabolic (hypothyroid,hypoparaT, hyperCa) Neuromuscular ( MMC, MD, spinal cord) Hirshsprungs
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Constipation- Treatment
Dietary: increased fluid/fibre Stool softeners or laxatives Lactulose Lansoyl PEG powder Bowel evacuation (enemas) Bowel/toileting regimen
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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
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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
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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
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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
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Umbilical hernia DDx: Refer to surgery if:
Small omphalocele (looks like fixed hernia) Supra-umbilical hernia Refer to surgery if: Ring defect > cm in diameter “elephant’s trunk” appearance Incarceration Not closing by 2 years of age
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UROLOGY / NEPHROLOGY
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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
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Hypospadius Sibling risk - 10% Undescended testes - 10-15%
Not associated with UT anomalies Do not circumcise
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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
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Enuresis Treatment Rule out underlying cause (UTI, constipation, IDDM)
Motivational maneuvers- star charts Alarm Medication- DDAVP, TCA
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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
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Proteinuria Tubular: Glomerular:
Hereditary- cystinosis, Wilson dis., RTA Acquired- antibiotics, ATN, cystic diseases, heavy metal Glomerular: Nephrotic syndrome Glomerulonephritis, tumour, drug, congenital
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Nephrotic Syndrome Minimal change disease the most common (76%)
Membranous (8%), Focal Segmental (7%) Diagnosis proteinuria(>40 mg/m2/hr) hypoalbuminemia hyperlipidemia edema
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Nephrotic Syndrome Treatment Renal biopsy Complications prednisone
Unusual age (<1yr, adol.) Steroid resistant/ frequent relapse HTN, decreased renal function Complications hypercoagulability infections Drug side effect- steroids, immunosuppressants
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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.
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Severe scrotal edema in a 6-year-old boy with nephrotic syndrome.
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Hematuria Microscopic (> 5 rbc/hpf) vs. Macroscopic
Approach based on anatomy: Kidney Ureter Bladder Urethra
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Hematuria Glomerular Tubulointerstitial Hematologic causes
ATN Infections Hypercalciuria Drugs Hematologic causes platelets, SS disease, renal vein thombosis Anatomic abnormalities Tumour, trauma, cysts, vascular Exercise
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Hematuria: Work-up STEP 1: STEP 2: STEP 3:
CBC, urine culture, Cr, C3, U/S 24 hr urine- Cr, protein, calcium STEP 2: ASOT/antiDNase-B, T/S, ANA, coags, urine RBC morphology, SS screen, VCUG (if infection/lower tract suspect) STEP 3: biopsy
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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
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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
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Hemolytic Uremic Syndrome
Treatment supportive lasix infusion Dialysis No role for antibiotics, steroids Prognosis: 10-30% morbidity 5-10% mortality
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RHEUMATOLOGY
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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)
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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%)
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Slide 1
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HSP - Gastrointestinal
45 to 85% of children with HSP major hemorrhage (5%) intussusception (2%) occult bleeding (33%)
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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
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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”
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Kawasaki Disease CVS Phases coronary aneurysms- 20% of cases
Risk < 5% if treated Phases Acute- febrile 1-10 days Subacute (peeling, afebrile, high platelets/ESR) days Convalescent (normalize plt/ESR) >21 days
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Kawasaki Disease Associated Features
Uveitis Hydropic gallbladder Carditis Pancreatitis arthritis Sterile pyuria (urethritis) Diarrhea Aseptic meningitis
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Kawasaki Disease Treatment IVIG Aspirin- high followed by low dose
Echo at baseline and at 6-8 weeks for coronary aneurysms
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ONCOLOGY
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Acute Lymphocytic Leukemia
Most prevalent malignancy under 15 yo- immature 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
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ALL- Clinical Features
Bone marrow failure: anemia, low plts, neutropenia Lymphadenopathy Hepatosplenomegaly Bone pain
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Acute Lymphocytic Leukemia
Relapse % bone marrow CNS testes Long term problems secondary tumours infertility learning disability
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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%
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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%
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Retinoblastoma Bilateral (40%) Unilateral (60%) hereditary - AD
osteogeneic carcinoma Unilateral (60%) sporadic
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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
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HEMATOLOGY
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Anemia Low Retics (underproduction) High Retics (increased loss)
MCV- Low- iron, thal,lead, chronic - Normal- renal, thyroid, infection - High- B12, folate, fanconi High Retics (increased loss) Blood Loss Hemolysis- intrinsic - extrinsic
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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
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Slide 1 .
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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
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From CD Atlas, MCCQE Toronto Notes, 2003
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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
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Sickle Cell Disease Newborn asymptomatic
first sign (6 mos) - hand-foot syndrome Crises sequestration vaso-occlusive aplastic(Parvovirus) hyperhemolytic infections Prevent infections (considered asplenic)
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From CD Atlas, MCCQE Toronto Notes, 2003
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Classic Hemophilia Factor VIII deficiency: Symptoms:
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
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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
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Classic Hemophilia Treatment: - prevention of trauma
- FVIII concentrates - strict avoidance of drugs that affect platelet function
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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
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CHILD ABUSE
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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
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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
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ADOLESCENCE
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Adolescence- HEEADSS Home Education Eating Activities Drugs Sexuality
Suicide
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Adolescent Suicide Warning Signs
Depression Psychosomatic complaints Acting out Previous attempt Family history
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ORTHOPEDICS
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Growing Pains 3 - 6 years Night time: poorly localized
Pain in shins, calves, thighs Heat, massage, Tylenol Normal physical exam
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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)
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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
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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
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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
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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
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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
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DERMATOLOGY
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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
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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
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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
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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
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Atopic Dermatitis Inflammatory skin disorder
erythema...edema...intense pruritus... exudation, crusting & scaling > risk to develop allergies & asthma
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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
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Atopic Dermatitis Other signs: “Mask of atopic dermatitis”
Hyperpigmentation of skin Lichenification
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Atopic Dermatitis Itch - scratch - itch cycle Rx: antihistamines
topical corticosteroids topical immune modulators (Protopic) hydrating lotions
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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
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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
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Staphylococcal diaper dermatitis
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.
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Irritant or ammoniacal diaper dermatitis
Irritant or ammoniacal diaper dermatitis. Note the involvement of the convex surfaces and the sparing of the intertriginous creases.
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Candidal diaper dermatitis
Candidal diaper dermatitis. The eruption is bright red with numerous pinpoint satellite papules and pustules. Intertriginous areas are prominently involved.
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Psoriatic diaper dermatitis
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.
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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.)
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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.)
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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
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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
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CLASS OF 2010 FACULTY OF MEDICINE UNIVERSITY OF OTTAWA
GOOD LUCK!
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