Management
•general:sitting up,0 2,sodium and water restriction, increased caloric intake
•pharmacologic:diuretics, afterload reduction (e.g. ACEI),(5-blockers;digoxin rarely used
•curative:correction of underlying cause
4 Key Features of CHF
2 Tachys and 2 Megalys
• Tachycardia
. Tachypnea
• Cardiomegaly
• Hepatomegaly
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P25 Paediatrics Toronto Notes 2023
Dysrhythmias
•can be transient or permanent, congenital (structurally normal or abnormal), or acquired (toxin,
infection, infarction)
Sinus Arrhythmia
•phasic variations with respiration (present in almost all normal children)
Sinus Tachycardia
•rate of impulses arising from sinus node is elevated (>150 bprn in infants, >100 bpm in older children)
•characterized by:beat-to-beat heart rate variability with changes in activity, P waves present/normal,
PR constant,QRS narrow
•etiology: H
'
l
'
N,fever, anxiety,sepsis, anemia/hypoxia, pain, PE, drugs, etc.
•differentiate from SVT by slowing the sinus rate (vagal massage, (5-blockers) to identify sinus P waves
Premature Atrial Contractions
•may be normal variant or can be caused by electrolyte disturbances, hyperthyroidism, cardiac
surgery, digitalis toxicity
Premature Ventricular Contractions
•common in adolescents
•benign ifsingle,uniform, disappear with exercise, and no associated structural lesions
•if not benign, may degenerate into more severe dysrhythmias
Supraventricular Tachycardia
•abnormally rapid heart rhythm originating above the ventricles- most frequentsustained
dysrhythmia in children
• no beat-to-beat HR variability, >220 bpm (infants) or >180 bpm (children), P waves absent/abnormal,
PR indeterminable, QRS usually narrow
•pre-excitation syndromes (subset of SVT): WPW syndrome, congenital defect (see Cardiology and
Paediatric vs.Adult ECG
Paediatric ECG findings that may be
normal:
. HR >100 bpm
. Shorter PR and OT intervals and ORS
duration
• Inferior and lateralsmall 0 waves
• RV larger than LV in neonates,so
normal to have:
. RAD
• Large precordial R waves
• Upright T waves
• Inverted T waves in the anterior
precordial leadsfrom early
infancy to teen years
Complete Heart Block
•congenital heart block can be caused by maternal anti-Ro or anti-La (e.g. mother with SLE)
•often diagnosed in utero (may lead to development of fetal hydrops)
•clinical symptoms related to level of block (the lower the block, the slower the heart rate and greater
the symptoms of inadequate cardiac output)
•symptomatic patients need a pacemaker
Heart Murmurs s
• 50-80% of children have audible heart murmurs at some point in their childhood
• most childhood murmurs are functional (e.g. "innocent") without associated structural abnormalities
and have normal ECti and radiologic findings
• in general, murmurs can become audible or accentuated in high output states (e.g. fever, anemia)
Table 15.Differentiating Heart Murmurs
Innocent Pathological
History and Physical Symptoms and signs ol cardiac disease (FIT.exercise
intolerance)
All diastolic, pansystolic, or continuous (except venous hum)
>316 (palpable thrill):harsh
May have lixed split orsingle S2
May be present
Unchanged
Asymptomatic
Timing
Cradc/Ouality
Splitting
Extra Sounds/Clicks
Change of Position
SEM
<316:sofllblowing/ vibralory
Physiologic S2
None
Murmur varies
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P26 Paediatrics Toronto Notes 2023
Table 16. Five Innocent Heart Murmurs
Location Timing Description Age Differential
Diagnosis
Type Etiology
Peripheral left upper sternal Systolic ejection
Pulmonic
Stenosis
Flo
*
into
pulmonary branch border
arteries from
Neonates,lowpitched.radiates
lo axilla andback
Neonates,usually PDA
disappears by Pulmonary
3-6mo stenosis
main,larger,
artery
Still's Murmur Left lower sternal
border
Systolic ejection 3-6 yr Subaortic stenosis
Small VSD
Flo
*
across the
pulmonic \raIre
leaflets
High-pitched,
vibratory.LLSB or
apex.SEM
Infradavicular
hum.continuous.
Venous Hum Altered flow in
reins
Infradavicular
(«>L)
Continuous 3-6yr PDA
RH
Flo
*
through the
pulmonic valve
Leftupperstemal
border
Systolic ejection Soft,blowing.
LUSB.SEM
Pulmonary Flow 8-14 yr ASD
Pulmonary
stenosis
Supraclavicular Systolic ejection
ArterialBruit
Iurbulenlflow
in the carotid
arteries
Supradavicular Low intensity,
above davides
Any age Aortic stenosis
Bicuspid aortic
valve
Infective Endocarditis
• see Infectious Pise.tses. 11)15
Development
Global Developmental Delay
•also known as Early Developmental Impairment
Definition
•significant delay (at least 2 SDs below the mean with standardized tests) in at least 2 developmental
domains (gross motor,fine motor,speech/language, cognitive,social/personal, activities of dailyliving) in a child <5 vr
•may predict a diagnosis of intellectual disability in the future
•after age 5,intellectual and physical disabilities are described (no longer a development‘delay’ as
catch up is not expected)
Epidemiology
•5-10% prevalence;50-70°
o of cases have a defined etiology
Etiology
Broad Category Possible Causes Upper Limit of Diagnostic Yield*
Prenatal Biological Factors Genetic abnormalities
Central nervous system deformities
Metabolic issues
Teratogens/toxins (substances of abuse,
medications,etc.)
Infections
4n
Prenatal EnvironmentalFactors 28 s
Perinatal Asphyxia and neonatal encephalopathy
Premature birth
Low birth weight
Neonatal complications
Neglect/unhealthy psychosocial environment 55%
Infections
Trauma
Severe jaundice (kernicterus)
Toxins
21%
Postnatal
•Percentage of totalrases of GOO or 10 withan identified etiologic diagnosis who fallinto this specific category
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Clinical Features
• key questions in addition to standard paediatric history:
detailed developmental milestones:rate of acquisition, regression ofskills
detailed prenatal, birth, postnatal history
detailed three-generation family history
detailed psychosocial history, including exposure to environmental toxins
associated problems:feeding,seizures, behaviour,sleep
• physical exam
micro/macrocephaly, dysmorphic features head-to-toe, hepatosplenomegaly, height, and weight
• neurodevelopmental exam (neurological exam, congenital abnormalities, cutaneous findings,
dysmorphic features, current developmental level)
• investigations (guided by history, physical examination, and CPS stepwise algorithm)
refer for formal vision and hearing tests, which may guide further management
first line:chromosomal microarray and Fragile X DNA testing
“Tier 1” lab investigations (defined by CPS) for inborn errors of metabolism:
blood:CBC, glucose, blood gas, urea, creatinine, electrolytes with anion gap, AST,ALT,TSH,
CK, ammonia, lactate, amino acids, acylcamitine profile,carnitine, homocysteine,copper,
ceruloplasmin, biotinidase
urine:organic acids, creatine metabolites, purines, pyrimidines,glycoaminoglycans
additional investigations:TSH,ferritin,Bn,lead, congenital infections
brain imaging:microcephaly, macrocephaly,seizures, or abnormal neurological findings
consider consultation with genetics or endocrinology
Management
• dependent on specific area of delay
« therapy services (e.g.speech and language therapy for communication delay, OT and/or PT for motor
delay), early intervention services(e.g.infant development services, Ontario Early Years Centres);
access to daycare can support developmental units
Intellectual Disability
Definition
« characterized by three domains:deficitsin intellectual function (confirmed by clinical assessment and
standardized intelligence testing, historically defined as Intelligence Quotient (IQ) <70),deficits in
adaptive function, and symptom onset during developmental period
• severity levels (mild, moderate,severe, profound) are based on adaptive function, not IQ
Epidemiology
• 1-3% of general population;M:F=1.5:1
Clinical Features
• history
» earlier age of onset correlates with greaterseverity of ID
» well below average general intellectual functioning
significant deficits in adaptive functioning in at least 2 of: communication,self-care, home-living,
social skills,self-direction, academic skills, work, leisure, health,safety
• physical exam
check growth,dysmorphic features, complete physical exam, detailed observation of behaviour/
phenotype (i.e.socialskills)
• investigations
standardized psychoeducational assessment (includes cognitive and adaptive functioning
measures)
vision, hearing, and/or neurologic assessment
genetic and metabolic testing asindicated
Management
• main objective:enhance adaptive functioning level
• requires an interprofessional team with strong case coordination
• emphasize community-based treatment and early intervention
• behaviour managementservices, therapy services (e.g.OT,SLP), medicationsfor associated
conditions
• medicationsfor associated conditions
• education:life skills, vocational training, communication skills, family education
• psychosocialsupport for individual and family; respite care, individual/family therapy
Prognosis
• higher rates of sensory deficits, motor impairment, behavioural/emotional disorders,seizures,
psychiatric illness
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P28 Paediatrics Toronto Notes 2023
Language Delay
Definition
• no universally accepted definition, but most often identified around 18 mo of age with enhanced well
baby visit
• if formally tested,at least one standard deviation below mean of age on standardized testing
• can be expressive (abilitv to produce or use language),receptive (ability to understand language), or
both
Epidemiology
• M>F
•
—10-15% of 2 y/ochildren have a language delay, but only 4-5% remain delayed after age 3
• -6-8% ofschool-aged children have specific language impairment (many of whom were not identified
before school entry)
Etiology
• intellectual disability
• selective mutism
• language specific learning disorder
• isolated language delay
• developmental disorders:cerebral palsy, autism spectrum disorder, constitutional language delay
• genetic/metabolic: DS, Fragile X syndrome, Williams syndrome, hypothyroidism, PKU, etc.
• mechanical problems:deft palate, cranial nerve palsy, hearing impairment
• medical conditions:seizure disorder (includes acquired epileptic aphasia),degenerative neurologic
disorders(i.e.Rettsyndrome, Leigh encephalopathy), CP, TORCH infection, iron deficiency, lead
poisoning,etc.
• psychosocial:neglect or abuse
Clinical Features
• historv
concerns about hearing, delay in language development or regression in previously normal
language development
delayed language milestones, presence of red flags, regression (see Table 9,Developmental
Milestones, PS )
must determine iflanguage delay is expressive,receptive, or mixed
• assesssocial communication skills,including use of gestures
determine differencesin behaviour at home,school, othersocial environments
risk factors:family history ofspeech and language delay, male, prematurity',low birth weight,
hearing loss
• physical exam
guided by history:look for abnormal growth, dysmorphisms, unusualsocial interactions(lack of
eye contact, not pointing)
• include full exam of the external/internal ear (e.g. TM scarring),oral pharynx (e.g.deft palate),
and neurologic system (including tone)
• investigations
• use of language specific screens in primary care setting:The Early Language Milestone,
Communication and Symbolic Behaviour Scales Developmental Profile Infant-Toddler Checklist
Clinical Adaptive Test/Clinical Linguistic and Auditory Milestone Scale (CAT/CLAMS),Modified
Checklist for Autism in Toddlers (M-CHAT), etc.
developmental evaluation and observation during informal interaction
hearing,dental, and vision screening (audiology,dentistry, and optometry referral)
CBC (to rule out anemia), venous blood lead levels, genetic/metabolic workup asindicated
Management
• specific to etiology'
• referral to SLP most important, consider referral to Otolaryngology Head and Neck Surgery (OHNS),
dental professionals,general support services
• consider other interventionsspecific to etiology
• prevention:parents can read aloud to their child, engage in dialogic reading,avoid baby talk,narrate
daily activities,etc.
Prognosis
• depends on etiology - best prognosis for developmental speech delay
• if language delay persists beyond age 5, more likely to have difficulties in adulthood
• persistent language delay is associated with poor academic performance, behavioural problems,social
isolation
Risk Factorsfor Sensorineural Hearing
Loss
• Genetic syndromes/family history
• Congenital (TORCH) infections
• Craniofacial abnormalities
• <1500g birth weight
• Hyperbilirubinemia/kemicterus
• Asphyxia/low APGAR scores
• Bacterial meningitis,viral
encephalitis
Primary care physiciansshould also
suspect a receptive language delay
in any young child with an expressive
language delay
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P29 Paediatrics Toronto Notes 2023
Specific Learning Disorder
Definition
• specific and persistent failure to acquire academic skills despite conventional instruction,adequate
intelligence, and sociocultural opportunity
• a significant discrepancy between a child'
s intellectual ability and their academic performance
• types: reading (dyslexia), writing, mathematics (dyscalculia)
Epidemiology
• prevalence: 10% (most commonly dyslexia)
• high incidence of psychiatric comorbidity: anxiety, dysthymia, conduct disorder, major depressive
disorder, oppositional defiant disorder, ADHD
Etiology
• pathogenesis is unknown, likely genetic factors involved
• learning disabilities may be associated with a number of conditions:
• genetic/metabolic (e.g.Turnersyndrome, Klinefelter syndrome)
• perinatal: prematurity, low birth weight, birth trauma/hypoxia
postnatal:CNS damage, hypoxia, environmental toxins, FAS, psychosocial deprivation
(understimulation), malnutrition
• poor visual acuity is NOT a cause
Risk Factors
• positive family history, prematurity, developmental and mental health conditions, neurologic
disorders(e.g. seizure disorders, neurofibromatosis), history of CNS infection/irradiation/traumatic
injury, prenatal alcohol exposure, chromosomal disorders
Clinical Features
• history and physical exam
school difficulties (academic achievement, behaviour, attention,social interaction, over-reliance
on teacher)
development of negative self-concept-> reluctance to participate even in areas ofstrength
social issues:overt hostility towards parents/teachers;difficulties making friends,bullying, and
anxiety
look for dysmorphisms,complete physical exam;signs and symptoms of OSA
• investigations
psychocducational assessment, educational history from school staff
• individual scores on achievement tests in reading, mathematics, or written expression (WISC 111,
VVRAT) >2 SD below that expected for age, education, and IQ
evaluate attention, memory, expressive language,coordination skills
Management
• proside quality instruction for specific learning disability
• advocate for schoolsupports:modifying the curriculum and/or providing accommodations (e.g.
scribe for writing, extra time for tests, photocopied notes,etc.)
• individualized Education Flan (1EP): a written plan that describes the strength and needs of the
student,services established to meet these needs, and how these servicesshould be delivered
• specialized education placements that can provide educational remediation
Prognosis
• limited information available about persistence of learning disabilities over time
• low self-esteem, poor socialskills,40% school drop-out rate
Fetal Alcohol Spectrum Disorder E
Definition
• term describing the range of effects of prenatal exposure to alcohol, including physical, mental,
behavioural, and learning disabilities
• spectrum from most to least severe: FAS (fetal alcohol syndrome), partial FAS, ARBI) (alcohol related
birth defects), and ARND (alcohol related neurodevelopmental disorder)
Epidemiology
• prevalence of 1-AS and FASD is 0.1% and 1.0%, respectively
• most common preventable cause of intellectual disability
• CDC estimates 10% of women drink alcohol during pregnancy, although abstinence isstrongly
recommended
r T
j
Pathogenesis
• specific mechanism of EASD is unknown, but hypotheses include nutritional deficits, toxic effects
of acetaldehyde, alteration of placental transport, abnormal protein synthesis, and altered cerebral
neurotransmission
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P30 Paediatrics Toronto Notes 2023
Diagnosis
• often misdiagnosed or missed entirely
• multidisciplinary team needed to make diagnosis and involves a complex physical exam and
neurodevelopmental assessment
• criteria for diagnosis of FAS
F
'
ASD with sentinel facial features: 1. presence of facial features, 2.maternal alcohol consumption
confirmed or unknown,3.evidence of neurodevelopmental impairment OR microcephaly in
infants and young children
F
'
ASD without sentinel facial features:evidence of neurodevelopmental impairment, maternal
alcohol consumption confirmed
• sentinel facial features:short palpebral fissures (<2 SD below mean),flattened philtrum, thin
upper lip (having all 3 featuresis highly specific for alcohol exposure
neurodevelopmental dysfunction (need >3):motorskills; neuroanatomy/neurophysiologv;
cognition; language; academic achievement;memory;attention;executive function (impulse
control and hyperactivity); affect regulation; adaptive behaviour,social skills or social
communication, or microcephaly in infant and young children
• diagnosis of AKBD and AKKD require evidence of maternal alcohol consumption during pregnancy
• criteria for diagnosis of AKBD
• congenital anomalies;malformations and dysplasias of the cardiac,skeletal,renal, ocular, and
auditor)'systems
• criteria for diagnosis of ARND
complex pattern of behavioural or cognitive abnormalities inconsistent with developmental level
that cannot be explained by familial background or environment alone
cannot be definitively diagnosed in children <3yr
Management
• early diagnosis is essential to prevent secondary disabilities by early connection to therapies and
supports
• no cure,but individuals with F
'
ASD and theirfamiliesshould be linked to community resources and
services to improve outcomes
• growth/dietshould be monitored closely as nutritional deficiencies are common
Prognosis
• secondary’disabilities include unemployment,mental health problems,difficulties with the law,
inappropriate sexual behaviour,disrupted school experience, peer problems
• prognosis may be improved if diagnosed before age 6,social and educationalsupports available,and
nurturing living environment
Attention Deficit Hyperactivity Disorder
• see Psychiatry, Neurodevelopmental Disorders,PS4T
Autism Spectrum Disorder
• see Psychiatry. Neurodevelopmental Disorders, Ps-}-
Motor Delay
• see Cerebral Palsy, P87and Medical Genetics. Duehenne Muscular Dystrophy, MGS
Endocrinology
Antidiuretic Hormone
Diabetes Insipidus
• see Endocrinology. E22 and Nephrology. NPI 2
Syndrome of Inappropriate Antidiuretic Hormone
• see Endocrinology. E22 and Nephrology. NPI 1
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P31 Paediatrics Toronto Notes 2023
Diabetes Mellitus
DIABETES MELLITUS TYPE 1
• see Endocrinology, E7
Epidemiology
• most common form of DM in children,M=T
• variable prevalence internationally, affects 32 in 100000 children in Canada
• can present at any age, but bimodal peaks at 5-9 y/o and at 10-14 y/o
Diagnostic Criteria tor DM (Types1and
2) in Children
1.Symptoms(polyuria, polydipsia,
weight loss,etc.) and hyperglycemia
(Random glucose >11.1 mmol/L)
Clinical Features OR
• can present with polyuria (may manifest as nocturia orsecondary enuresis), polydipsia, weight loss
(lack of insulin leading to a catabolic state), polyphagia, perineal candidiasis (younger children),
visual disturbances, and DKA (30%, with greater incidence in younger children)
2.Two of the following on one occasion:
. Fasting glucose >7.0 mmol/L
. 2 h plasma glucose during OGTT >11.1
mmol/L
• HbAlc i6.5%
Management OR
• patients and families are best managed with a family-centred paediatric multidisciplinary team able
to provide education, ongoing care, and psychosocial support surrounding survival skills, meal plans,
and insulin injections as a cornerstone of treatment
• diet with consistent levels of carbohydrates, avoiding foods with high glycemic index is advised
-60 min aerobic exercise recommended daily, extensive activity may cause prolonged
hypoglycemia or hyperglycemia
administer influenza immunization yearly to avoid complications to management
• blood glucose monitoring is especially important in children asthey are more susceptible to
hypoglycemia (lethargy, unusual behaviour, tremor, pallor,tachycardia, diaphoresis,seizure, coma)
administersimple PO carbohydrate (i.e.sweetened fruit juice) for mild hypoglycemia and 1M
glucagon or IV dextrose forsevere hypoglycemia
screen for micro- and macrovascular complications(regular ophthalmology assessments,
microalbuminuria, diabetic foot exam), concurrent autoimmune diseases (thyroiditis, celiac disease,
etc.),mental health issues (depression, eating disorders, etc.), HTN, dyslipidemia
Prognosis
• no cure currently
• short
-term complications
• hypoglycemia
» due to missed/delayed meals, excess insulin or exercise, illness, alcohol ingestion,
psychosocial factors
can lead to seizures and/or coma as well as permanent neurologic complications
hyperglycemia
due to intercurrent illness, carbohydrate-to-insulin mismatch
risk of end-organ damage
DKA:due to missed insulin doses, infection;most common cause of death
• long-term complications
microvascular:retinopathy, nephropathy, neuropathy
• macrovascular:metabolic syndrome,CVD,CAD, PVD
increased risk of other autoimmune diseases
• hypertension, dyslipidemia
DIABETIC KETOACIDOSIS (DKA)
• approximately 40% of children with new onset diabetes will have DKA,and 0.5-1% of DKA cases are
complicated by cerebral edema
• symptoms: anorexia, nausea/vomiting, abdominal pain
• signs: Kussmaul breathing, tachycardia, reduced skin turgor, drowsiness, lethargy, coma
• warning signs of neurological deterioration: headache, bradycardia, irritability, decreased LOG,
incontinence,specific neurologicalsigns
• management with paediatric-specific protocols:
ABCs, 100% Oa,admit,monitor, correct fluid losses (use isotonic fluids)
• administer insulin
avoid insulin bolus and delay infusion until 1 h afterfluid resuscitation
SC insulin if mild DKA;IV infusion if moderate orsevere
normalize glucose level gradually
frequently monitor BG, electrolytes,fluid ins/outs, neurological status
• ensure maintenance fluids contain potassium, add glucose to fluids once BG reachesspecific threshold
• if cerebral edema issuspected, give mannitol, restrict IV fluids, and move to ICU; imaging only after
patient is stabilized
• see Endocrinology. E9
3. One of the following on two separate
occasions*
• Fasting glucose i7.0 mmol/L
• 2 h plasma glucose during OGTT zll.1
mmol/L
. HbAlc >6.5%
'HbAlc Isnot recommended oslire soledegrade totin
children and adolescents
'HbAlchas reducedrelioMy whenhemogM<no<»ll>es
aincreasedRBC turnover (i.e.G6P0)present
Blood Glucose Targets
Current Diabetes Canada guidelines
recommend an HbAlc target of <7% for
children with Type 2 diabetes, with a
less stringent target of <7.5% for children
with Type 1Diabetes to minimize
hypoglycemia.
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P32 Paediatrics Toronto Notes 2023
DIABETES MELLITUS TYPE 2
• see l-
'
amilv Medicine, FM25 and Endocrinology. E8
- impaired glucose metabolism due to increased peripheral insulin resistance and relative impairment
in insulin secretion
Epidemiology
• rare before age 10, but more common in older children/adolescents(mean age of -14 y/o)
• prevalence is rising mainly due to the increased incidence of childhood obesity
• risk factors:first orsecond degree relative with type 2 diabetes, high risk ethnic group,obesity,
impaired glucose tolerance, polycystic ovarian syndrome (PCOS), exposure to diabetesin utero,
acanthosis nigricans, hypertension,dvslipidemia, non-alcoholic fatty liver disease, atypical
antipsychotic medications(see Endocrinology, E8)
• risk reduced with breastfeeding
Clinical Features
• clinical features maybe similar to that of T1DM, though most children are asymptomatic (
-40%)
may present in DKA or hyperglycemic hyperosmotic nonketotic state
• screening at least every 3 yr recommended in overweight or obese asymptomatic children after
puberty or >10 y/o if >1 risk factors
• screening and diagnostic investigations-fasting plasma glucose recommended, 2 h oral glucose
tolerance test (higher detection in severe obesity, BM1 >99th percentile, and with multiple risk
factors),HbAlc
• consider pancreatic autoantibodies(anti-glutamate decarboxylase,anti-islet and anti-insulin
antibodies) to excludeT1DM as 10-20% of children with clinical T2DM diagnosis may have T1DM
Set landraatkPiedafrt IntistaMe for mote
infonnatiocostOMT.»4«idetaIsttt effica ly of
t hree treatments ased at Kfce«n9 durable glycemic
control in ctildmandadolescents with recent-onset
type 2 diabetes.
See Landmark PeedzrtI-alstablefor more
nformaboo on EUIPS.wfnk detaisthe safety and
e ffectiveness of kraglsWeand metfoemm combined
therapy for yootb nrr:type 2 diabetes.
Management
• initial therapy with insulin used forsevere metabolic decompensation at diagnosis (DKA, HbAlc
>9%),can wean off
• initiate lifestyle modification program, including diet, weight loss, physical activity (moderate to
vigorous activity for at least 60 min/d;screen time less than 2 h/d)
• if glycemic targets not achieved within 3-6 mo from diagnosis with lifestyle intervention alone,either
metformin (first line),glimepiride, or insulin should be initiated
metformin can be initiated at diagnosis if HbAlc >7%
• if glycemic target not met with metformin,add liraglutide with/without basal insulin (especially if
severe hyperglycemia - HbAlc >8.5%)
• monitor HbAlc every 3mo
• advise patient to monitor finger-stick blood glucose levels if on medication with risk of hypoglycemia,
are changing medication regimen, have not met treatment goals,or have intercurrent illness
• screening -same as TIDM plus annualscreening for PCOS and nonalcoholic fatty liver disease
(NAFLD)
Prognosis
• includes microvascular and macrovascular complicationssimilar toTIDM
Growth
• see l
'
aihtre to thrive, P15
SHORT STATURE
Definition
• shortstature:height <3rd percentile
• poor grow th evidenced by growth deceleration (height crosses major percentile lines,decreased
growth velocity
Short Stature DOx
Epidemiology
• -2.5% of the population by definition ABCDEFG
Al one (neglected infant)
Bone dysplasias (rickets,
scoliosis,mucopolysaccharidoses,
achondroplasia)
Chromosomal(Turner.Down)
Delayed growth (CDGP)
Endocrine (hypopituitary.low GH,
Cushing,hypothyroid)
Familial (familial short stature)
Gl malabsorption (cetiac.Crohn's)
Etiology
. ABCDEFG (see Short Stature DDx Memory Aid)
Pathologic shortstature (if reduced growth velocity)
Non-pathologic short stature (if normal growth velocity)
Clinical Features
• history and physical exam
family history of growth and pubertal onset
plot on growth curve (special growth charts available for Turnersyndrome, achondroplasia, DS,
and other genetic syndromes)
decreased growth velocity often more worrisome than actual height
assess for dysmorphic features,disproportionate short stature
• assess for headaches, vision changes,stigmata of endocrine abnormalities
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P33Paediatrics Toronto Notes 2023
risk factors for GH deficiency: previous head trauma, history of intracranial bleed or infection,
head surgery or irradiation, positive family history, breech delivery
•investigations
calculate mid-parental height:children are usually in a percentile between their parents’
height
mid-parental height male = (mother + father’
s height in cm + 12.5 cm)/2
mid-parental height female = (mother + father’
s height in cm -12.5 cm)/2
likely low mid-parental height in familialshortstature (HSS)
AP x-ray ofleft hand and wrist for bone age
Constitutional delay of growth and puberty (CDGP) may be distinguished from KSS based
upon delayed bone age
• further investigations recommended with severe shortstature or decreased growth velocity,
guided by history/physical (e.g.endocrine (TSH/T4,GH testing, etc.), chronic illness(e.g.CBC,
creatinine, electrolytes, celiac screen,sweat chloride,etc.), genetic (e.g. microarrav,karyotype if
aneuploidy suspected), etc.
Management
•depends on etiology and severity of problem as perceived by parents/child
•no treatment for non-pathological shortstature,except for idiopathic shortstature (height <3rd
percentile without any endocrine, metabolic,or other disease etiology)
•GH therapy for GH deficiency:if administered at an early age, can help patients achieve adult height
requirements
GH shown to be deficient by 2 differentstimulation tests (with arginine,glucagon,insulin)
growth velocity <3rd percentile or height <3rd percentile
bone age x-rays show unfused epiphyses/delayed bone age
•support and management of resultant self-image issues,social anxiety, etc.
Short Stature
!
I
IUGR NolUGR
|
1
Primordial
•Height,weight,and head circumference
are affected
•Chromosomal (e.g. Turner, Down syndrome)
•Teratogen,placental insufficiency,
infection
Proportionate Disproportionate
•Skeletal dysplasia
Normal Growth Velocity Slow Growth Velocity
Constitutional Delay of Growth and Puberty
• Delayed puberty
• May have family history of delayed puberty
• May need short-term therapy with androgens/
estrogens
• Delayed bone age
• Often mid-parental height is normal
Familial
• Normal bone age
•Treatment not indicated
•Family Hx of short stature
Endocrine (height affected more than weight)
• GH deficiency
• Hypothyroidism/Hyperthyroidism
• Hypercortisolism
• Hypopituitarism
• Adrenal insufficiency
Chronic disease (weight affected more than height)
• Cyanotic CHD
• Celiac disease. IBD. CF
• Chronic infections
• Chronic renal failure (often height more affected)
Psychosocial neglect (psychosocial dwarfism)
• Usually decreased height and weight (decreased
head circumference if severe)
Figure 7.Approach to the child with shortstature
TALL STATURE
•height greater than 2 SDs above the mean for a given age,sex, and race
Etiology
•constitutional/familial
•endocrine:Beckwith-Wiedemann syndrome, hyperthyroidism, hypophyseal gigantism, precocious
puberty
•genetic homoevstinuria, Klinefeltersyndrome,Marfan syndrome, Sotossyndrome
n
Hypercalcemia/Hypocalcemia/Rickets
• see Endocrinology, E43, E44, E48
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Hyperthyroidism and Hypothyroidism
• may be congenital or acquired (for acquired causes,see Endocrinology,E26)
CONGENITAL HYPERTHYROIDISM
• also known as neonatal Graves’disease
Epidemiology
• ~1 in 25000 neonates,M=E
Etiology
• typically caused by transplacental transfer of TSH receptor antibody (TRAb)
• rare causesinclude mutations in the TSH receptor pathway
Clinical Features
• history and physical exam
maternal history of thyroid pathology and management
low birthweight,1UGR, microcephaly, premature birth, tachycardia, irritability, frontal bossing,
triangular facies, hepatosplenomegaly, goitre,flushing,sweating
Investigations
• TSH receptor antibody levels during the 3rd trimester or in the cord blood
• neonatal TSH,T3, free T4
Management
• methimazole and (3-adrenergic blocker (e.g.propranolol)
Prognosis
• with prompt treatment, hyperthyroidism improves
• however, long-term cognitive and CNS problems can still occur
• risk for development of central hypothyroidism later in life
CONGENITAL HYPOTHYROIDISM
Epidemiology
• incidence:1 in 2000-4000 newborn births; l
:
:M=2:l
• one of the most common preventable causes of intellectual disability
Etiology
• may be classified as permanent or transient congenital hypothyroidism (CH)
subcategorize into primary (85% thyroid dysgenesis, 15% inborn errors of thyroid gland hor
biosynthesis),secondary/central (pituitary/hypothalamic issue),or peripheral CH (deficits in
thyroid hormone transport, metabolism, or action)
• causes of transient hypothyroidism: maternal antibody-mediated, iodine deficiency (rare in developed
countries), prenatal exposure to antithyroid medications; neonatal iodine deficiency/excess,
congenital liver hemangiomas, certain gene mutations
Clinical Features
• history and physical exam
• usually asymptomatic in neonatal period because maternal T4 crosses the placenta
• prolonged jaundice, feeding difficulty,lethargy, constipation, umbilical hernia, macroglossia,
large fontanelles, puffy face,swollen eyes, hypotonia (signs/symptoms develop over first few mo)
examine for congenital malformations (especially cardiac) and dysmorphic features
• central hypothyroidism associated with hypoglycemia, micropenis, undescended testes, features
of diabetes insipidus
most commonly presents as a positive newborn screen result
• investigations
• all infantsshould be screened for primary CH
• repeat screening at 2 wk for infants at high-risk: preterm, SGA, infants in N1CU,specimen
collection <24 h of life, multiple births
diagnosis through newborn screening of TSH (most sensitive for primary CH) or free T4;
abnormal results should be confirmed with serum levels from venipuncture
tT SH, 4free T4 in primary CH
4TSH, 4free T4 in secondary CH
• primary CH (optional):radioisotope scanning/ultrasound of thyroid for severity,serum
thyrogiobulin, maternal antithyroid antibodies, urinary iodine
• secondary CH: MR1, gene analysis, eye exam for optic nerve hypoplasia (assess pituitary)
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Management
• thyroxine replacement, hormone normalization should be done within 2 wk to avoid cognitive
impairment
• counsel against using soy based formulas
Prognosis
• excellent outcome if treatmentstarted within 1-2 mo of birth
• if treatment started after 3-6 mo of age, may result in permanent developmental delay and/or
disability (mild to profound), intellectual impairment, poor growth, hearing loss
Disorders of Sexual Development
AMBIGUOUS GENITALIA
Definition
• newborn or child whose sex is difficult to assign based on the appearance of genitalia
• subtype of DSD: a condition in which development of chromosomal,gonadal, or anatomic sex is
atypical
• subtypes:46,XX DSD,46,XY DSD,ovotesticular DSD (true hermaphrodite)
Epidemiology
• incidence of genital abnormalities at birth is as high as 1 in 300
• prevalence of complex anomalies with true sexual ambiguity much lower at ~1 in 5000
Etiology
• 46,XY DSD
• inborn error of testosterone biosynthesis or Leydig cell hypoplasia
5-a-reductase deficiency, androgen receptor deficiency'or insensitivity'
LH/hCG unresponsiveness
• 46,XX DSD
virilizing CAH (most common)
maternalsource:virilizing ovarian or adrenal tumours, untreated maternal CAH, placental
aromatase deficiency
• ovotesticular DSD
both ovarian follicles and seminiferous tubules in the same patient with a 46,XX karyotype
• mixed gonadal dysgenesis
Risk Factors
• parental consanguinity, positive family history of ambiguous genitalia, early childhood illness/death,
or primary amenorrhea, maternal medications during pregnancy (e.g.androgens, progesterones,
danazol, phenytoin, aminoglutethimide, endocrine disruptors)
Clinical Features
• history
thorough obstetrical history, including prenatal screens, maternal medications,and maternal
virilization in pregnancy
» family history:autosomal recessive pattern may suggest CAH, X-linked recessive pattern may
suggest androgen insensitivity syndrome
• physical exam
XY:small phallus, hypospadias, bilateral cryptorchidism (undescended testicles)
XX:clitoromegaly, labioscrotal fusion
look for concurrent midline defects,dysmorphic features,and congenital abnormalities
• investigations
karyotype and genetic workup, including FISH for SRY gene, asindicated
blood work:electrolytes and renin (evidence ofsalt-wasting in CAH);17-OH-progesterone,
androgens,FSH and LH,glucose
imaging:abdominal and pelvic U/S to look for gonads, uterus, and vagina
Management
• avoid announcement of probable sex or use of personal pronouns until all tests are complete
• continuous psychosocialsupport for parents and child during development
• promote individualized management with respect to sex of rearing,surgical intervention, hormonal
therapy, and preservation of fertility
CONGENITAL ADRENAL HYPERPLASIA
Definition
• autosomal recessive disorder characterized b
cortisol and aldosterone production in the a
• adrenal cortex normally produces balanced levels of aldosterone, cortisol, and androgens
jy a defect in varioussynthetic enzymes required for
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Epidemiology
• occurs in ~1 in 15000 live births
• most common cause of ambiguous genitalia in genotypically normal females(46,XX)
Etiology
• 21-OH deficiency Is responsible for
-95% of CAH cases
• results in * cortisol and aldosterone production with shunting toward 11 androgens
• cortisol deficiency leadsto elevated ACT'
H, which causes adrenal hyperplasia
• rarer causes include deficiencies in 11-OH, cholesterol desmolase, 17-OH, and 3-HSD
Clinical Features
• depends on which enzyme in cortisolsynthesis pathway is defective
• presentation of 21-OH deficiency can be divided into:
classic deficiency with salt wasting:inadequate aldosterone resulting in FIT, hyperkalemia,
hyponatremia, hypoglycemia, acidosis (majority of classic CAH types)
• classic deficiency without salt wasting:simple virilization with adequate aldosterone levels
females typically present with genital ambiguity, amenorrhea, precocious puberty, polycystic
ovaries, hirsutism
males typically asymptomatic at birth,may show hyperpigmentation (from overproduction of
melanocyte stimulating hormone), penile enlargement, rapid growth, and accelerated skeletal
maturation; present with signs of virilization later in life
non-classic CAH - mild androgen excess,sometimes asymptomatic, precocious puberty
and/or virilization present later in life,rarely associated with Addisonian crises(may be
indistinguishable from PCOS)
• 21-OH deficiency screening is part of many newborn screening programs across North America (nonclassical variant rarely detected)
• high serum levels of 17-OH progesterone in random blood sample diagnostic for 21-OH deficiency
• assess plasma ACT'
H,serum electrolytes, plasma glucose, plasma aldosterone, plasma renin
activity,blood gas
ultrasound -look for enlarged adrenal gland and presence of uterus
Management
• correct any abnormalities in fluids, electrolytes, orserum glucose
• provide glucocorticoids (e.g. hydrocortisone)/mineralocorticoids (fludrocortisone) to reduce ACT'
H
levels, extra glucocorticoids in times ofstress
• psychosocial support
Prognosis
• complications if untreated include virilization, acne,salt wasting, hypotension
NORMAL PUBERTAL DEVELOPMENT
Physiology
• puberty occurs with the maturation of the HPG axis
• t pulsatile release of GnRH * t release of LH and l-
'
SH » maturation of gonads, release of sex steroids
* secondary sexual characteristics
• adrenal production of androgens also required
Females
• onset:ages 8-13 (may start as early as 7 in girls of African descent)
• usual sequence
1.thelarche:breast budding
2. pubarche: axillary hair, body odour, mild acne
3.growth spurt
4.menarche: mean age 12.5 yr;indicates that growth spurt is almost complete;menses may be
irregular in duration and length of cycle
• early puberty is common and often constitutional,late puberty is rare (rule out organic causes)
Males
• onset:ages 9-14
• usual sequence
1. testicular enlargement
2. penile enlargement
3. pubarche: axillary and facial hair,body odour, mild acne
4.growth spurt:occurs later in boys
• early puberty is uncommon (rule out organic causes),late puberty is common and often constitutional
• gynecomastia (transient development of breast tissue) is a common self-limited condition seen in 50%
of males during puberty (but any discharge from nipple or fixed massshould be investigated)
Maturity Rating (formerly Tanner Staging)
• scale used in paediatricsthat defines physical measurements of development based on external
primary and secondary sex characteristics
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FEMALE BREAST
Stage 1: Papilla elevation only Stage 2: Breast and papilla Stage 3: Enlargement of Stage 4; Areola and papilla Stage 5:Mature, nipple projects,
elevated as small mound, breastandareola. no contour form secondary mound no secondary mound
enlargement of areola separation
FEMALE GENITAL
Stage I: No hair
I
, prepubertal Stage 2: Stnall
T
amount of long. Stage 3: Oarker
T , coarser, Staged: Adult
T-type It Bir,no T
straight or curled, slightly curlier hair distributed eaten sion to medial thighs
pigmented hail along labia majora sparsely over pubs
Stagefi Mature distribution with
spread to medial thighs
MALE GENITAL
T I T Y 7 i
\ / ii /
Stage 1 Nohair, piepubBital Stage 2: Small amount of long, Sl»gu 3 Darker, coarser, curlier Staged: Adult - type hair, no Stagufi Mature distribution with jy
straight or curled, slightly be•
distributed sparsely exten sion to medial thighs
pigmented hair along base of over pubis, Longlhonvtg of Increase in ponloclrcumfernnco
penis Enlargement ol tosles penis, further enlargement Df and length, development of glands,
toslos and scrotum
spread to madial thighs Adult sire a.
further enlorgomont ol teslas and
scrotum,darkening of scrota I skin
end scrotum, taddenng
of scrotal skin
Figure 8. Tanner staging
PRECOCIOUS PUBERTY
Definition
• development of secondary sexual characteristics 2-2.5 SDs before population mean
• <8 yr for females, <9 yr for males
Epidemiology
• 1 in 10000; F>M
Etiology
• usually idiopathic in females (90%), more suggestive of pathology in males (50%)
• central (GnRH dependent)
hypergonadotropic hypergonadism; hormone levels as in normal puberty
premature activation of the HFG axis
differential diagnosis:idiopathic or constitutional (most common in females), obesity, CNS
disturbances (tumours, hamartomas, post-meningitis, increased 1CP, radiotherapy), NF,primary
severe hypothyroidism
• peripheral (GnRH independent)
hvpogonadotropic hypergonadism
• differential diagnosis
males:testicular tumour, gonadotropin/hCG secreting tumour (hepatoblastoma, intracranial
teratoma,germinoma)
females: ovarian cysts/tumours
both: adrenal disorders (CAH, adrenal neoplasm), exogenous steroid administration,
McCune-Albright syndrome, aromatase excess syndrome, rarely primary hypothyroidism
(Van Wyk-Grumbach syndrome)
Clinical Features
history
symptoms of puberty,family history of precocious puberty, medical illness
• physical exam
growth velocity
prepubertal:minimum 4 cm/yr
growth spurt: males 10-14 cm/yr,females 8-12 cm/yr
complete physical exam, including Tanner staging and neurological assessment r i
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initial screening tests: bone age,serum hormone levels (estradiol, testosterone, LH, FSH, TSH,
free T 4, DHEA-S, 17-OH-progesterone, prolactin)
secondary tests:MR1 head, pelvic U/S, (5-hCG, GnRH, and/or ACTH stimulation test
A child (generally boys and girls <6/7 y/o)
with proven central precocious puberty
should receive an MRI of the brain
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Management
• indicationsfor medical intervention to delay progression of puberty:rapid advancement of puberty,
early age, risk of compromise of final adult height, psychological
• central causes:goals are to preserve height and alleviate psychosocial stress; GnRH agonists(e.g.
leuprolide) most effective
• peripheral causes:goal is to limit effects of elevated sex steroids; medications that decrease the
production of a specific sex steroid or block its effects (e.g. ketoconazole,spironolactone, tamoxifen,
anastrozole);surgical intervention
DELAYED PUBERTY
Definition
• failure to develop secondary sex characteristics by 2-2.5 SDs beyond the population mean
for males:lack of testicular enlargement by age 14
• for females:lack of breast development by age 13 OR absence of menarche by age 16 or within 5 yr
of pubertal onset
Epidemiology
• M>F
Etiology
• usually constitutional delay in males, more suggestive of pathology in females
• central causes
constitutional delay in activation of HPG axis(most common)
• hypogonadotropic hypogonadism (e.g. various genetic syndromes (e.g. Kallmann syndrome),
hypothalamic/pituitary disorders,chronic illness, hypothyroidism, hyperprolactinemia, poor
nutrition, excessive exercise, etc.)
• peripheral causes
hypergonadotropic hypogonadism (e.g.primary gonadal failure,gonadal damage,Turner
syndrome, Klinefeltersyndrome,hormone deficiency, androgen insensitivity syndrome, etc.)
Clinical Features
• history:weight loss,shortstature,family history of puberty onset, medical illness, high performance
athletes(females), congenital anomalies, or neurologic symptoms
• physical exam
growth velocity
prepubertal: minimum 4 cm/yr
growth spurt:males 10-14 cm/yr,females 8-12 cm/yr
complete physical exam, including Tanner staging and neurological assessment
• investigations
initial screening tests:bone age,serum hormone levels (estradiol, testosterone, LH, 1
;
SH,TSH,
free T
'
4, IGF-1),CBC, electrolytes, BUN,Cr, Ll-Ts,liver enzymes, HSR, CRR,IGF-1, urinalysis
secondary tests:MR1 head, pelvic U/S, karyotype, 1BD panel, celiac disease panel, LH levels
following GnRH agonist, prolactin
Management
• identify and treat underlying cause
• patients with constitutional delay or GnRH deficiency may be offered “ jump start" therapy to induce
puberty: cyclic estradiol and progesterone for females, testosterone for males
• refer to paediatric endocrinologist for hormone therapy
Total Body Water Fluids and Electrolytes i
*
Intracelluar
HuidllCF)
Extracelluar
Fluid (ECF)
Approach to Infant/Child with Dehydration 2/3 I 3
1
*
Etiology
• decreased intake: poor oral intake during acute illness, breastfeeding difficulties, eating disorders
• increased losses: common sites include Gl tract (diarrhea, vomiting, bleeding),skin/mucous
membranes (fever, burns, hemorrhage,stomatitis), urine (osmotic diuresis (e.g. hyperglycemia,
DKA)),diuretic therapy, Dl, post-obstructive/post ATN recovery diuresis, and respiratory tract
(tachypnea,bronchiolitis, pneumonia)
Intravascular Interstitial
Fluid Fluid (ISF)
1/4 2 4
Figure 9. Body fluid compartments
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P3V Paediatrics Toronto Notes 2023
Management
• if suspect dehydration based on history (acute illness, decreased number of rvet diapers,lethargy,
changes in mental status, increased thirst, etc.), you must:
1) Determine degree of extracellular volume contraction
Assessment of Severity of Dehydration
C BASE HrO
Capillary refill
B
Table 17. Assessment of Degree of Extracellular Volume Contraction Based on Physical Exam - Anterior fontanelle
Skin turgor
Eyes sunken
Mild Moderate Severe
<2 yr SV 10V 15V
HR
3 > '
2 yr 6%‘ 9%‘ Oral mucosa
Pulse Normal, lull Output of urine
Normal
Rapid
low to normal
Rapid, weak
Decreased in shock (very lale
finding in paediatrics and very
dangerous)
Anun'
a
Parched
Markedly sunken
Markedly sunken
Tenting
Increased (>3s)
Blood Pressure
Urine Output
Oral Mucosa
Anterior Fontanelle
Decreased
Slightly dry
Normal
Normal
Normal
Normal|*3 s)
Markedly decreased
Dry
Sunken
Sunken
Decreased
Normal to increased
Eyes
Skin Turgor
Capillary Relill
*
Note that percentage*
refer to percent to**
ot pre-illness body weight
2) Determine the likely electrolyte disturbance
• dependent on etiology of dehydration and type of fluid loss (isotonic vs. hypertonic vs. hypotonic)
Table 18. Electrolyte Content of Various Bodily Fluids
Bodily Fluid Na" (mmol/L) K (mmoiyi) Ch(mmol/L) HCQ3-(mmol/L)
Saliva
Gastric Juice
Pancreatic Juice
30 30 20 70 30
GO 80 15 100 0
140 5-10 60 90 40100
Bile 140 5 -10 100 40
Small Bowel
Large Bowel
Sweat
140 20 100 2550
75 30 30 0
20-70 5-10 40-60 0
• for moderate and severe dehydration, initial investigationsshould include urinalysis and blood work
examining electrolytes(Na *, K '
,Cl), glucose, acid-base disturbances ( blood pH, p(.0:, HCO.i-), and
impaired renal function (creatinine, BUN )
3) Determine if the child requires PO or IV rehydration
• dehydrated child must receive adequate fluid management, including replacing deficits, ongoing
losses, and maintenance fluids
• oral rehydration therapy (ORT) indication: mild to moderate dehydration
advantages:
* cost, no IV needed, no increase in incidence of iatrogenic hyper/hyponatremia,
parental involvement in therapy
• indications for IV rehydration therapy:severe dehydration requiring close monitoring and frequent
assessment of electrolytes, inability to tolerate ORT (e.g. vomiting, alteration in mentalstatus, ileus,
monosaccharide malabsorption, etc.), inability to provide ORT,failure of ORT in providing adequate
rehydration (e.g. persistent diarrhea or vomiting)
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4) Return the child to a normal volume and electrolyte status by replacing current
deficits and ongoing losses
Degree of Dehydration
i 1 Special Consideration-S1ADH
• Clinical Signs:hyponatremia and
excretion of concentrated urine
• Risk Factors:certain medications
(e.g.morphine),postoperative,
pain.N'V.pulmonary disease (e.g.
pneumonia).CNS disease (e.g.
meningitis)
• Caution:acute hyponatremia is
associated with rapid administration
of hypotonic IV fluids,this can lead to
cerebral edema and brain herniation
or central pontine myelinolysis
No dehydration Mild dehydration Moderate dehydration Severe dehydration
I i I
1. Rehydrate with ORT at
50 mL/kg over 4 h
2. Replace ongoing losses
with ORT
3. Age-appropriate diet
after rehydration
1. Rehydrate with ORT at
100 mL/kg over 4 h
2. Replace ongoing losses
with ORT
3. Age-appropriate diet
after rehydration
1. IV resuscitation with
NS 20 mlAg bolus
2. Reassess and
repeat if necessary
3. Begin ORT when
patient is stable
4. Replace ongoing
losses with ORT
5. Age-appropriate
diet after
rehydration
Figure 10. Algorithm for deficit replacement and replacement of ongoing losses in the dehydrated child
1. Age-appropriate diet
2. Replace ongoing losses
5) Provide the appropriate fluid and electrolyte maintenance daily requirements
Table 19. Maintenance Fluid Requirements
Body Weight 100:50:20 Rule (24 h maintenance fluids) 4:2:1 Rule (hourly rate of maintenance fluids)
I-10 kg
II-20 kg
100 cc/kg/d
1000 cc
- 50 cc/kg/d for every kg »10 kg
1500 cc + 20 cc/kg/d for every kg »20 kg
4 cc/kg/h
40 cc 2cci'kg/h for every kg »10 kg
60 cc
-
»20 kg 1 cc/kg/h for every kg »20 kg
• prior to starting IV' fluids,serum electrolyte values should be measured
• in children, all maintenance fluids should have a dextrose component due to their higher risk of
hypoglycemia, especially if they are NPO
• common IV’ fluid combinations used in paediatrics
NS bolus for dehydration
for maintenance:
newborn: D10YV
first mo of life:D5W/0.45 NS + KC120 mHq/L (only add KC1 if voiding well)
children withoutspecial considerations:D5W/NS + KCI 20 mHq/L - decreased risk of
hyponatremia
other options: D5\V0.45%NS + KG 20 mHq/L
• most important thing to remember when correcting Na+ aberrations due to fluid deficits
risk of cerebral edema with rapid rehydration with hypotonic or isotonic solutions (Le. NS)
therefore replace fluid slowly with close monitoring
aim to adjust (increase or decrease) plasma [Na i by no more than 12 mmol/L/d
• management depends on etiology,severity of symptoms, and timing (acute vs.chronic)
6) Continue to monitor fluid and electrolyte status
• accurate monitoring of daily fluid intake (PO and IV'
) and ongoing losses (urine output,diarrhea,
emesis,drains)
• if child receiving >50% of maintenance fluids through IV,serum electrolyte valuesshould be
monitored daily and therapy adjusted accordingly
• avoid iatrogenic hyper/hvponatremia, keep the possibility of S1ADH in mind (indicated by
hyponatremia and concentrated urine)
Gastroenterology
Vomiting
History
• characteristic of emesis (e.g. projectile, bilious, bloody, etc.)
• pattern of emesis (e.g. association with feeds, cyclic, morning, prolonged, positional, etc.)
• associated symptoms (e.g. anorexia, diarrhea, abdominal pain, hematochezia,fever, headache, etc.)
• red flags: bilious or bloody emesis, projectile vomit, abdominal distension and tenderness, high fever,
signs of dehydration, worse when lying down
• remember that vomiting without diarrhea is not always gastroenteritis
• post-tussive vomiting is also common with coughing fits in children
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Physical
• vital signs to determine clinical status and hydration state
• abdominal examination for evidence of obstruction or focal tenderness
• neurologic assessment for signs of increased 1CP
Investigations
• if child appears well and no worrisome features, often investigation is not required
• CBC, electrolytes, BUN,Cr, amylase, lipase, glucose, liver enzymes, urinalysis done routinely
• in sick child, add: HSR, venous blood gases,C&S (blood,stool), imaging (x-ray, U/S)
Table 20. Common Differential Diagnosis, Associated Findings, and Diagnostic Approach Based
on Age
Cause Suggestive Findings Diagnostic Approach
NEONATES- NON-BILIOUS
Tracheoesophageal Fistula Excessive secretions soon alter birth(e.g.
drooling,choking,respiratory distress/
pneumonia),inability to feed,cyanosis (esp
with feeds),emesis
Projectile non-bilious emesis within 30min
after feeding,fatigue,dehydrated,palpable
“olive"in RUO.decreased stools,hunger
Fussiness after feeds,spit ups.arching of
back,poor weight gain
Fever,lethargy,tachycardia,tachypnea,
widening pulse pressure
Inability to advance NG tube.CXR.upper Gl
series with water-soluble contrast
Pyloric Stenosis CSC.electrolytes.Cr.SUN.ASG (hypokalemic,
hypochloremic metabolic alkalosis).U/S of
pylorus,upper Glstudy (if U/Snondiagnostic)
Empiric trial of acid suppression.pH
monitoring study,upper Gl study,endoscopy
CBC.PT/PTT.electrolytes.Cr.BUN.tils,
bilirubin,lactate,urinalysis,cultures (blood,
urine.CSF).CXR
Electrolytes.ABG (hyponatremic.hyperkalemic
metabolic acidosis).lactate,ammonia.LFTs.
BUN.Cr.serum glucose,bilirubin.PT/PTT.CBC
GERD
Sepsis
Inborn Error of Metabolism Poor feeding.FTT,jaundice,
hepatosplenomegaly,cardiomyopathy,
dysmorphia.developmental delay,neurologic
manifestations
NEONATES-BILIOUS
Intestinal Obstruction - Malrotation with
Volvulus.Meconium Ileus,etc.
Duodenal Alresia/Stenosis
Bilious emesis,abdominal distension,pain, AXR.upper Glseries.contrast enema
bloody stool,shock
Bilious emesis,abdominal distension,often
seen in DS.jaundice,polyhydramnios during
pregnancy,hypokalemic,hypochloremic
metabolic alkalosis
Bilious emesis,abdominal distension,pain,
failure to pass stool
Premature neonate,bilious emesis,bloody
stools,abdominal distension,intolerance of
feeds,electrolytes.Cr.BUN.blood culture
AXR.upper Glseries ('double bubble' sign)
Hirschsprung's Disease AXR.contrast enema,rectal biopsy
Necrotizing Enterocolitis AXR,CBC,electrolytes,Cr.BUN.blood culture
CHILDREN AND ADOLESCENTS
Acute Viral Gastroenteritis Generally clinical diagnosis:if severe:CBC.
electrolytes,stool studies
Periumbilical discomfort thatlater localizes to Abdominal U/S
RLO.fever,anorexia
Colicky progressive abdominal pain,drawing Abdominal U/S.AXR (rule out other etiologies
ol legs up to chest,lethargy,bloody “red and perforation)
currant jelly" stool (Triad)
Fever,localized findings depending on cause Cultures (CSF.blood,urine),brain imaging.
Diarrhea,fever,abdominal discomfort,
myalgia,sick contact,recent travel
Appendicitis
Intussusception
Non-GI Infection (e.g. Meningitis,
pyelonephritis, acute otitis media)
IncreasedICP
CXR
Brain CT without contrast
Therapeutic LP in idiopathic intracranial HTN
Nocturnal wakening,progressive recurrent
headache worse with Valsalva,focal
neurologic deficits,gait disturbance
Findings vary by substance - toxidrome. often a Qualitative and sometimes quantitative levels
(urine,blood)
Amenorrhea,morning sickness,bloating. Urine jt-hCG
breast tenderness
At least 3 self-limited episodes of vomiting Diagnosis of exclusion
lasting12 h.7 d between episodes,no organic
cause of vomiting
Toxic Ingestion
history of ingestion
Pregnancy
Cyclic Vomiting
Management
• rehydration (see Fluids and Electrolytes,P38)
• treat underlying cause and correct metabolic/electrolyte abnormalities
• antiemetic drugs can be used in older infants, children, and adolescents with severe vomiting:
ondansetron, promethazine, prochlorperazine, metodopramide
• not recommended when unknown etiology or anatomic abnormalities
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