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History

• signs and symptoms variable and dependent on age,duration of illness, and host response to infection

• infants:fever,lethargy,irritability, poor feeding, vomiting, diarrhea, respiratory distress,seizures

• children:fever, headache, photophobia, N/V, confusion, back/neck pain/stiffness, lethargy, irritability

Physical Exam

• infants:toxic, hypothermia, bulging anterior fontanelle, respiratory distress,apnea, petechial/

purpuric rash, jaundice

• children:toxic,decreased LOG, nuchal rigidity, Kernig’s and Brudzinski'

ssigns,focal neurologic

findings, petechial/purpuric rash

Investigations

• blood work:GBC, electrolytes,Cr, BUN,glucose, C&S, PTT/1NR

• LP required for definitive diagnosis

• Gram stain, bacterial C&S, WBC count and differential, KBC count, glucose, protein

concentration

acid-fast stain if suspect TB

PGR for specific bacteria if available (helpful if already treated with antibiotics)

urinalysis and urine G&S in infants.Gram stain and culture of petechial/purpuric lesions

HSV and enterovirus PGR if suspected

contraindications: thrombocytopenia, DIG,signs of raised 1GP, unstable patient, known/

suspected underlying anatomical abnormalitiesto the lumbar region

decision making around LP should NOT delay empiric antibiotic therapy

Table 28. CSF Findings of Meningitis

Component Normal Child Normal Newborn Bacterial

Meningitis

Viral Meningitis Tuberculosis

Meningitis

s5 0-30 10-1000 (can be

normal)

100-10000 (can be Usually <100

normal)

Usually <100 50-1000 (can be

normal)

Usually <100

Lymphocytes

|x10*/l)

Neutrophils («10 M.) 0 0

Glucose (CSF:Blood ) >0.((or >2.5mmol/L) ?0.6|or »2.0 mmol / L) <0.4 (can be normal) Usually normal

Protein (g/l)

<0.3(can be normal)

<0.4 *1.0 >1.0 (can be normal) 0.4 1-5(Can be normal) -1.0 (can be

normal)

Moditied from https://www.rclt.org.au/difiicolguide/guidelineJndex/CSFJnterpietation/

Management

• supportive care

preservation of adequate cerebral perfusion by maintaining normal BP and managing IGP

close monitoring of fluids, electrolytes, glucose,acid-base disturbances, coagulopathies

• bacterial meningitis

ifsuspected or cannot be excluded, commence empiric antibiotic therapy while awaiting cultures

or if LP contraindicated or delayed

adjuvant dexamethasone BK1-ORE antibiotic for Hib meningitis; consider for those >6 wk with

pneumococcal meningitis

isolation with appropriate infection control procedures until 24 h after culture-sensitive antibiotic

therapy

fluid restrict if any concern for SIADH

hearing test

report to Public Health; prophylactic antibioticsfor close contacts of Hib and N.meningitidis

meningitis

• viral meningitis

mainly supportive (except for HSV)

acyclovir for HSV meningitis

report to Public Health

• prophylaxis:appropriate vaccinationssignificantly decrease incidence of bacterial meningitis (see

Routine Immunization, PS)

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Table 29. Antibiotic Management of Bacterial Meningitis

Ago Main Pathogens Antibiotics

Signs of Meninglsmus

0-28 d CBS, f. coli,listeria

Other:Gram-negative bacilli

Overlap of neonatal pathogens and those seen Cefotaxime vancomycin (+ ampicillin if

immunocompromised)

S. pneumoniae.H.meningitidis,H. influenioe Ceftriaxone * vancomycin

(If penicillin alergic:vancomycin •rifampin)

Ampicillin * cefotaxime

BOMConthehead

Brudzinski'ssign

Opisthotonos*

Nuchal rigidity

Kernig's sign

'Opisthotonos:rigid spasm of the body,

with the back fully arched and the heels

and head bent back

28-90d

in older children

>90 d

Complications

• mortality:neonate 15-20%,children 4-8%; pneumococcus > meningococcus > Hib

• acute:S1ADH,subdural effusion/empyema,brain abscess, disseminated infection (osteomyelitis,

septic arthritis, abscess),shock/DIC

• chronic: hearing loss, neuromotor/cognitive delay, learning disabilities, neurological deficit,seizure

disorder, hydrocephalus

Mumps

Definition

• acute,seif-limited viral infection that is most commonly characterized by adenitis and swelling of the

parotid glands

Epidemiology

• incidence in Ontario has declined since introduction of two-dose MMR vaccination schedule

• average of 25 reported cases per yr

• majority of reported cases in children age 5-10 yr

Etiology

• mumps virus(RNA virus of the genus Rubulavirus in the Paramyxoviridae family)

• transmission via respiratory droplets, direct contact, fomites

• incubation period: usually 14-16 d (range 12-25 d)

• infectivity period:7 d pre-parotitis to 5 d post-parotitis

• viral replication in upper respiratory tract,drains to local lymph nodes, then spreads to secondary

sites (salivary glands, gonads, pancreas, meninges, kidney, heart, thyroid)

History

• non-specific prodrome of fever,headache, malaise, myalgias(especially neck pain)

• usually followed within 48 h by parotid swelling secondary to parotitis (bilateral, preauricular,ear

pushed up and out)

• parotid gland is tender and pain worsened with spicy orsour foods

• one third of infections do not cause clinically apparentsalivary gland swelling and may simply present

asanURT!

Investigations

• clinical diagnosis, but may be confirmed with IgM positive serology

• may also use PCR or viral cultures from oral secretions, urine, blood, and CS1*

• blood work:CBC (leukopenia with relative lymphocytosis),serum amylase (elevated)

within 4 wk of acute infection

Management

- mainly supportive:analgesics, antipyretics,warm or cold packs to parotid may be soothing

• admit to hospital if serious complications (meningitis, pancreatitis)

• droplet precautions recommended until 5 d after onset of parotid swelling

• prophylaxis: routine vaccination (see Routine Immunization, P5)

Complications

• common:aseptic meningitis,orchitis/oophoritis

• less common:encephalitis, pancreatitis, thyroiditis, myocarditis, arthritis,GN,ocular complications,

hearing impairment

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P68 Paediatrics Toronto Notes 2023

Pertussis

Definition

• prolonged respiratory illness characterized by paroxysmal coughing and inspiratory “whoop”

Epidemiology

• -10 million children <1 yr affected worldwide, causes up to 400000 deaths peryr

• greatest incidence among children <1 yr (not fully immunized) and adolescents (waning immunity)

Etiology

• B. pertussis:Gram-negative pleomorphic rod

• highly contagious; transmitted via respiratory droplets released during intense coughing

• incubation period:6-20 d; most contagious during catarrhal phase but may remain contagiousfor wk

after

History

• prodromal catarrhal stage

lasts 1-7 d; URT'

l symptoms (coryza, mild cough,sneezing) with NO or low-grade fever

• paroxysmal stage

lasts 4-6 wk; characterized by paroxysms of cough (“100 day cough”),sometimes followed by

inspiratory whoop (“whooping cough")

infants <6 mo may present with post-tussive apnea,whoop is often absent

onset of attacks precipitated by yawning,sneezing, eating, physical exertion

± post-tussive emesis, may become cyanotic before whoop

• convalescentstage

lasts I -2 wk; characterized by occasional paroxysms of cough, but decreased frequency and

severity

non-infectious,but cough may last up to 6 mo

Investigations

• NP specimen using aspirate or N P swab

gold standard:culture using special media (Regan-Lowe agar)

• PCR to detect pertussis antigens

• blood work:CBC (lymphocytosis) and serology (antibodies against B. pertussis)

Management

• admit if paroxysms of cough are associated with cyanosis and/or apnea and give O’

• supportive care with attention on nutrition in young infants

• antimicrobial therapy indicated if B.pertussisisolated orsymptoms present for <21 d

use macrolide antibiotics (azithromycin, erythromycin, or clarithromycin)

• droplet isolation until 5 d of treatment and report to Public Health

• prophylaxis

macrolide antibiotics for all household contacts

• prevention with vaccination in infants and children (Pentacel*), and booster in adolescents

(Adacel*) (see Routine Immunization, PS )

Complications

• pressure-related from paroxysms:subconjunctival hemorrhage,rectal prolapse, hernias, epistaxis

• respiratory:sinusitis, pneumonia, aspiration, atelectasis, pneumomediastinum, pneumothorax,

alveolar rupture

• neurological:seizures (

-3%), encephalopathy, ICH

• mortality: ~0.3%; highest risk in infants <6 mo

Pneumonia

• see Infectious Diseases.1D7 and Pneumonia, P93

Periorbital (Preseptal) and Orbital Cellulitis Cardinal Signs of Orbital Cellulitis

• Ophthalmoplegia/diplopia

• Proptosis

• Decreased visual acuity

• Pain with extraocular eye movement

• sco < Iphth.tlmologv, I > IH >

Sexually Transmitted Infections r

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• see Family Medicine, FM46 and Gynaecology, GY28

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P69 Paediatrics Toronto Notes 2023

Sinusitis

• see Family Medicine, FM47

• complication of S10% of URTIsin children

• clinical diagnosis

• diagnostic imaging is NOT required to confirm diagnosis in children

• routine CT not recommended, but consider ifsuspect complications ofsinusitis, persistent/

recurrent disease, need forsurgery

• antibiotic therapy (amoxicillin) for all children (although nearly half resolve spontaneously within 4

wk)

• complications: preseptal/orbital (preseptal/orbilal cellulitis, orbital abscess, osteomyelitis, etc.),

intracranial (meningitis,abscess, etc.), Pott's Fully tumour (presents with tender soft tissue

erythematous swelling of the forehead;symptoms include headache, photophobia, and fever;managed

with IV antibiotics and HNT consult)

Urinary Tract Infection

Definition

• infection of the urinary bladder (cystitis) and/or kidneys (pyelonephritis)

Epidemiology

• overall prevalence in infants and young children presenting with fever is 7%

• <4-6 wk: more common in males

• >1 yr:females have 2-4x higher prevalence

Etiology

• majority (>95%) have a single cause (

-70% U.coli)

• Gram-negative bacilli: E. coli, Klebsiella, Proteus, Enterobacter, Pseudomonas,Citrobacter

• Gram-positive cocci: S.sapropliyticus, Enterococcus

Risk Factors

• non-modifiable:female gender. White, previous UTIs, FMHx

• modifiable: urinary tract abnormalities(VUK. neurogenic bladder, obstructive uropathy, posterior

urethral valve),dysfunctional voiding, repeated bladder catheterization, uncircumcised males, labial

adhesions,sexually active, constipation, toilet training

Features Suggestive of Pyelonephritis

• High-grade fever

• Flank or high abdominal pain

• CVA tenderness on palpation

Bagged urine specimen not useful for

ruling in UTI (high false positive rate

>85%).but useful for ruling out UTI (high

sensitivity)

History

• infants and young child: often just fever or non-specific symptoms(poor feeding, irritability, FIT,

jaundice if <28d, vomiting)

• older child:fever, urinary symptoms(dysuria, urgency, frequency, incontinence, hematuria),

abdominal, and/orflank pain

Prophylasis Alter First febrile Urinary Tract

Infection In Children!

*

Multicentre. Randotaiied

Controlled, Noninferiority Trial

Pediatrics 2008:122:1064-107

Study: Randomized,controlled, open-label.2 armed.

rorinferiority trial.

Patients: 3 33 patients 2 rroto </ yrwho had a first

episode ol febrile Ull.

Intervention: Ho prophylaxis vs. prophylaxis.

Outcome:Recurrence rate of febrile Ull and rate of

renalscarring.

Results:Hu significant difference in recurrence

rate or in the rate of renalscarring between be

prophylaxis and no prophylaxis group.

Physical Exam

• infants and young child: toxic vs. non-toxic, febrile, ITT, jaundice; look for external genitalia

abnormalities(phimosis, labial adhesions) and lower back signs of occult myelodysplasia (e.g. hair

tufts), which may be associated with neurogenic bladder

• older child:febrile,suprapubic and/or costovertebral angle (CVA) tenderness,abdominal mass

(enlarged bladder or kidney); may present with shortstature, FIT,or HTN secondary to renal scarring

from previously unrecognized or recurrent UTIs

Investigations

• urinalysis, microscopy, C&S

sterile specimen: clean catch, catheterization,suprapubic aspiration, or‘Tap and Rub’

technique

• bag specimen can only be used for urinalysis and only to rule out diagnosis

• urinalysis:leukocyte esterase, nitrites, erythrocytes, hemoglobin

• microscopy: bacteria, leukocytes, erythrocytes

• diagnosis established if urinalysis suggests infection AND if >50000 colony-forming units(CFUs)/mL

in catheterspecimen OR >100000 Cl-

'

Us/mL in clean catch specimen

Management

• admit if: age <2 mo, urosepsis, persistent vomiting, inability to tolerate oral medication, moderatesevere dehydration, immunocompromised, complex urologic pathology, inadequate follow-up,failure

to respond to outpatient therapy

• supportive care:maintenance of hydration and adequate pain control

• antibiotics

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base on local antimicrobial susceptibility patterns

commence broad empiric therapy until results of urine C&S known, and then tailor as

appropriate

neonates:IV ampicillin and aminoglycoside

infants and older children:oral antibiotics(based on local t. coli sensitivity) if outpatient; IV

ampicillin and gentamicin if inpatient

duration 7-10 d

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•imaging

• renal and bladder VIS for all febrile infants (<2 yr), recurrent febrile UT Is (any age) looking for

anatomical abnormalities, hydronephrosis, abscess

VCUG not recommended after 1st febrile UT1 unless U/S reveals hydronephrosis, obstructive

uropathies or other signs suggestive of high-grade VUR

•follow- up:

outpatients to return in 24-48 h if no clinical response

seek prompt medical evaluation for future febrile illnesses

•prophylaxis: generally not recommended unless higher grades of VUR

Complications

•long-term morbidity:focal renalscarring develops in 8% of patients;long-term significance unknown

Neonatology

Gestational Age and Size

Definitions

• classification by CIA

preterm:<37 wk (extremely preterm <28 wk, very preterm 28-32 wk, moderate-late preterm 32-37

Dubowitz/Ballard Scares

GA can be determined after birth using

Dubowitz/8allard scores:

• Assessment at delivery of physical

maturity (c.g. plantar creases, lanugo,

ear maturation) and neuromuscular

maturity (e.g. posture, arm recoil)

translates into a score from -10 to +50

• Higher score means greater maturity

(increased GA)

• -10-20 wk;+5 -44 wk

• Ideal-35-40,which correspondsto GA

38-40 wk

• Only accurate ± 2 wk

• May be inaccurate in infants who are

preterm, postterm,SGA infants

wk)

• term: 37-42 wk

• post-term:>42 wk

• classification by birth weight

• SGA: 2 SD < mean weight for GA or <10th percentile

• AGA: within 2 SD of mean weight for GA

LGA:2 SD > mean weight for GA or >90th percentile

• classification of preterm infants by birth weight

• low birthweight (LBW) <2500 g

• very low birthweight (VLBVV ) <1500 g

» extremely low birthweight (liLBW) <1000 g

Table 30. Abnormalities of Gestational Age and Size

Features Causes Problems

Preterm Infants

<37 wk

Spontaneous:cause unknown

Maternal disease: H1N.0H, cardiac anil renal

disorders

Fetal conditions:multiple pregnancy,

congenital abnormalities, macrosomia. R8C

isoimmunization, (etal inlection

Pregnancy issues: placental insufficiency,

placenta previa, uterine malformations,

previous preterm birth, infection, placental

abruption

Behavioural and psychological contributors:

smoking, alcohol,drug use. psychosocial

stressors

Sociodemographic factors: advanced age. low

socioeconomic status

Most cases unknown

Increased in first pregnancies

Previous post-term birth

Genetic factors

RDS. apnea of prematurity, chronic lung

disease, bronchopulmonary dysplasia

Feeding dilficullies, NFC

Hypocalcemia, hypoglycemia, hypothermia

Anemia, jaundice

Retinopathy ol prematurity

ICH /IVH

PDA

Increased nskol slillbitlh or neonalaldealh

Increased birthweight

Fetal "postmaturity syndrome":impaired

growth due to placental dysfunction

Meconium aspiration

Perinatal hypoxia

Hypoglycemia, hypocalcemia , hypothermia,

hyperviscosity (polycythemia), jaundice.

Post-term Inlanls

>42 wk

SGA Intants

*10th percentile

Asymmetric ( head-sparing):

late onset, growth arrest

SGA Intants

Symmetric:early onset, lower growth

txtrinsic causes: placental insufficiency, poor

nutrition. HTN. multiple pregnancies, drugs,

alcohol,smoking,familial (actors,fibroids

Intrinsic causes:maternal infections (TORCH ),

congenital abnormalities,syndromal.

idiopathic

Maternal DM

Racial or familial factors

Increasing parity

Previous LGA infant, high BMI. large pregnancy

weight gain

Certain syndromes

PDA

LGA Infants

»90th percentile

Birth trauma, perinatal depression (meconium

aspiration)

RDS.TIN

Jaundice, polycythemia

Hypoglycemia, hypocalcemia

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P71 Paediatrics Toronto Notes 2023

Routine Neonatal Care

• history taking

passage of meconium in 24-48 h, urination/number of wet diapers

feeding: breast milk or formula, route (breast or bottle), duration, frequency and volume of feeds

• issues: jaundice, poor feeding, difficulty breathing, cyanosis,seizures

weight: discharge weight (close follow-up if >10% below birth weight), initial weight gain (goal

20-25 g/d), number of days until birth weight regained (should regain by day 10-14 of life)

• erythromycin ointment:applied to both eyes for prophylaxis of ophthalmia neonatorum ( N.

gonorrhoeae); no longer recommended by Canadian Paediatric Society but required by law in some

provinces/territories

• vitamin K 1M:prophylaxis against VKDB

• newborn screening tests in Ontario

• in Ontario, newborn screening tests for:

metabolic disorders (amino acid disorders, organic acid disorders, fatty acid oxidation

defects, biotinidase deficiency, galactosemia)

blood disorders (sickle cell disease, other hemoglobinopathies)

endocrine disorders(CAH, congenital hypothyroidism)

others (CP,severe combined immunodeficiency)

congenital hearing loss

• if mother Rh negative:send cord blood for blood group and DAT (also considersending DAT for O

positive mothers)

• if household contact is HBsAg positive:start hepatitis B vaccine series (and if mother is positive, give

HBlg within 12 h of birth); the US and some Canadian provinces give Hep B vaccine at birth routinely

Neonatal Resuscitation Apgar

i

Score

Appearance (colour)

Pulse (heart rate)

Grimace (Irritability)

Activity (tone)

Respiration (respiratory effort)

Or: "How Ready Is This Child?"

• assess Apgar score at 1 and 5 min

• if <7 at 5 min then reassess q5 min, until >7

• do not wait to assign Apgar score before initiating resuscitation

Table 31. Apgar Score

Sign 0 1 2

Heart Rate

RespiratoryEffort

Irritability

Tone

Colour

Absent

Absent

Ho response

<K)0/min

Slow,irregular

6rimace

Some flexion of extremities

Body pink,extremities blue

(acrocyanosis)

>tOO/min

Good,crying

Cough/cry

Active motion

Completely pink

Use of 100% Oxygen in Neonatal Resuscitation

Circulation 2015:132(suppl 2|:S543-S560

The 201S neonatal resuscitation guidelines hare

provided the following recommendatioi:"Since an

oxygen saturation of 100% may correspond to a PaO)

anywheie between >10 and S00 niaHg.in general

it is appropriate loWNH the HOi lor a saturation ol

100%. provided the oxyhemoglobin saturation can be

maintained >941." (Class llb.lOE |C .

Limp

Blue,pate

Initial Resuscitation

• anticipation: know maternal history, history of pregnancy,labour, and delivery

• stepsto take for all infants

» pre-delivery team debriefing including assigning roles,checking equipment, and discussing

possible complications and management plan

warm (radiant heater, warm blankets) and dry the newborn (remove wet blankets)

stimulate infant: rub lower back gently or flick soles of feet

o position airway (“sniffing” position) and clear orsuction if necessary

• assess breathing and HR

if apneic or ineffective respiration and HR <100:bag and mask ventilation (PPV) with room air

(or 30% if preterm infant).Continue until HR >100 and breathing spontaneously

if HR <60: establish airway for effective ventilation and start chest compressions; turn oxygen to

100%

if meconium present:a team with advanced resuscitation skillsshould be present.If the newborn

is hypotonic with ineffective respirations, routine intubation for tracheal suction is not suggested

unlessskilled at intubation. Do initial resuscitation and administer PPV as required

Corrective

0

Actions for PPV in Neonatal

Resuscitation

MR SOM

Mask readjustment

Reposition airway

Suction mouth and nose

Open mouth

Pressure increase

Alternative airway

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P72 Paediatrics Toronto Notes 2023

Table 32. Interventions Used in Neonatal Resuscitation

Intervention Indications Comments

Epinephrine

(adrenaline)

0.1-0.3 ml/kg/dose of1:10000 HR <60 andnotrlsing

10.01 0.03 mg/kg) IV

0.5-1mL/ kg/dose of 1:10000

(0.05- 0.1 mg/kg) endotracheally

can be considered while awaiting

IV access(IV preferred )

Can be repealed q3-5 mill CRN

10 ml/kg

May need lobe repeated

Avoid giving loo rapidly aslarge

volume rapid infusions can be

associated with IVH

Side effects:tachycardia. HIM,

cardiac anhyllimias

Fluid Bolus

(NS.PRBC)

Evidence of hypovolemia

Approach to the Depressed Newborn

• a depressed newborn has ineffective respiratory effort and cyanosis

• approximately 10% of newborn babies require assistance with breathing after deliver)'

Table 33. Etiology of Respiratory Depression in the Newborn

Etiology Examples

Respiratory Problems RDS/hyaline membrane disease

Pulmonary hypoplasia

CMS depression

MAS

Pneumonia

Pneumothorax

Pleural effusions

Congenital malformations

Erythroblastosisfetalis

Secondary hydrops letalis

Drugs/anesthesia (opiates,magnesium sulphate)

Anemia (severe)

MaternalCauses

DM

Congenital Malformations/Birth Injury Nuchal cord, perinatal depression

Bilateral phrenic nerve injury

Potter'ssequence

Antepartum hemorrhage

Transposition of the great arteries with intact ventricular septum

Hypothermia

Hypoglycemia

Infection

Shock

CHD

Other

Diagnosis

• vital signs including pre- and post-ductal oxygen saturations and -I limb BP. hyperoxia test

• detailed maternal and labour history: include prenatal care, illnesses, use of drugs, previous high-risk

pregnancies, infections during pregnancy (including GBS status),duration of ruptured membranes,

maternal fever orsigns of chorioamnionitis during labour/delivery, blood type and Rh status,

serologies,amniotic fluid status, GA, meconium, Apgarscores

• clinical findings (observe for signs of respirator)'distress such as cyanosis, tachypnea, retractions,

grunting, temperature instability, poor tone, abnormal movements, no spontaneous movements)

• laboratory results (CBC, blood gas, blood type and DAT, glucose ± blood culture)

• transillumination of chest to evaluate for pneumothorax if sudden change in respiratory status/

worsening distress

• CXR, BCG, echocardiogram, MR1, cerebral function monitoring/EEG

Management

• see Neonatal Resuscitation, P71,identify and treat underlying cause

Common Conditions of Neonates

Apnea

Definition

• periodic breathing: normal respiratory pattern seen in newbornsin which periods of rapid respiration

are alternated with pauseslasting 5-10 s

• apnea: absence of respiratory gas flow for >20 s (or less if associated with bradycardia or desaturation)

• three types of apnea

central: no chest wall movement, no signs of obstruction

• obstructive: chest wall movement continues against obstructed upper airway, no airflow

• mixed:combination of central and obstructive apnea

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Differential Diagnosis

• in term infants, apnea requiresfullseptic workup (CBC and differential, blood and urine cultures ±

LP, CXR)

• other causes

CNS:seizures, ICH

apnea of prematurity (<34 wk):combination of CNS immaturity and obstructive apnea;resolves

by 36 wk GA;diagnosis of exclusion

hypoxic injury

infectious;sepsis, meningitis, NEC

Gl:GEKD, aspiration with feeding

metabolic:hypoglycemia, hyponatremia, hypocalcemia, inborn error of metabolism

cardiovascular: anemia, hypovolemia, PDA, heart failure

medications:morphine

Management

• O’

,ventilatory support, maintain normal blood gasses

• tactile stimulation

• correct underlying

• medications: methylxanthines (caffeine) stimulate the CNS and diaphragm and are used for apnea of

prematurity (not in term infants)

• if apnea of prematurity is diagnosed,infants should receive cardiorespiratory monitoring in a

neonatal intensive care unit

cause

Bleeding Disorders in Neonates

Clinical Features

• oozing from the umbilical stump, excessive bleeding from peripheral venipuncture/heel stick sites/IV

sites,large caputsuccedaneum, cephalohematomas (in absence of significant birth trauma),subgaleal

hemorrhage,and prolonged bleeding following circumcision

Etiology

• 4 major categories

increased platelet destruction:maternal 1TP or SLE, infection/sepsis, D1C,neonatal alloimmune

thrombocytopenia, autoimmune thrombocytopenia

decreased platelet production/function: pancytopenia, bone marrow replacement, l-

'

anconi

anemia,Trisomy 13 and 18

metabolic: congenital thyrotoxicosis, inborn error of metabolism

coagulation factor deficiencies (see Hematology.H55):hemophilia A/B, VKDB

NEONATAL ALLOIMMUNE THROMBOCYTOPENIA

Definition

• maternal antibodies directed towards neonatal platelets, causing thrombocytopenia (platelets

<15()()00/pL)

Epidemiology

• 1 in 4000-5000 live births

Pathophysiology

• platelet equivalent of Rh disease of the newborn

• occurs when mother is negative for HPA and fetus is positive

• development of maternal IgG antibodies against HPA antigens on fetal platelets

Clinical Features

• petechiae, purpura, thrombocytopenia in otherwise healthy neonate

• severe disease can lead to intracranial bleeding

Diagnosis

• maternal and paternal platelet typing and identification of platelet alloantibodies

Treatment

• IV Ig to mother prenatally starts in second trimester ± steroids ± fetal platelet transfusions

• platelet transfusion is the mainstay of treatment. HPA specific (e.g. HPA-la negative) platelets are

preferred, however can use random donor platelets. Maternal washed platelets are effective but

practically often not feasible.

• concomitant IV1G treatment could be considered (insufficient evidence to support routine use)

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