Tcell

lymphoblastic, and matureT cell lymphoma (anaplastic large cell)

rapidly growing tumour with distant metastases(unlike adult non-Hodgkin lymphoma)

signs and symptoms related to disease site:most commonly abdomen (intussusception),chest

(mediastinal mass), head and neck region

• investigations:CBC and differential, peripheral blood smear, extended electrolytes, uric acid, LDH,

renal function, liver enzymes and function, ESR, and blood culture if concerns for infection. CXR (AP

and lateral) and CT of neck/chest/abdomen/pelvis. Specialized tests: BM aspirate and biopsy ± LN

biopsy. LP. PET scan

Constitutional symptoms-fever, chills,

nightsweats, unexplained weight toss

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P56 Paediatrics Toronto Notes 2023

Management

• Hodgkin lymphoma

combination chemotherapy and radiation

increasing role for use of PET scanning to assess early disease response and plan therapy

• non- Hodgkin lymphoma

• combination chemotherapy

no added benefit of radiation in paediatric protocols

Prognosis

• Hodgkin lymphoma:>90% 5 yr survival

• non-Hodgkin lymphoma: 75-90% 5 yrsurvival

Brain Tumours

• see Neurosurgery. NS11

Wilms’ Tumour (Nephroblastoma)

Epidemiology

• usually diagnosed between 2-5 yr; M«l

:

• most common primary renal neoplasm of childhood

• 5-10% of cases both kidneys are affected (simultaneously or in sequence)

Differential Diagnosis

• hydronephrosis, polycystic kidney disease, renal cell carcinoma, neuroblastoma

Clinical Features

• 80% present with asymptomatic, unilateral abdominal mass

• may also present with HTN, gross hematuria, abdominal pain, vomiting, fever, UT1, anemia

• may have pulmonary metastases at time of diagnosis (respiratory symptoms)

Associated Congenital Abnormalities

• WAGR syndrome (Wilms’tumour, Aniridia,Genitourinary anomalies, mental Retardation) with

llpl3 deletion

• Beckwith-Wiedemann syndrome:

characterized by enlargement of body organs(especially tongue), hemihypertrophy, renal

medullary cysts, and adrenal cytomegaly

• also at increased risk for developing hepatoblastoma, and less commonly adrenocortical tumours,

neuroblastomas,and rhabdomyosarcomas

• Denys-Drash syndrome: characterized by gonadal dysgenesis and nephropathy leading to renal failure

Management

• staging ± nephrectomy

• chemotherapy, radiation for higher stages

Prognosis

. 90% 5-yr survival

• prognostic factorsinclude tumour histology and size,molecular and genetic markers, age

Investigations

• CBC,electrolytes, Cr, BUN, urinalysis,coagulation studies

• imaging: U/S, contrast-enhanced CT or MR1 chest/abdomen/pelvis

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Neuroblastoma

Epidemiology

• most common cancer occurring in first yr of life

• neural crest cell tumour arising from sympathetic tissues (neuroblasts)

Clinical Features

• can originate from any site in sympathetic nervoussystem, presenting as mass in neck, chest,or

abdomen (most common site is adrenal gland)

• signs and symptoms of disease vary with location of tumour

thoracic: dyspnea, Horner’ssyndrome

• abdomen: palpable mass, pain, constipation, enuresis

paravertebral:spinal cord compression, localized back pain, weakness

• metastases are common at presentation (>50% present with advanced stage disease):

usually to bone or bone marrow (presents as bone pain,limp)

can also present with periorbital ecchymoses, abdominal pain, emesis, fever, weight loss,

anorexia, hepatomegaly, “blueberry muffin" skin nodules

• paraneoplastic: HTN, palpitations,sweating (from excessive catecholamines),diarrhea, FI T

'

(from

vasoactive intestinal peptide secretion),opsomyoclonus

Management

• depends on prognostic factors and may include combination of:surgery, radiation, chemotherapy,

autologousstem cell transplantation, immunotherapy

Prognosis

• prognosis is often poor due to late detection

• good prognostic factors

“age and stage"

are important determinants of better outcome: <18 mo,stage 1, 11, 1V-S disease

(“S" designates a “Special” classification only pertaining to infants)

primary site: posterior mediastinum and neck

more differentiated histology

tumour cell markers: aneuploidy, absent MYCN oncogene amplification

Investigations

• CBC,electrolytes, urinalysis, urine, catecholamine metabolites (H VA and VMA),Cr

• imaging: MRI or CT, M1BG scan

• biopsy: required for definitive diagnosis and classification

• definitive diagnosis needs one of the following:

• unequivocal histologic diagnosis from tumour tissue

• evidence of bone marrow metastases on aspirate biopsy with elevation of urinary/serum

catecholamines or metabolites

Bone Tumours

• see Orthopaedic Surgery. OR50

Cancer Predisposition Syndromes

• suspected in cases of multiple primary neoplasms, especially early onset for cancer type and/or family

history consistent with known cancer predisposition syndrome (critical to obtain family history and

refer ifsyndrome suspected)

• cancer predisposition syndromes with paediatric onset include Li-l raumenisyndrome (soft tissue

sarcomas, osteosarcoma,CNS tumours, and adrenal cortical carcinoma),hereditary retinoblastoma,

and l

'

anconi anemia (leukemias and oral cancers)

• early recognition of new malignancies through surveillance limits required therapies

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P58 Paediatrics Toronto Notes 2023

Infectious Diseases

Fever

Definition

• fever:a practical definition is >38°C/100.4°1

:

oral or rectal

• fever without a source/focus:acute febrile illness (typically <10 d duration) with no identifiable cause

of fever even after careful history and physical

• fever of unknown origin: daily or intermittent feversfor at least 2 consecutive wk of uncertain cause

after careful history and physical, and initial laboratory assessment

Etiology

• infectious: anatomic approach (CNS, ears, upper and lower respiratory tract, (il, (iU,skin,soft tissue,

bones and joints, etc.)

• inflammatory: mainly autoimmune (Kawasaki disease,|1A,1BD,Sl.fi, etc.)

• malignancy:childhood cancers (leukemia, lymphoma, neuroblastoma, etc.)

• miscellaneous:drugs and toxins, post

-immunization,familial dysaulonomia, factitious disorder, etc.

Diagnosis

• history:duration, height and pattern of fever, associated symptoms, exposures, constitutional

symptoms, recent antipyretic use, ethnic or genetic background, daycare,sick contacts, travel, tick or

other bug bites, age of child

• physical exam:toxic vs. non-toxic, vitals, growth,complete head-to-toe exam to identify any focus of

infection

• investigations:guided by history, physical exam, and clinical suspicion

Fever

£ i

Age: <26 d Aye: 26-90 d Age: 3 mo-3 yr

1

1

.

I I I

Admit,Full SWU ! NON-TOXIC and All others

empiric antibiotic1 Reliable lollow-upland

Low risk'

eriteria

TOXIC NON-TOXIC and NO FOCUS

1

1

4 1

i

Admit,Full SWU'

,

empiric antibiotic

’

T >39,

’C T <39T

i I

Partial SWlf+Abx Admit.Full SWU'.

May consider empiric antibiotid

treating

as outpatient

Urine R&M Urine R&M

CBC observation

1

4 V

or WBC >15 WBC <15 Consider observation

without antibiotics 4 4

Blood C&S

if NO source of infection con be identified,

then empirical treatment con be used

lie. amoxicillin or ceftriaxone

SOmglkg IM should bo statlodl

Urine C&S

Acetaminophen

Blood C&S

Observation

Acetaminophen

follow-up1

in 24 h

Rochester Criteria - Developed toIdentify

Infants <60 dof Age with fever atlow-risk of

Serious Bacterial Infection

Clinically

WBC Count

Bands

Urinalysis

Well

5 ISi10'

/l

UstWl

<10 W8C.

,bigti - power

NOTES

t. SWU - Septic Workup

2. Partial SWU blood C&S. CBC and differential, urine R&M. C&S. LP. CXR it respiratory symptoms,stool C&S if Gl symptoms

3. Follow up is crucial - if adequate follow up is not assured, a more aggressrve diagnostic and therapeutic approach may be Indicated

4. Low risk (Rochester!criteria

5.Considerable practice variation exists in terms of empiric antibiotic treatment

6.Important principles -the younger the child, the greater the difficulty to clinically assessthe degree of illness

fed

Stool (ifdiarrhea) <5 WBUhighpowtt

held

Past Health 8otn >37 vrk

HomewiBi/beforeEoni

No hosprtalizaboas

No prior anbhiobcase

No prior treatment

for oneipla tired

hyperbilirubinemia

Nothtomedisease

Figure 12. Approach to the febrile child

Evaluation of Neonates and Infants with Fever

• several protocols exist that attempt to identify neonates and young infants at low-risk of serious

bacterial infection (e.g. Rochester Criteria)

• such protocols are not assensitive in the 1-28 d age group; therefore, febrile neonatesshould he

considered high-risk regardless of clinical features and laboratory findings

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Management

• admit to hospital if appropriate

• treat the source if known

• replace fluid losses (e.g. from vomiting, diarrhea); maintenance fluid needs are higher in a febrile child

• reassure parents that most fevers are benign and self-limited

• antipyretics (acetaminophen and/or ibuprofen) may be given if child is uncomfortable

Acute Otitis Media

•all of:

1. presence of middle ear effusion

2. presence of middle ear inflammation

3. acute onset ofsymptoms of middle ear effusion and inflammation

Pneumococcal ConjugateVaccineslor Preventing

Acnte OtitlsMedia inChildren

Cochrane OBSyst He.2019:C00OU8O

Purpose: losyiterubully review the uu of

pneumococcal conjugal vaccinesin preventing AOU

in children <13yearsof age.

Methods:fiCTs comparing the use of pneumococcal

conjugate vaccineslo placebo or control vaccine mere

metuded in this review.

•esutts:14 studies based on 11 trials with a total

of 60733 children were included in thsreview.

During early infancy administration of licenced

CRM197 PCV 7 and PHi D-CV10 vaccinesis associated

with a large relative reduction in pneumococcal

MM.No beneficial effect wasseen for all cause

MM in high-risk infants,after early infancy,or in

older chldren with a history of respiratory ilness.

Mild adverse reactions(local redness oiswelling,

level, poin,tenderness) were seen ootecemmonly

in the groop receiving the pneumococcal conjugate

vaccines compared to placebo or control vaccines.No

dfferences in severe adverse effects were seen.

Epidemiology

•60-70% of children have at least 1 episode of AOM before age 3

•6-24 mo is the most common age group

commonly develops within a wk after a viral URI

•one third of children have had S3 episodes hy age 3; peak incidence January to April

Etiology

•bacterial- S. pneumoniae (decreasing since the introduction of PCV7 and PCV13), H. influenza, M.

calarrhalis, group A Streptococcus (GAS)

•less common - anaerobes (newborns) , Gram-negative enterics(infants)

•viral- more likely to spontaneously resolve

Risk Factors

•Eustachian tube related:

dysfunction/obstruction (URT1, allergic rhinitis, chronic rhinosinusitis,adenoid hypertrophy,

barotrauma)

inadequate tensor veil palatini function (deft palate)

genetic syndromes(DS,Crouzon, Apert)

cilia disruption (Kartagenger’ssyndrome, CE)

•genetic predisposition (family history, ethnicity - First Nations peoples and lnuit, low levels of

secretory IgA,or persistent biofilm in middle ear)

•behavioural and environmental exposures(not breastfed orshorter duration of breastfeeding,

prolonged bottle feeding, bottle feeding laying down,pacifier use,second-hand smoke exposure,

crowded living conditions/daycare,sick contacts)

•immunosuppression/deficiency (chemotherapy,steroids, DM, hypogammaglobulinemia,Cl;

)

Pathogenesis

•obstruction of Eustachian tube -» air absorbed in middle ear -> negative pressure (an irritant to middle

ear mucosa) -> edema of mucosa with exudate/effusion -> infection of exudate from nasopharyngeal

secretions

Minagcment of Atilt OtitlsMedia inChildren Sli

Months at Age and Older

JPaediatr Child Health 2016:21(l):39 44

Recommendations

• Mider disease is usually due lo viruses or low

virulence bacteria

• Resolves equity qiKkly with or without

antibiotics

• Bnlging tympanacmembcane (especially if yellow

or hemorrhagic) hasa high sensitivity for MM and

isamajor diagnostic criterion

• likelyhacttr.il

" -V

'

I : JJ

- ;u il l" c : : ;v. Ill

purulent discharge indicates bacterial AOM

• Indications foe immediate antibiotic treatment:

• Highly febrile ( >39'C|

• Moderately to severely systemcilly III

• Very severe olalgia

Significant rllnessfor 43 h

- Aotibiotic thevapjregime:

• Amonicil . n remains the clear drug ol choice

• 10-d course for children <2yrr

• S-d course for children >2 yr

•

-

:le; ins, p aaNrtaSMSSIMIt

at 48 Ir OR pwide an antibiotic prescription lo

parents to 6II il the child does not improve in 48 h

Clinical Features

•acute onset ofsymptoms

•triad of otalgia (best predictor of AOM), fever (especially in younger children), and conductive hearing

loss - not all symptomssuch as fever or hearing loss may be present

•rarely tinnitus, vertigo, and/or facial nerve paralysis

•otorrhea if tympanic membrane perforated

•infants/toddlers:ear-tugging (this alone is not a good indicator of pathology), hearing loss, balance

disturbances (rare),irritable, poor sleeping, vomiting and diarrhea, anorexia

•otoscopy of TM:hyperemia, bulging, pus may be seen behind TM,loss of landmarks(e.g. handle and

long process of malleus not visible), discolouration (hemorrhagic, grey, red,yellow)

Diagnosis

•requires middle ear eflfusion and signs of inflammation (most important is a bulgingTM)

•accurate diagnosis of AOM is very important to prevent antibiotic overuse

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P60 Paediatrics Toronto Notes 2023

Management

• symptomatic therapy: antipyretics/analgesics (e.g. acetaminophen or ibuprofen)

• watchful waiting if criteria met

• antibiotic therapy if <6 mo or moderate-severe illness:

• 1st line:high dose amoxicillin 75-90 mg/kg/d dosed BID x 5 d (10 d if age <2 yr, perforated I

'M, or

recurrent AOM) (if penicillin allergic: cefuroxime-axetil, ceftriaxone)

2nd line:amoxicillin-davulanic acid, cephalosporins: cefuroxime axetil, ceftriaxone, cefaclor,

cefixime

used when AOM unresponsive and clinical signs/symptoms persist beyond 48 h of antibiotic

treatment, or for treatment of otitis-conjunctivitissyndrome

• signs of a perforated TM should always be treated with antimicrobial therapy (most commonly topical

Ciprodex) and examined for complications

• prevention: parent education about risk factors, pneumococcal and influenza vaccines,surgery (e.g.

tympanostomy tubes)

• choice of surgical therapy for recurrent AOM depends on whether local factors (Eustachian

tube dysfunction) are responsible (use ventilation tubes), or regional disease factors (tonsillitis,

adenoid hypertrophy,sinusitis) are responsible

Complications

• extracranial: hearing loss and speech delay (secondary to persistent middle ear effusion (MEE),

TM perforation, extension ofsuppurative process to adjacent structures (mastoiditis, petrositis,

labyrinthitis), cholesteatoma, facial nerve palsy, middle ear atelectasis, ossicular necrosis, vestibular

dysfunction

• intracranial:meningitis, epidural and brain abscess,subdural empyema, lateral and cavernous sinus

thrombosis, carotid artery thrombosis

Management of Acute Otitis Modia

T

>6 mo of ago, generally healthy

Acute onset of illness

With or without fever and may or may not manifest other signs of middle

car dysfunction le g vomiting) or pain, depending on age and verbal skills

Suspected acute otitis media

Perforated tympanic

1

membrane

*

with purulent drainage

MEE present Without MEE

OR with MEE but non-bulging or midly

erythematous tympanic membrane

AM

Bulging tympanic membrane 4

Treat with antimicrobials for 10 d

Consider viral etiology such as RSV,

influenza, etc. or other infection

Reassess in 24-48 h if not clinically

improved or earlier if clinically

Irritable, difficulty sleeping, poor response worscning, 10 von(Y presence of olfusion

to antipyretics, severe otalgia

OR >39'C in absence of antipyretics

OR >48 h of symptoms

Mildly ill

Alert, responsive,no rigors,responding

to antipyretics,mild otalgia, able to sleep

<39'

C in absence of antipyretics

<48 h of illness

Moderately or scvcrly ill

and signs of middle car inflammation

such as bulging tympanic membrane

i 4

Treat with anbmicrobials for 10 d

if B mo-2 yr of age

and for 5 d if 22 V

After discussing with caregivers,observo

for 24-48 h and ensure follow-up

medical care (recommend analgesia)

If not clinically improved or if worsening,

treat with anbmicrobials 110 d

if 6 mo-2 yr of age and 5 d if >2 yr)

Figure 13. Management of acute otitis media

Flow diagram lor the management of children with suspected and confirmed acute otitis media -from CPS statement Feb 2016

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Otitis Media with Effusion

Definition

• presence of fluid in the middle ear without signs or symptoms of ear infection

Epidemiology

• most common cause of conductive hearing loss in children

• 90% of cases resolved by 3 mo

• 80-90% of all children have one episode before 6 yr

• 30-40% of affected children will experience recurrent episodes

Risk Factors

• same as AOM

Clinical Features

• fluctuating conductive hearing losst tinnitus

• fullness in ear, balance problems

• ± pain, low grade fever

« otoscopy of TM

• discolouration -amber or dull grey

meniscus fluid level behind TM

air bubbles

retraction pockets/TM atelectasis

flat tympanogram

most reliable finding with pneumatic otoscopy is immobility

Management

• expectant management appropriate if low risk for speech/language/learning difficulties

• ENT referral if unilateral OME >6 mo, bilateral OME >3 mo with hearing loss,or structural tympanic

membrane damage

• consider early ENT referral for children with craniofacial abnormalities or immunodeficiency

• surgical options include myringotomy with tympanostomy (ventilation) tubes ± adenoidectomy (if

tonsils enlarged or on insertion of second set of tubes after first set falls out)

• no role for antibiotics,glucocorticoids, antihistamines, or decongestants

Complications

• hearing loss,speech delay, learning problems in young children

• chronic mastoiditis

• ossicular erosion

• cholesteatoma especially when retraction pockets involve parsflaccida

• retraction of tympanic membrane, atelectasis, ossicular fixation

Gastroenteritis

• see Gastroenterology.G15

HIV Infection

• see Infectious Diseases. IL)

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P62 Paediatrics Toronto Notes 2023

Infectious Paediatric Exanthems

Table 27. Common Infectious Paediatric Exanthems

Disease Incubation

Period

Communicability Mode of

Transmission

Associated

Features

Management Outcomes and

Complications

Pathogen(s) Rash

Parvovirus B19 Low-risk ol

transmission once

symptomatic

Respiratory

secretions or

infected blood

Initial 7-10 d of flu- ltke

illness and fever

Rash maybe warm,

non-tender, and

pruritic

less common

presentations include

Supportive Rash fades over

dtowk.butmay

reappear mo later

with sunlight,

exercise

Transient Aplastic

crisis (especially if

chronic hemolytic

anemia)

Erythema

Infecliosum (i.e.

Fifth Disease/

Slapped Cheek)

4 -14 d Appearance:

uniform,

erythematous.

maculopapular

‘lacy'rash

liming: 10 -17 d

after symptoms

(immune response) ‘gloves and socks

Distribution: syndrome' or STAR

bilateral cheeks complex (sore throat,

(‘slapped cheeks') arthritis,rash)

with circurnoral

sparing;may

affect trunk and

extremities

Gianotti-Crosti

Syndrome

(i.e.Papular

Acrodermatitis)

EBV and Hepatitis Variable

B virus

(majority)

Supportive

Pain control

None None Asymptomatic or Resolves in 3-12 wk

pruritic

Appearance:

symmetric papules and/or

Distribution:lace, hepatosplenomegaly

cheeks,extensor

surfaces of the

extremities, spares

trunk

Viral prodrome

May have

lymphadenopalhy

Hand.Foot,and Coxsackie group A 3-5 d

Mouth Disease

Likely 1-7 d after Direct and indirect

symptomsbut may be contactwith

up to months

Enanthem:vesicles

in the POSTERIOR

Appearance: Supportive

vesicles and

pustules on an oral cavity (pharynx,

erythematous base longue)

Distribution:mouth,

buttocks,acral,bul

may extend up the

extremity

Resolves inIwk

Mainly dehydration

infected bodily

fluids,fecal-oral

Herpes Simplex HSV1.2 1-26 d Direct contact,

often through

saliva,vertical

transmission at

barlh.or sexual

contact

Grouped vesicles on Enanthem:vesicles/

an erythematous erosions in the

ANTERIOR oral cavity

Ibuccal mucosa,

tongue)

May present with

herpetic whitlow

(autoinoculation)

Mainly supportive

Consider oral or

topical antivirals

Local:secondary

skin infections,

keratitis,

gingivostomatitis

CNS:encephalitis

Disseminated

hepatitis. DIC

Eczema herpeticum

base

Kawasaki Disease SeeP9S

Morbillivirus 8 13 d 4 d before and alter Airborne Prodrome of cough,

cotyra.conjunctivitis

PCs)

Enanthem:Koplik’s

Infected:

supportive,some

evidence for

vitamin A.

Unimmunized

contacts:measles

vaccine within

72 hoi exposure

or IgG within 6 d of

exposure

Respiratory

isolation,report to

Public Health

Prevention:MMR

vaccine

Supportive

Diagnosis

confirmed using

viral cultures

(nasopharyngeal

andrcclal swabs)

Supportive

Secondary bacterial

infections:

AOM.sinusitis,

pneumonia

Encephalitis

Rare:myocarditis.

pericarditis.

thrombocytopenia.

Stevens-Johnson

syndrome,GN.

subacute sclerosing

panencephalitis

Measles Appearance:

erythematous

maculopapular

Timing:3 d after

start ofsymptoms spots

Distribution:starts 1-2 d before rash

rash

at hairline and Desquamation

spreads downwards Positive serology for

withsparing of measles IgM

palms and soles

Non-Specific

Enteroviral

Exanthems

Enteroviruses Variable Direct and indirect

contactwith

infected bodily

fluids

Polymorphous rash Systemic involvement

(macules,papules, israre,but possible

vesicles,petechiae.

urticaria)

Variable Self-limiting

Droplet transmission Saliva

Perinatal:

transplacental

infection,getmline

cell integration

High grade lever 3-5 d

Common:

Self-limiting

CNS:febrile

seizures (10-25%),

aseptic meningitis

Thrombocytopenia

Roseola Human herpes virus S-15 d

(HHV) 6

Appearance:

blanching,pink,

maculopapular irritability,anorexia.

Timing:appears lymphadenopalhy,

once fever subsides eiythcmalous IM and

Distribution:starts pharynx.Nagayama

at the neck and spots (erythematous

trunk and spreads papules on soft palate

to the face and and uvula)

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extremities less common:cough,

coiyza.bulging

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P63 Paediatrics Toronto Notes 2023

Table 27. Common Infectious Paediatric Exanthems

Disease Pathogen(s) Incubation

Period

Communicability Mode of

Transmission

Associated

Features

Outcomes and

Complications

Rash Management

14-21 d 7 d before and alter Droplet

eruptions

Prodrome of low grade Supportive

fever and occipital/ Deport to Public

retroauricular nodes Health

STAR complex (sore Prevention: MM It

Rubella Rubivirus Appearance:pink,

maculopapular

Timing:1-5 d after

start olsymptoms

Distribution:starts throat, arthritis,rash) vaccine

on lace and spreads Positive serology lor

to neck and trunk rubella IgM. Caution to

pregnanlwomenwith

Excellent prognosis

with acquired

disease

Arthritis may last

days to weeks

Encephalitis

Irreversible defects

in congenitally

infected patients

(i.e. congenital

rubella syndrome)

exposure

Scarlet Fever

Varicella

See«5

10 -21 d 1-2 d pre-eruptions Direct contact,

and 5 d post-eruption inhalation of

lesion aerosols,

aerosol!red

respiratory

secretions

Appearance:groups Significant pruritus

of skin lesions,

polymorphic,from

macules lopapules lesions which may

to vesiclestocxusls become pustular or

Timing:1-3d after ulcerate. Caution to

start olsymptoms pregnant women

Distribution:

generalized

Supportive

Avoid salicylates suptainfedion,

(due to risk of Reye necrotizing fasciitis

syndrome)

Consider antivirals encephalitis and

Respiratory and cerebellar ataxia

Systemic: hepatitis.

Varicella zoster Skin:bacterial

virus Malaise,fever

Enanlhcm: vesicular

CNS: acute

contact

isolation, report lo DIC

Congenital

varicella syndrome

if intrapartum

infection

Public Health

Prevention:

varicella vaccine

Infectious Mononucleosis

Definition

• systemic viral infection caused by EBV with multiviscera] involvement; often called “ the great

imitator"

Epidemiology

• peak incidence betss'een 15-19 yr

• -50% of children in developed countries have a primary EBV infection by 5 yr, but <10% of children

develop clinical infection

Etiology

• EBV: a member of herpesviridae

• transmission is mainly through infected saliva ( “kissing disease”) and sexual activity (less

commonly); incubation period of 1-2 mo

Risk Factors

• infectious contacts,sexually active, multiple sexual partners

History

• prodrome: 2-3 d of malaise, anorexia

• infants and young children: often asymptomatic or mild disease

• older children and adolescents: malaise, fatigue, fever,sore throat, abdominal pain (often LUQ),

headache, myalgia

Physical Exam

• classic triad:febrile, generalized non-tender lymphadenopathy, pharyngitis/tonsillitis (exudative)

• ± hepatosplenomegaly

• ± periorbital edema, ± rash (urticarial, maculopapular,or petechial) - more common after

inappropriate treatment with (3-lactam antibiotics

• any “-itis" (including arthritis, hepatitis, nephritis, myocarditis, meningitis, encephalitis, etc.)

Investigations

• heterophile antibody test (Monospot'test)

• 85% sensitive in adults and older children, but only 50% sensitive if age <-l yr

false positive results with HIV, SLE, lymphoma, rubella, parvovirus

• EBV titres (if negative heterophile test or clinical suspicion remains high)

• CBC and differential, blood smear:reactive lymphocytes, lymphocytosis, Downey cells ± anemia ±

thrombocytopenia

• throat culture to rule outstreptococcal pharyngitis

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Management

• supportive: adequate rest, hydration,saline gargles, and analgesics forsore throat

• splenic enlargement is often not clinically apparent so all patients should avoid contactsports for 6-8

wk

• if airway obstruction secondary to nodal and/or tonsillar enlargement is present (especially younger

children), admit for steroid therapy

Prognosis

• most acute symptoms resolve in 1-2 wk,though fatigue may last for mo

• short-term complications:splenic rupture, Guillain-Barre syndrome

Infectious Pharyngitis/Tonsillitis

Definition

• inflammation of the pharynx, especially the tonsils if present, causing a sore throat

Etiology

• viral (~80%): adenoviruses, enteroviruses, coxsackie, upper respiratory tract viruses, HBV,CMV,

COV1D-19

• bacterial (~20%):mainly GAS, Af. pneumoniae (older children),N.gonorrhoeae (sexually active),C.

diphtheriae (unvaccinated), /•

'

. necrophorum (anaerobe causing Lemierre syndrome)

• fungal:Candida

Epidemiology

• season: GAS pharyngitis more common in late winter or early spring; viral all year long

• age:GAS pharyngitis peak incidence at 5-12 yr and uncommon <3 yr; viral pharyngitis affects all ages

Presentation

• GAS:sore throat (may be severe), febrile, malaise, headache, abdominal pain, N/ V, absence of other

UKTT symptoms,pharyngeal/tonsillar erythema and exudates, enlarged (>1 cm) and tender anterior

cervical lymph nodes, palatal petechiae,strawberry tongue,scarlatiniform rash

• viral:sore throat (often mild), conjunctivitis,cough, rhinorrhea, hoarseness, diarrhea, flu-like

symptoms (fever, malaise, myalgias), absent/mild tonsillar exudates, minor and non-tender

adenopathy, viral exanthems

Investigations

• scores are used to predict if throat culture will be positive (e.g.m-CENTOR score)

» these score systems have not been found to be sensitive or specific enough to diagnose GAS in

children and adolescents with sore throat

• suspected diagnosis of GAS pharyngitisshould be confirmed with a rapid streptococcal antigen test

and a follow-up throat culture if the rapid test is negative

Management

• antibiotics (for GASIS. pyogenes)

• penicillin V or amoxicillin or erythromycin (if penicillin allergy) x 10 d

• can prevent rheumatic fever if given within 9 d ofsymptoms;does NOT alter risk of post

-

streptococcal GN

• supportive: hydration and acetaminophen for discomfort due to pain and/or fever

• follow-up: if uncomplicated course, no follow-up or post-antibiotic throat cultures needed

• prophylaxis: tonsillectomy may be considered for severe, recurrent streptococcal tonsillitis

Complications

• preventable with antibiotics: AOM,sinusitis,cervical adenitis, mastoiditis, retropharyngeal/

peritonsillar abscess,sepsis

• immune-mediated complications:scarlet fever, acute rheumatic fever, post-streptococcal GN, reactive

arthritis, paediatric autoimmune neuropsychiatric disorder associated with GAS (PANDAS)

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P65 Paediatrics Toronto Notes 2023

SCARLET FEVER

• diffuse erythematous eruption

• delayed-type hypersensitivity reaction to pyrogenic exotoxin produced by GAS

• requires prior exposure to S.pyogenes

• acute onset of fever, sore throat,strawberry tongue

• 24-48 h after pharyngitis, rash begins in the groin, axillae, neck, antecubital fossa; Pastia’

slines may

be accentuated in flexural areas

• within 24 h,sandpaper rash becomes generalized with perioral sparing, non-pruritic, non-painful,

blanchable

• rash fades after 3-4 d, may be followed by desquamation

• treatment is penicillin, amoxicillin,or erythromycin x 10 d

RHEUMATIC FEVER

• inflammatory disease due to antibody cross-reactivity following GAS infection

• affects ~1 in 10000 children in developed world;much more prevalent in developing nations; peak

incidence at 5-15 yr

• clinical diagnosis based on|ones Criteria (revised)

requires 2 major OR 1 major and 2 minor PLUS evidence of preceding strep infection (history of

scarlet fever, GAS pharyngitis culture, positive rapid Ag detection test,ASOIs)

major:carditis and valvulitis, arthritis,CNS involvement (Sydenham chorea),subcutaneous

nodules,erythema marginatum

minor: arthralgia,fever, tESR or CRP, prolonged PR interval

• treatment: penicillin or erythromycin for acute course x 10 d, prednisone ifsevere carditis

• secondary prophylaxis with daily penicillin or erythromycin

• complications

acute:myocarditis, conduction system aberrations (sinustachycardia, atrial fibrillation),

valvulitis (acute mitral regurgitation), pericarditis

chronic:valvular heart disease (mitral and/or aortic insufficiency/stenosis), infectious

endocarditis ± thromboembolic phenomenon

» onset of symptoms usually after 10-20 yr latency from acute carditis of rheumatic fever

m-CENTOR Score for Probability of

Streptococcal Pharyngitis

For patients presenting with sore throat/

pharyngitis and URTI symptoms:

Must be >3 yr

Cough — no cough (+1)

Exudates or Swelling — tonsillar

exudates/swelling (+1)

Nodes — anterior cervical adenopathy

Ml

Temperature-history of fever or

temperature >38°C (+1)

Only Young — patients <15 y/o (+1)

Rarely Elder- patients >45 y/o (-1)

Interpretation

m-CENTOR Probability Recommendation

Score olstrep

POST-STREPTOCOCCAL GLOMERULONEPHRITIS pharyngitis

• most common in children ages 4-8 yr; M>1

;

• antigen-antibody mediated complement activation with diffuse, proliferative GN

• occurs 1-3 wk following initial GAS infection (skin or throat)

• clinical features vary from asymptomatic, microscopic and macroscopic hematuria (cola-coloured

urine) to all features of nephritic syndrome (see Nephritic Syndrome, P83)

• diagnosed upon clinical findings of acute nephritis and recent GAS infection.It can be confirmed

with elevated serum antibody titres againststreptococcal antigens(ASOT, anti-DNAase B),low serum

complement (C3)

• management

symptomatic:fluid and sodium restrictions;loop diureticsfor HT'N and edema

in severe cases, may require dialysis if renal function significantly impaired

treat with penicillin or erythromycin (if penicillin allergy) if evidence of persistent GAS infection

. 95% of children recover completely within 1-2 wk;5-10% have persistent hematuria

0 1-2.5% No further testing or

antibiotics 1 $•10%

2 11-17% Consider rapid

strep testing aod.br

culture

Consider rapid

strep testing and/

or culture. Empiric

antibiotics nay

be appropriate

depending on

scenario

3 28-35%

»4 51-53%

Meningitis

Definition

• inflammation of the meninges surrounding the brain and spinal cord

Epidemiology

• peak age: < I yr;90% of paediatric cases occur in children age <5 yr

Etiology

• viral: enteroviruses, human parechoviruses, HSV

• bacterial: age-related variation in specific pathogens

• fungal and parasitic meningitis also possible

• most often due to hematogenousspread or direct extension from a contiguoussite

Risk Factors

• unvaccinated

• immunocompromised: asplenia, DM, HIV, prematurity

• recent or current infections: AOM,sinusitis, orbital cellulitis

• neuroanatomical:congenital defects, dermalsinus, neurosurgery, cochlear implants, recent head

trauma

• exposures:daycare centres, household contact,recent travel

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