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P-12 Paediatrics Toronto Notes 2023

Gastroesophageal Reflux

Epidemiology

• extremely common in infancy (up to 50%) but rarely causes pathology (i.e.GERD)

Clinical Features

• passage ofstomach contents into esophagus,may cause regurgitation or vomiting typically soon after

feeding, non-bilious, rarely contains blood,small volume (<30 mL)

• should suspect GEKD,defined as when gastroesophageal reflux causes troublesome symptoms/

complications:

infant:poor weight gain, irritability,sleep disturbance,respiratory symptoms(coughing,

choking,wheezing)

older chiId /adolescent:abdominal pain/heartbum, dysphagia, asthma, recurrent pneumonia/

upper respiratory infections (if aspirating), recurrent otitis media, upper airway symptoms

(chronic cough, hoarseness), dental erosions

Investigations

• thriving baby requires no investigation

• GERD generally can be a clinical diagnosis,diagnostic investigations rarely done but may include:

upper Gl series- assesses anatomy and motility disorder

» esophageal pH - assessesfrequency and duration of acid exposure, not a definitive diagnostic test

upper endoscopy and esophageal biopsy -rule out other conditions that mimic GERD symptoms

(e.g. eosinophilic esophagitis), assesses GERD-related esophageal injury

• warning signs of associated disorders requiring further investigations: bilious vomiting, Gl tract

bleeding, forceful vomiting,fever, lethargy, hepatosplenomegaly, bulging fontanelle, micro/

macrocephaly,seizures, abdominal tenderness/distension,suspected genetic, metabolic syndrome,or

chronic disease

Management

• conservative (infant):thickened feeds,frequent and smaller feeds, elevation of head,changing formula

to hydrolyzed protein or amino acid based formula,starting solid foodsif age appropriate

breastfeeding infants-sequential elimination diet by mother including milk, beef,soy, and egg

• conservative (older children/adolescent):same as adult management

• medical

• short

-term parenteral feeding to enhance weight gain

PPI, H2-blocker:decreases gastric acidity,decreases esophageal irritation

recommended when failure of conservative measures, moderate -severe disease or biopsyproven esophagitis

D2 antagonist (domperidone,metodopramide): generally not recommended for GERD, reserved

when concurrent gastroparesis

acid-suppressants or motility agents not recommended for infants with uncomplicated rcllux

• interventional (indicated for failure of medical therapy):

Nissen fundoplication

insertion of gastrojejunal tube for post-pyloric feeds

• several of these recommendationsshould be used cautiously in preterm infants given higher risk of NEC

Complications

• esophagitis, oral feeding aversion, poor weight gain, aspiration,strictures, Barrett'

s esophagus

Tracheoesophageal Fistula

• see General and Ihoracic Suruerv. GS75

Pyloric Stenosis

• see General and Ihoracic Surgery, GS73

Duodenal Atresia

• see General and Ihoracic Surgery,GS74

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Malrotation of the Intestine

• see General and Ihoracic Surgery, GS73

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P13 Paediatrics Toronto Notes 2023

Diarrhea

•definition of diarrhea varies with diet and age (stool normalcy difficult to define in children)

•infants > increase in stool frequency to twice as often per d ; older children > 3+ loose or watery

stools/d

•duration: acute:<2 wk; chronic: >2 wk

Pathophysiology

•osmotic:due to non-absorbable solutes in Cil tract (e.g. lactose intolerance)

•secretory:increased secretion of Cl ions and water in intestinal lumen (e.g. bacterial toxin)

•malabsorption:less time for absorption due to increased motility or fewer villi to absorb (e.g.short

bowel syndrome)

History

•frequency, duration, quality of diarrhea

•associated symptoms (e.g. fever, vomiting, abdominal pain, hematochezia)

•recent antibiotic use or travel

•elements of diet

Physical

•vital signs and complete examination to determine clinical status and hydration state

Investigations

•acute diarrhea (well child with non-bloody diarrhea often requires no further investigations)

• stool for C&S,O&P, electron microscopy for viruses, difficile toxin, microscopy ( leukocytes

suggestive of invading pathogen), blood and urine cultures, CBC, electrolytes, BUN, Cr, glucose,

abdominal imaging

•chronic diarrhea

• serial heights, weights, growth percentiles

if child growing well and thriving, workup is limited (stool cultures as above,stool reducing

substances)

• red Hags: poor growth, chronic rash, other serious infections, hospitalizations for dehydration

(require full workup)

stool: consistency, pH, reducing substances, microscopy,occult blood, O&P,C&S, difficile

toxin, 3 d fecal fat. a-l

-antitrypsin clearance, fecal elastase

urinalysis, urine culture

CBC, differential, ESR/CKP,smear, electrolytes, total protein, albumin, carotene, Ca1 , POt}-,

Mg-'

, l e, ferritin, folate, fat-soluble vitamins, P I T, INK

sweat chloride, celiac screen, thyroid function tests, urine VMA and HVA, HIV test, lead

levels

CXR, upper Gl series and follow-through

specialized tests: endoscopy,small bowel biopsy

Differential Diagnosis

Diarrhea is defined as an increase in

frequency and/or decreased consistency

of stools compared to normal

Normal stool volume

Infants:5-10 g/k g/d

Children: 200 g/d

Diarrhea Red Flags

Bloody stool, fever,pctechiae or

purpura, signs of severe dehydration,

weight loss/FTT

Common

o

Antibiotics that Can Lead to

C. difficile Infection

• Fluoroquinolones

, Clindamycin

• Penicillin < broad spectrum)

• Cephalosporins (broad spectrum)

Table 21. Differential Diagnosis of Diarrhea

Infectious Non-infectious

Viral

Rotavirus

Norwalk

Enteric adenovirus

Bacterial

Solmonello

Campylobacter

Shigella

Pathogenic f. coli

Yersinia

C. difficile

Parasitic

Ciordio lamblia

[nlamoeba histolytica

Antibiotic-induced

Non-specific: associated vrith systemic

inlection

Hirschsprung's disease

Toxin ingestion

Primary disaccharidase deficiency

Intussusception

Acute

Chronic 0-3 mo 3 mo- 3 yr 3 — 18 yr Uncommon

Drug-induced

Chronic constipation

NoFTT Gl infection Gl infection

Toddler's diarrhea

Gl infection

Lactase deficiency

Irritable bowel syndrome DTI

Disaccharidase deficiency. Celiac disease

food protein induced

allergic proctocolitis (FPIAP)

FTT IBD Short bowel syndrome

Endocrine (thyrotoxicosis, Shwachman-Diamond syndrome

Addison's)

Neoplastic

Ipheochromocytoma,

lymphoma)

i- y

CE Autoimmune Enteropathy

Hirschsprung's Disease Eosinophilic Gastroenteritis

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P I I Paediatrics Toronto Xotes 2023

Gastroenteritis

History

• non-specific:diarrhea, vomiting, fever, anorexia, headache, myalgias, abdominal cramps

• viral causes most common, bacterial and parasitic agents more common in older children (2-4 yr)

• recent infectious contacts:symptoms usually begin 24-48 h after exposure

Physical Exam

• febrile

• dehydrated: must assess extent (see Approach to Infant/Child with Dehydration, P3S )

Investigations

• not usually necessary in young children

• CBC,electrolytes, and stool studies may be indicated in severe cases, if IV hydration required or

atypical presentation

• stool analysis:leukocytes/erythrocytessuggests bacterial or parasitic etiology

Complications

• viral gastroenteritis usually self-limiting (lasts 3-7 d in most cases)

• adverse effects related to hypovolemia,shock, tissue acidosis, and rapid onset and over-correction of

electrolyte imbalances

• death in severe dehydration (rare in developed countries)

Table 22. Gastroenteritis

Viral Infection Bacterial Infection

Etiology Most common cause of gastroenteritis

Commonly:rotaviruses (most common), enteric

adenovirus,norovirus|typically older children)

Salmonella,Campylobacter,Shigella,pathogenic

f. co//. Yersinia. C.difficile

Clinical Features Severe abdominal pain

High fever

Slight fever,malaise, vomiting, vague abdominal pain Bloody diarrhea

Daycare.

Bacteria

Associated with URTIs

Resolves in 3-7 d

Risk Factors young age. sick contacts,immunocompromised

I infection:travel,poorly cooked meat,poorly refrigerated foods, antibiotics

Prevention and treatment of dehydration most important (see Approach to lolaol/Child with Dehydration.P3S\

Early refeeding advisable, with age- appropriate diet upon completion ofrehydralion

Ondansetron for suspected gastroenteritis with mild to moderate dehydration or failed ORT and significant vomiting

Antibiotic or anliparasitic therapy when indicated, antidiarrheal medications not indicated

Management

Notify Public Health authorities if appropriate

Promote regular hand- washing and return to school 24 h after last diarrheal episode to prevent transmission

Rotavirus vaccine

Toddler’s Diarrhea

Epidemiology

• most common cause of chronic diarrhea during infancy

• onset between 6-36 mo of age,resolves spontaneously between 2-4 yr

Clinical Features

• diagnosis of exclusion in thriving child

• 4-6 bowel movements per d

• diet history (e.g. excess juice intake overwhelms small bowel resulting in disaccharide malabsorption)

• stool may contain undigested food particles

• excoriated diaper rash

Management

• reassurance that it is self-limiting

• IIs (adequate Fibre,normal Fluid intake, lower dietary Fat (35-40%), discourage excess Fruit juice)

Lactase Deficiency (Lactose Intolerance)

Clinical Features

• chronic, watery diarrhea and abdominal pain, bloating associated with dairy intake

• primary lactose intolerance: crampy abdominal pain with loose stool (older children, more common

in Fast Asian and African descent)

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j

• secondary lactose intolerance: older infant,persistent diarrhea (decreased lactase production post

viral/bacterial infection, celiac disease,or IBD)

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P-15 Paediatrics Toronto Notes 2023

Diagnosis

• investigations usually not needed, trial of lactose-free diet

• symptom assessment with validated questionnaire after oral lactose load

• positive breath hydrogen test if >6 yr after oral lactose load with simultaneoussymptom assessment

• tests for lactase deficiency:small bowel biopsy, genetic testing

• demonstration of lactose malabsorption should be combined with assessment of intolerance

symptoms

Management

• lactose-free diet

• lactase-containing tablets/capsules/drops(e.g. Lacteeze’, Lactaid*)

Irritable Bowel Syndrome

• see Gastroenterology. G26

Celiac Disease

Celiac disease is associated with an

increased prevalence of IgA deficiency.

Since fTG is an IgA-detecting test you

must order an accompanying IgA level

•

Gastroenterology,G21 in children:presents at any age, often 6-24 mo with the introduction of gluten

in the diet

• poor weight gain, poor appetite, irritability,apathy, rickets, wasted muscles,flat buttocks,rarely

distended abdomen

• GI symptoms: N/V, edema, anemia, abdominal pain,diarrhea

• non-(il manifestations:iron-deficiency anemia,dermatitis herpetiformis,dental enamel hypoplasia,

osteopenia/osteoporosis,shortstature, delayed puberty, behavioural changes

• associated with other autoimmune disorders(e.g. Tl DM, thyroid disease)

A Celiac disease diet must avoid gluten

present in "BROW” foods

Barley

Cow’s Milk Allergy Oats(controversial)

Wheat

Pathophysiology

• cow’s milk allergy (CM A) may be either an IgE-mediated reaction or a non-lgE mediated reaction,

which is further classified as a food protein-induced allergic proctocolitis (EPIAP), food proteininduced enterocolitissyndrome (I

'

PIES),or food-protein-induced enteropathy

Clinical Features

• IgE-mediated CM A reactions occur within hours of exposure and are present on the skin

(i.e. urticarial, pruritus, etc.), upper and lower resp tractsymptoms(i.e. wheeze, cough, etc.),

gastrointestinal symptoms (i.e.abdominal pain, nausea/vomiting, diarrhea, etc.)

• non-lgE-mediated CMA reactions occur hoursfollowing ingestion, within few mo, presents with:

EPIAP: mild diarrhea,small amounts of bloody stools (common in young infant)

1-PIES:severe vomiting, and diarrhea,anemia, hematochezia

food protein-induced enteropathy:FIT,chronic diarrhea, hypoalbuminemia

• up to 50% of children intolerant to cow’s milk may be intolerant to soy protein as well

Investigations

• food challenge (gold standard),skin prick test,serum measurement of allergen-specific IgE, patch

testing

Management

• IgE-mediated CMA:stop exposure, epinephrine for acute anaphylactic reactions

• non-lgE-mediated CMA:stop, reintroduce milk at 6-8 mo, vast majority (>90%) will outgrow by 1 yr

• casein hydrolysate formula (Nutramigen*, Pregestimil*) or mother may sequentially remove cow’

s

milk protein, all bovine protein,soy protein, legumes (7 d washout), and continue breastfeeding (with

adequate calcium and vitamin D intake)

Inflammatory Bowel Disease

• see (itistroeiUerology. Ci22

Cystic Fibrosis

• see Respirolouv, KI 2

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P-16 Paediatrics Toronto Notes 2023

Constipation

•decreased stool frequency (<3stools/wk) and/or stool fluidity (hard, pellet-like)

FUNCTIONAL CONSTIPATION

•99% of cases of constipation

•Rome IV criteria for infants and toddlers <4 y/o:

>2 of the following for at least 1 mo:

<2 defecations/wk

history of excessive stool retention

history of large-diameter stools

history of painful or hard bowel movements

evidence of large fecal mass in rectum

• in toilet-trained children, the following additional criteria may be used:

at least 1 episode/wk of incontinence alter the acquisition of toileting skills

history of large-diameter stools that may obstruct toilet

Pathophysiology

•lack of fibre in diet or change in diet, poor fluid intake, behavioural

• infants:often occurs when introducing cow'

s milk after breast milk due to high fat and solute

content, lower water content

toddlers/older children: can occur during toilet training,starting school, or due to pain on

defecation,leading to withholding ofstool

» adolescents: often related to school stressors, anxiety/eating disorders

Management

•education:explanation of mechanism of functional constipation for parents/older children

•clean out: PEG 3350 flakes (1-1.5 g/kg/d, max 100 g/d), picosalax, PEGlyte*

•maintenance: adequate fluid intake (if <6 mo, 150 mL/kg/d), adequate dietary fibre (fruit, vegetables,

whole grains),stool softening (PEG 3350, mineral oil), appropriate toilet training technique (dedicated

time for defecation: 3-10 min, 1-2 x/d)

•children should be treated for at least 3-6 mo, and should not be weaned from maintenance therapy

until they arc having regular bowel movements without difficulty

•regular follow-up with ongoing support and encouragement is essential

Complications

•pain retention cycle: anal fissures and pain from withholding passing stool, chronic dilatation ±

overflow incontinence

HIRSCHSPRUNG’S DISEASE (Congenital Aganglionic Megacolon)

•see General and Ihoracic Surgery.GS74

OTHER ORGANIC DISORDERS CAUSING CONSTIPATION

•endocrine:hypothyroidism, DM, hypercalcemia

•neurologic:spinal cord abnormalities/trauma, NF

•anatomic:bowel obstruction, anus (imperforate, atresia,stenosis,anteriorly displaced)

•drugs:lead, chemotherapy, opioids

•celiac disease

•others

Abdominal Pain

ACUTE ABDOMINAL PAIN

History

• description of pain (location, radiation, duration, constant vs. colicky, relation to meals)

• associated symptoms: N/V,diarrhea,fever

Physical Exam

• abdominal exam,rectal exam, rash

Investigations

• may include CBC, differential, liver enzymes,lipase, bilirubin, creatinine, CKP, glucose, blood gas

urinalysis to rule out UTI, (J-HCG, abdominal, pelvic, and/or testicular imaging

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PI7 Paediatrics Toronto Notes 2023

Table 23. Differential Diagnosis of Acute Abdominal Pain

Gastrointestinal Hepatobiliary Miscellaneous

Tract

Genitourinary Hematologic Metabolic Drug and Toxins Pulmonary

Gaslrocntcritis Hepatitis Utl Sickle cell crisis Diabetic

ketoacidosis

Hypoglycemia

Porphyria

Erythromycin Pneumonia Functional pain

Appendicitis Cholecystitis Henoch Schonlein

purpura

Hemolytic uremic

syndrome

Urinary calculi Salicylates Diaphragmatic Infantile colic

pleurisy

Mesenteric Aden it’

s Cholelithiasis dysmenorrhea Lead poisoning Pharyngitis

Constipation Spleen -infarction.

rupture

Pancreatitis

Mittelschmerz Venoms Angioneurotic edema

Mediterranean lever

Neoplasms (i.e.

Wilms' tumour,

neuroblastoma, etc.)

Ileus

Abdominal Trauma

PID

threatened abortion

Intestinal Obstruction

(incarcerated hernia,

intussusception,

volvulus)

Peritonitis

Peptic Ulcer

Meckel's Diverticulum

Ectopic pregnancy

Hephtolilhiasis

tcsticulai torsion

Ovarian torsion

Ruptured ovarian cyst

Endometriosis

Hematocolpos

IBS

Food Poisoning

Lactose Intolerance

APPENDICITIS

• sec General and Thoracic Surgery. (iS35

• most common cause of acute abdomen alter aye 5

• clinical features:low grade fever, abdominal pain, anorexia, N/V (after onset of pain), peritoneal signs

(generalized peritonitis is a common presentation in infants/young children)

• treatment:surgical

• complications:perforation (common in young children), abscess

INTUSSUSCEPTION

• telescoping of segment of bowel into distalsegment causing ischemia and necrosis

Epidemiology

• 90% idiopathic, children with CF or GJ tube at significantly increased risk; M:F=3:2

• 60% <12 mo, 80-90% before age 2

Pathophysiology

• usual site: ileocecal junction; jejunum in children with GJ tubes

• lead point of telescoping segment may be swollen Peyer’s patches, Meckel’s diverticulum, polyp,

malignancy, bowel wall edema or submucosal bleeding secondary to HSP,structural abnormalities

Clinical Features

• “classic triad" (<15% patients) - abdominal pain, vomiting, red currant jelly stools

• often preceded by URTT

• sudden onset of recurrent, paroxysmal,severe periumbilical pain associated with inconsolable crying

and raising legs toward abdomen with pain-free intervals

• later vomiting (may be bilious) and rectal bleeding (late finding)

• shock and dehydration; lethargy may be only presenting symptom

Diagnosis

• air enema: both diagnostic and therapeutic

• AXR, U/S

Management

• air or saline/contrast enema can be therapeutic ( reduces intussusception in 75% of cases), reduction

under hydrostatic pressure,surgery rarely needed

• recurrence rate 10-15%, need to consider pathologic lead point

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P-18 Paediatrics Toronto Notes 202J

Chronic Abdominal Pain

Epidemiology

• prevalence: 10% ofschool children (peak at 8-10 yr),F>M

Etiology

• organic (<10%)

gastrointestinal

» constipation (cause vs. effect), infectious

IBD, esophagitis, peptic ulcer disease, lactose intolerance

anatomic anomalies, masses

pancreatic, hepatobiliary

« celiac disease

genitourinary causes:recurrent UT1, nephrolithiasis, chronic PID, Mittelschmerz

• neoplastic

• functional abdominal pain (90%): can be diagnosed when there are no alarming signs orsymptoms,

physical exam is normal; no further testing is required,unless high suspicion for organic cause

alarming symptoms include involuntary weight loss, deceleration of linear growth,G1 blood

loss,significant vomiting, chronic severe diarrhea, persistent upper or right lower quadrant pain,

unexplained fever,family history of IBD

can be furthersubclassified into functional dyspepsia ( pain in upper abdomen), irritable bowel

syndrome (alternating bowel movements), abdominal migraine (paroxysmal abdominal pain,

associated with anorexia, nausea, vomiting, pallor),functional abdominal pain syndrome

Chronic Abdominal Pain

Rule of 3s

3episodes of severe pain

Child >3y/o

Over 3 mo period

Red Flagsfor Organic Etiology of

Chronic Abdominal Pain

• Age <5

• Fever

• Localizes pain away from midline

. Anemia

• Evidence of Gl blood loss

. Rash

• Pain wakes child at night

• Travel history

• Prominent vomiting, diarrhea

. Weight loss or failure to gain weight

• Deceleration in linear growth

• Joint pain

,

Family history of IBD

, Abnormal or unexplained physical

exam findings

FUNCTIONAL ABDOMINAL PAIN

Clinical Features

• clustering episodes of vague, crampy periumbilical/epigastric pain,vivid pain description

• seldom awakens child from sleep, less common on weekends

• aggravated by exercise, alleviated by rest

• psychological factors related to onset and/or maintenance of pain,school avoidance

• psychiatric comorbidity: anxiety,somatoform, mood, learning disorders,sexual abuse, eating

disorders, elimination disorders

• diagnosis of exclusion

Investigations

• fecal studies (calprotectin, occult blood) and others based on clinical suspicion (e.g.CBC, HSR,

urinalysis,imaging, etc.)

Management

• continue to attend school

• manage any emotional or family problems, counselling,CBT

• trial of high fibre diet,or trial of lactose-free diet may be considered

medication rarely used,should be for symptom relief - acid reduction therapy for dyspepsia,

antispasmodic agents,smooth muscle relaxants for pain, non stimulating laxatives or

antidiarrheals for altered bowel pattern

• possible role for amitriptyline or gabapentin

• reassurance

Prognosis

• pain resolvesin 30-50% of children within 2-6 wk of diagnosis

• 30-50% of children with functional abdominal pain have functional pain as adults(e.g.IBS)

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P-19 Paediatrics Toronto Notes 2023

Abdominal Mass

Table 24. Differential Diagnosis for Abdominal Mass

Non-malignant Malignant

Renal(role: 50% of abdominal masses in

newborns aicicnalin origin)

Hydronephrosis

Polycystic kidney disease

Hamartoma

Nephroblastoma (Wilms' tumour)

Renal cell carcinoma

Adrenal Neuroblastoma

Ovarian tumours

lymphoma

Rhabdomyosarcoma

Retroperitoneal sarcoma

Ovarian

Other

Ovarian cysts

Hepatomegaly/splenomegaly

Pyloric stenosis

Abdominal hernia

leratoma

Fecal impaction

Table 25. Renal Etiologies of an Abdominal Mass

Abdominal Mass Benign or Malignant Clinical Features Management

Hydronephrosis Benign Usually asymptomatic

Urinary tract obstruction

Vesicoureteial reflux

Genetic counselling

Unilateral hydronephrosis >4 mm

in second trimester,a follow up

US scan in third trimesteris

performed

Persistent hydronephrosis >10

mm require postnatal evaluation

BP controlwith ACE inhibitors

Dietary sodium restrictions

Statins

Vasopressin receptor antagonists

Polycystic Kidney Disease Benign Progressive renal failure,

hypertension,urinary tract

infection,concentrating defects,

hematuria,nephrolithiasis,

flank pain

Asymptomatic abdominal

swelling

Abdominal pain (30-40%)

Hematuria (12-25%)

Fever and hypertension (25%)

Asymptomatic abdominal

swelling

Abdominal pain (30-40%)

Hematuria (12-25%)

Fevei and hypertension (25%)

Classic triad of Hank pain,

hematuria, and palpable

abdominal renal mass

Hamartoma Benign Surgery,chemotherapy,radiation

Wilm's Tumour Malignant Surgery,chemotherapy,radiation

Forlocalircd RCC.surgery is

curative

For advanced RCC.

immunotherapy and radiation

Renal Cell Carcinoma Malignant

Upper Gastrointestinal Bleeding

• sec Gastroenterology, (i28

Lower Gastrointestinal Bleeding

•see (

lastroenterolostv,(i30

Etiology

•acute

infectious(bacterial, parasitic)

antibiotic-induced (C. difficile)

NEC in preterm infants

anatomic

malrotation /volvulus, intussusception

Hirschsprung disease

Meckel’s diverticulitis

anal fissures, hemorrhoids

vascular/hematologic

HSP

HUS

coagulopathy

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P50 Paediatrics Toronto Notes 2023

•chronic

anal fissures (most common)

infectious colitis

IBD

IP1AP

allergic (milk protein)

structural

polyps (most are hamartomas)

coagulopathy

neoplasms (rare)

Physical Exam

•general exam: hemodynamic status,evidence of poor growth, fever

•anal and rectal exam: tags, fissures, anal fistulas, polyps, foreign body, blood per rectum

•stool appearance

• NG aspirate

•lower Cil bleed may present as melena (if it involves the small bowel) or hematochezia

Investigations

•stool cultures (C&S, C. difficile toxin)

•urinalysis and microscopy

•CBC,smear,differential, HSR,CRP, electrolytes, urea, Cr, 1NR, PTT, albumin, iron studies, amoeba

titers

•radiologic investigations

•Meckel s radionuclide scan

•Colonoscopy

Management

•acute stabilization:ABCs, volume and blood replacement, bowrel rest (NPO, NG tube)

•treatment dictated by etiology

•once stable, endoscopy and/or surgery as indicated

Genetics,Dysmorphisms,and Metabolism

• see Medical Genetics

Hematology

Approach to Anemia

CLASSIFICATION

• mechanism: decreased production (inadequate reticulocyte response) vs. increased destruction or loss

(adequate reticulocyte response)

• in the context of anemia, a normal reticulocyte count is inappropriate Normal Hb Values by Age

Age Hb Range (g1)

Anemia Newborn UI 20t

|

2«t 130-200 I I

Decreased reticulocytes Increased reticulocytes 3 mo 95-145

I I I

6 mo-6 yr

7-12 yr

Adult female

Adult male

105 -M0

Production problem Hemolysis Blood loss 110-160

t

1 120-160 4 I 140-180

Microcytic Normocytic Macrocytic Extrinsic to BBC

(antibody mediated)

Intrinsic to RBC

Iron deficiency

I 4 : ; t i 4 4

anemia,

thalassemia,

anemia of

chronic

disease,

lead poisoning,

sideroblastic

anemia

Megaloblastic

anemia

diseases IJIA. (Buand folate

SLE, IBD, RA), deficiency),

recent blood hypothyroidism,

alcohol

Anomia of

chronic Non-immunc

hemolysis

IDAT-)

Hemoglobinopathies Membrane Enzyme Immune

problem problem hemolysis

(DATA l 4 4

4

r i

loss L J

SCO, thalassemia Hereditary G6PD

spherocytosis deficiency TTP, HUS

Figure 11. Approach to anemia +

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P5I Paediatrics Toronto Notes 2023

Physiologic Anemia

•

• after

high

utero

birth

Hb

and

{>

,

increased

170

levels

g/L

start

) and

erythropoietin

to

reticulocyte

fall due to shorter

levels

count at

fetal

birth

RBC

is caused

lifespan

by

,decreased

a relatively

RBC

hypoxic

production

environment

(during

in

first

m

6-8 wk of life, there is virtually no erythropoiesis due to new Ol rich environment), and increasing

blood volume secondary to growth

• lowest levels about 100 g/1.at 8-12 wk (earlier and more exaggerated in premature infants); levels rise

spontaneously with activation of erythropoiesis

• red flags suggesting non-physiologic anemia may include Hb level lower than expected with

physiologic anemia,signs of hemolysis, orsymptoms of anemia

• usually no treatment required

Mean corpuscular volume (MCV) in

childhood varies with age

General rule:lower normal limit of MO/ -

70 age (yr) until 80 ft (adult standard)

Ferritin is an acute phase reactant,

therefore,normal or high ferritin does

not exclude iron deficiency anemia

during inflammation (e.g. infection)

Iron Deficiency Anemia

• most common cause of childhood anemia

• full term infants exhaust iron reserves by age 6 mo

• premature infants have lower iron reserves, therefore exhausted by age 2-3 mo if not supplemented

• common diagnosis between 6 mo-3 yr and 11-17 yr due to periods of rapid growth and increased iron

requirements; adolescents may also have poor diets and menstrual losses

Etiology

• children at risk:premature,maternal iron deficiency, LBW,low socioeconomic status (SES),etc.

• dietary risk factors:cow’

s milk in first year of life

age >6 mo: <2 servings/d of iron-fortified cereal,red meat,or legumes

• age <12 mo: use of low-iron formula (<10 mg/L); primary diet of cow, goat, orsoy milk

age 1-5 yr: >500 ml/d of non-iron fortified milk

• malabsorption syndrome (i.e. celiac disease, Crohn'

s disease, short bowel syndrome,etc.)

• blood loss

iatrogenic: repeated blood sampling (especially in hospitalized neonates)

allergic: cow's milk protein-induced colitis

gastrointestinal:1BD

Clinical Features

• usually asymptomatic until marked anemia

• symptoms may include:pallor,fatigue, pica (eating non-food materials), tachycardia,systolic murmur,

angular cheilitis, koilonychia (spoon nails)

Investigations

• CBC:low Hb, and MCV, reticulocyte count normal or high (absolute number low)

• Mcntzcr index (MCV/RBC) can help distinguish iron deficiency anemia from thalassemia

ratio <13 suggests thalassemia

ratio >13 suggests iron deficiency

• blood smear:hypochromic,microcytic RBCs, pencilshaped cells, poikilocytosis

• iron studies:low ferritin,other (low iron, high total iron binding capacity, high transferrin,low

transferrin saturation)

Prevention

• breastfed term infants:begin iron supplementation (1 mg/kg/d) at 4-6 mo, continuing until able to eat

S2 feeds/d of iron-rich foods

• non-breastfed (<50% of diet) term infants: give iron-fortified formula from birth

• premature infants: give iron supplements beginning at 2 wk (2-4 mg/kg/d, max 15 mg), continue at

least 2 mg/k/d until 1 yr

• no cow’s milk until 12 mo,early introduction of red meat and iron-rich vegetables:total daily iron

should be 11 mg (ages 6-12 mo), 7 mg (ages l-3yr)

• consider screening Hb levelsin infants not receiving iron-fortified formula at 9-12 mo, and earlier if

other risk factors present

Management

• encourage diverse, balanced diet, limit homogenized milk to 500 mL/d (ideally after meals)

• oral iron therapy: 4-6 mg/ kg/d elemental iron, divided BID to TID, for 3-6 mo to replenish iron stores

• increased reticulocyte count in 2-3 d (peaks d 5-7)

increased hemoglobin in 4-30 d

repletion of iron storesin 1-3 mo

repeat hemoglobin levels after 1 mo of treatment

• poor response to oral iron therapy: non-adherence,medication intolerance,ongoing blood loss, 1BD,

celiac disease,incorrect diagnosis

Complications

• can cause irreversible effects on development if untreated (behavioural and intellectual deficiencies)

• angular cheilitis, glossitis, koilonychia (spoon nails)

Iron deficiency is rare in children <6

mo in the absence of blood loss or

prematurity

r T

L J

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P52 Paediatrics Toronto Notes 2023

Vitamin K Deficiency

Etiology

• most commonly in infants <6 mo due to hepatic immaturity not efficiently utilizing vitamin K (in

preterm infants), having poor vitamin K stores,and low vitamin K content in milk,leading to vitamin

K deficiency bleeding (VKDB) previously known as hemorrhagic disease of the newborn (HDNB)

• non-classic presentation acquired later in life, often in association with chronic malabsorption (Le.CF,

celiac disease, IBD, biliary atresia, primary biliary cholangitis, primary sclerosing cholangitis,etc.),

liver failure, medications (i.e.antibiotics)

risk factorsfor non-classic presentation:maternal medication (i.e.antiepileptic drugs),chronic

malabsorption, no prophylaxis

Clinical Features

• VKDB due to relative deficiencies of vitamin K-dependent coagulation factors

generalized bleeding; cutaneous bleeding, mucosal bleeding (Gl, umbilicus),and/or intracranial

hemorrhage

early-onset (in first 24 h), classic (27 d),and late-onset (2-12 wk up to 7 mo,high occurrence of

ICH)

• acquired vitamin K deficiency symptoms may include:easy bruising,mucosal bleeding (i.e. epistaxis,

Gl bleed, hematuria, etc.)

Management

• VKDB managed urgently with 1V/SC vitamin K (1-2 mg).If there issevere bleeding,also administer

fresh frozen plasma or prothrombin complex concentrate

• prevented with vitamin K 1M injection (0.5-1 mg) at birth,can also be given orally as vitamin K

(doses:first feed, 1, 4,8 wk) for breastfed, term infants but higher risk of VKDB

• bleeding due to vitamin K deficiency of other acquired etiologies managed with PO/IM/SC/IV vitamin

K,with dose dependent on condition

Anemia of Chronic Disease

• see Hematology, H16

Sickle Cell Disease

• see Hematology.H21

Thalassemia

• see Hematology, H19

Hereditary Spherocytosis

• see Hematology, H24

Glucose-6-Phosphate Dehydrogenase Deficiency i i

G6PD deficiency protects against

• see Hematology parasitism of R8Cs(Le.malaria)

, H24

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P53 Paediatrics Toronto Notes 2023

Bleeding Disorders

• see Hematology. H28

Table 26. Evaluation of Abnormal Bruising/Bleeding

PFA PT PTT VllhC VWF Platelets Fibrinogen Extensive bruising in the absence

of lab abnormalities:consider child

maltreatment

Hemophilia A

Hemophilia B

von Willebrand Disease t

N II t N N *

N N t N N N N

II HOF t Nor

*

a N II

OIC N o r t t t a N a a

Vitamin K Deficiency

thrombocytopenia

N » N N N N

t N N N N a N

N-normii;OIC •disseminated intravascular coagulation:PFA •platelet function assay:VllhC •Factor VIII coagulant activity:VWF •von Willebrand

Factor

Immune Thrombocytopenic Purpura

Definition

• IIP is isolated thrombocytopenia (platelet count <100000/pL with normal white blood cell count and

hemoglobin)

Epidemiology

• most common cause ofsymptomatic thrombocytopenia in childhood

• peak age:2-5 yr, M>1

;

(slightly)

• incidence 5 in 100000 children per yr

Etiology

• caused by autoantibodies that bind to platelet membranes-> Pc-receptor mediated splenic uptake >

destruction of platelets

Clinical Features

• 60% present within 1 mo alter viral illness (e.g. UR'

11. chicken pox)

• sudden onset of petechiae, purpura, bleeding in an otherwise well child

• clinically significant bleed in only 3% (severe bleed more likely with platelet count <10) with <0.5%

risk of intracranial bleed

• no lymphadenopathy, no hepatosplenomegaly

• diagnosis made in well appearing patients with mucocutaneous bleeding without other systemic

symptoms orsigns and lab confirmation of1TP (diagnosis of exclusion)

• labs:thrombocytopenia with normal RBC, WBC

• bone marrow aspirate only indicated if red flags on history,exam, or lab studies

• differential diagnosis:leukemia, drug-induced thrombocytopenia, HIV, infection (viral),

immunodeficiency syndromes, autoimmune (SLE, autoimmune lymphoproliferative syndrome,

autoimmune hemolytic anemia)

Management

• involve family in management;shared decision-making

• no or mild bleeding - watchful waiting

• moderate bleeding (i.e.severe skin manifestations with some mucosal lesions and some troublesome

epistaxis or menorrhagia) -IVlg (1 g/kg) or steroids; if Rh-positive or DAT-negative can use anti-D

• severe (i.e. prolonged epistaxis, Cil bleeding, or intracranial hemorrhage) - immediate treatment with

IV steroids and IVlg; may use tranexamic acid as adjunct therapy

• treatment with IVlg or prednisone if mucosal or internal bleeding, platelets <10, or at risk of

significant bleeding (surgery, dental procedure, concomitant vasculitis, or coagulopathy)

• life-threatening bleed:additional platelet transfusion ± emergency splenectomy

• persistent (>3-12 mo) or chronic (>12 mo):re-evaluate;treat ifsymptoms persist

• supportive:avoid contactsports and ASA/NSAIDs

Diagnosis and Management olTypkalNevriy

Diagnosed Primary Immune thrombocytopenia

(IIP) of Childhood

J Pediatr Child Health 20t9;24(1):54

Recommendations

• Bane -narrow examination Is unnecessary in

children and adolescents with the typicalfeatures

of IIP or who fail IVlg therapy

• Children with no bleeding or mild bleeding (defined

asskin manifestations only,such as Musing and

petechiae) may he managed with observation

alone regardless olptatefet count

•Children with moderate hteedvig may hemanaged

with a single dose of IVlg (0.8-1giVg) or a short

course ol corticosteroids (typically prednisone 4

mg/kgiVf for 4 d)

•Children with severe bleeding(prolonged

epistaxis. lil Weeding,or ICH) require immediate

management with IV stem ds and IVlg aswell as

consideration lor IV traneiamic acid (IV 10 mg/kgl

dose every8 h)

• IVlg is used if a more rapid increase in the platelet

count isdesired

• Anti-0 therapy isonly nsedin Rti-posShre children

and not advised in children with a bemogotnn

concentration that isdecreased due to bleeding,or

with evidence ol autoimmune hemolysis

Suggestions

• Bone -narrow examination is also notnecessary in

similar patients prior to initiation of treatment with

corticosteroids or before splenectomy

• losinglot inhnudear antibodies is not necessary

In the evaluation of children and adolescents with

suspected IIP

Hemophilia

• see Hemalolottv. H32

von Willebrand’s Disease

• see Hematology, H3I +

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P54 Paediatrics Toronto Notes 2023

Oncology

• cancer is the second most common cause of death after injuries in children >1 yr

• cause is rarely known,but increased risk for children with:chromosomal syndromes (e.g.Trisomy 21),

cancer predisposition syndromes (e.g. Li-fraumenisyndrome), prior malignancies, neurocutaneous

syndromes, immunodeficiency syndromes,family history,exposure to radiation, chemicals, biologic

agents

• leukemias are the most common type of paediatric malignancy (30%),followed by brain tumours

(25%) and lymphomas(15%)

• some malignancies are more prevalent in certain age groups

• newborns: neuroblastoma, Wilms'

tumour, retinoblastoma

• infancy and childhood:leukemia, neuroblastoma,(.

'

NS tumours, Wilms’ tumour, retinoblastoma

adolescence:lymphoma, leukemia, gonadal tumours, germ cell tumours, thyroid cancers,

melanoma, bone tumours

• unique treatment considerations in paediatrics because radiation, chemotherapy, and surgery can

impact growth and development, endocrine function, and fertility

• good prognosis: treatments have led to remarkable improvements in overallsurvival and cure rates for

many paediatric cancers (>80%)

Most common cause of acute bilateral

cervical lymphadenopathy is viral illness

Lymphadenopathy

Clinical Features

• features of malignant lymphadenopathy:firm,discrete (not often), non-tender, enlarging, immobile,

worrisome location (i.e.supraclavicular or generalized), abnormal imaging findings or Woodwork,

constitutional symptoms

• fluctuance, warmth, or tenderness are more suggestive of benign nodes (infection)

Differential Diagnosis

• infection

• viral: URTI, EBV.CMV, adenovirus, HIV, measles,mumps, rubella, Hep B

bacterial: S.aureus,GAS, anaerobes, Mycobacterium (e.g. typical and atypical TB), cat scratch

disease (Bartonella), Rickettsia

other:fungal, protozoan

• autoimmune:rheumatoid arthritis,SLE,serum sickness

• malignancy:lymphoma,leukemia,metastatic solid tumours

• storage diseases:Niemann-Pick,Gaucher

• other:sarcoidosis, Kawasaki disease, histiocytoses

Investigations

• assess location,size, consistency, fixation, and tenderness of each node

• generalized lymphadenopathy (S2 body areas)

• GBG and differential, blood culture

• inflammatory markers (ESR, GRP)

serology: EBV, CMV and others as indicated by history and physical exam (e.g. HIV,fungal,

toxoplasmosis)

uric acid, LDH, electrolytes

-

CXR

tuberculin skin test

if indicated other blood work i.e. inflammatory panel (ANA, R1-, dsDNA)

biopsy:late biopsy (within 4 wk) if increasing in size,or >2 cm and unclear diagnosis or no

response to treatment. Do early biopsy ifsupraclavicular nodes, nodes >4 cm,or groups of nodes

with total diameter >3cm

• regional lymphadenopathy (I body area)

• period of observation if asymptomatic

trial of oral antibiotics

• ultrasound

biopsy (especially if persistent >4 wk and/or constitutional symptoms)

ifsupraclavicular lymphadenopathy:CXR to rule out mediastinal mass

Leukemia

r T

• see Hematology, H39 LJ

Definition

• leukemia is a cancer that startsin the bone-forming tissue (e.g. bone marrow), causing abnormal

blood cell production +

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P55 Paediatrics Toronto Notes 2023

Epidemiology

• mean age of diagnosis 2-5 yr but can occur at any age

• heterogeneous group of diseases

ALL (80%)

• AML (15%)

. CML (<5%)

• children with DS are 15 times more likely to develop leukemia

Clinical Features

• infiltration of leukemic cells into bone marrow results in bone pain and bone marrow failure (anemia,

neutropenia, thrombocytopenia)

• infiltration into tissues results in lymphadenopathy, hepatosplenomegaly, CNS manifestations,

testicular disease

• fever,fatigue, weight loss, bruising, bone pain, and easy bleeding

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

renal function, and blood culture

• specialized tests: BM ± lymph node biopsy, flow cytometry, cytogenetics, molecular studies

• hyperleukocytosis (total WBC >100 x lO’VL) is a medical emergency

presents clinically with respiratory or neurological distress caused by hyperviscosity of blood and

leukostasis

risk of 1CH, pulmonary leukostasissyndrome, tumour lysissyndrome

management:fluids, allopurinol/rasburicase,fresh frozen plasma/platelets to correct

thrombocytopenia, induction chemotherapy, avoid transfusing RBCs unlesssymptomatic (and

then use very small volumes),or leukapheresis in some centres

Management

• combination chemotherapy using non-cross resistant chemotherapy agents; allogeneic stem cell

transplantation for particular genetic subtypes, poorly responsive disease, or recurrent disease

• supportive care and management of treatment complications

febrile neutropenia:see Infectious Diseases, 1D44

tumour lysissyndrome:see Hematology, H54

Prognosis

• 80-90% 5-yr event-free survival for ALL, 50-60% 5-yr survival for AML

• patients are stratified into standard risk and high-risk based on WBC and age; other prognostic factors

include presence of CNS/testicular disease, immunophenotype, cytogenetics, and initial response to

therapy (most important prognostic variable)

Back pain in children must always be

investigated!

Unlike adults, back pain in children often

pointsto a pathological process

Lymphoma

• see Hematology, H47

Epidemiology

• Hodgkin lymphoma: incidence is bimodal, peaks at ages 15-34 and >50 yr

• non- Hodgkin lymphoma: incidence peaks at 7-11 yr

Clinical Features

• Hodgkin lymphoma

most common presentation is persistent, painless, firm,rubbery, cervical orsupraclavicular

lymphadenopathy

can present as persistent cough or dyspnea (secondary to mediastinal mass) orless commonly as

splenomegaly, axillary, or inguinal lymphadenopathy

constitutional symptoms in 30% of children

• contiguous spread

• non-Hodgkin lymphoma

• presents as enlarging, non-tender lymphadenopathy

• includes most commonly mature B cell lymphoma (Burkitt, diffuse large B cell),