BUDAK

MEDIK
NOTES
PAEDS
COMPILED BY: ANAR

MAY SUCCESS BE WITH YOU ALWAYS😊

 DEVELOPMENTAL MILESTONES

Sit at 6
Stranger
anxiety
Stretch hand
Switch hand
Schmooze
(bubble)

Pull to stand
Pincer grasper
“papa, mama”
Play peek-a-
book
Understand
“bye-bye”, “no”

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DEVELOPMENTAL DELAY

= when child does not reach their dev milestones at the

expected times

GLOBAL DD (GDD) = delay in ≥ 2 developmental domains,

affecting children under age of 5 years

SPECIFIC DD = delay in single domain

Intellectual disability (ID) = after 5 years when cognitive & adaptive fxn can reliably tested.

IMPORTANT POINT WHEN ASSESSING CHILD W DEV DELAY

• Child must be cooperative, not tired, fretful, hungry or sick.
• Allowance must be made for prematurity up to 2 years.
• Note parental account of what child can or cannot do & concerns on gait, speech etc.
• Ensure child’s hearing & vision are normal.
• Normal speech & language development is essential for normal social, intellectual & emotional development.

History Physical Examination

• Significant fam hx, consanguinity • Head circumference, growth, dysmorphic features,
• Antenatal: maternal illness, ingestion of drugs, neurocutaneous markers
alcohol, smoking. • Neurological abn
• Birth: prematurity, perinatal asphyxia • Full developmental assessment
• Postnatal: severe NNJ, hypoglycaemia or seizures • Observation of behavior, social interaction & play
• Serious childhood infections, hospital admissions or
trauma
• Home environment, stimulation (environmental
deprivation)

CLINICAL POINTS TO CONSIDER REFER TO PAEDIATRIC NEUROLOGIST

History Physical Examination

• Regression or possible regression inc significant • Neurological signs: dystonia, ataxia, chorea, focal
change in behaviour signs, cranial neuropathy, peripheral neuropathy,
• Possible or definite seizures arthrogryposis/ joint contractures
• Movement disorder: continuous or paroxysmal • Cerebral Palsy picture w/o a clear cause/hx
• Muscle pain/fatigue • Ocular signs: cataract, nystagmus, eye movement
• New onset sensory impairment (eg: significant disorder, abn fundi
decline in visual acuity)
• Cognitive decline/ behavioural change in a child w
epilepsy or ASD

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ABNORMAL DEVELOPMENT

1. Motor

Causes –
Central motor deficit (eg – cerebral palsy)
Cong myopathy/ primary muscle dis
Spinal cord lesions (eg - spina bifida)
Global developmental delay (GDD)

Hand dominance: 1-2y or later

Asymmetry of motor skills during the 1st year of life is always abn & may suggest underlying hemiplegia
Functional ability is described using GMFCS

2. Speech & language

Causes:
Hearing loss
GDD
Difficulty in speech production from an anatomical deficit (eg: cleft palate) or oromotor incoordination (eg: CP)
Environmental deprivation/ lack of opportunity for social interaction
Normal variant/ fam pattern

3. Social/ communication

Common in boys
Usually btwn 2-4y
Presents w a triad of difficulties & associated co-morbidities
If some of the behaviors present → autistic features not spectrum
Asperger syndrome: a child w the social impairments of an ASD but at the milder end, & near-normal speech
dev.

*ASD: impairment of social interaction, speech & language disorder & imposition of routines w ritualistic &
repetitive behavior, usually managed by behavior modification

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MANAGEMENT

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 DOWN SYNDROME

= congenital disorder that make extra copy of chromo 21, l/t IQ impairment & physical abnormalities.

(Trisomy 21 (47 (XX/XY, + 21 = child has 47 chromosomes, with 3 copies of chromosome 21

KARYOTYPING RECURRENCE RISK

Non-disjunction trisomy 21
(95%)
*related to maternal age
Robertsonian-translocation
(3%)
Mosaicism (2%)
Chromosome not split
Extra chromo 21 join
another chromo (14)
*need parental
chromosomal analysis!
Cell mixed
1% or age-related risk
(whichever higher)
Both parents normal - <1%
Carrier mother – 10%
Carrier father – 2.5%
Either parent t(21q:21q) –
100%
<1%

RISK FACTOR - maternal age > 35 years, Mom already had DS child, parent who are carrier for genetic
translocation of DS

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CLINICAL FEATURES “CHILD HAS PROBLEM”
CHD (AVSD) / cataract, glaucoma/
clinodactyly
Hypotonia
Infertility (male)
Leukemia/ lung probs
Dementia/ DM-1/ duodenal atresia/ dev
delay

Hypothyroid/ hearing loss/ Hirschsprung

Atlanto-axial instability/ Alzheimer
Short stature/ sandal gap/ single
transverse crest/ smooth philtrum

Protruding tongue/ pyloric stenosis

Rolling eye (nystagmus)/ round face
Occiput flat
Behavior prob/ brachycephaly
Learning difficulty/ low set ears/ low nasal
bridge
Epicanthic fold
Mental retard

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MEDICAL PROBLEMS

Newborn Infancy & childhood Adolescence & adulthood

Cardiac defect (50%) Delayed dev milestone Boy
AVSD, VSD, TOF, PDA Intellectual impairment (IQ 30-70) Infertile (low testosterone - impair
Autistic spectrum dis & ADHD spermatogenesis)
GIT (12%) Maladaptive behavior (eg: use ↑ risk of dementia
Duodenal atresia (bilious vomiting, social distraction to avoid given Shorter life expectancy
no abd distension & double bubble task & stubbornness)
sign on AXR) Susceptibility to infection Girls
Pyloric stenosis – visible peristalsis, Hearing loss from secretory OM Delayed menarche
non-bile vomit, olive mass (>60%) Fertility presumed
(doughnut sign on abd usg) Visual impairment - squint,
Anorectal malformation cataract, nystagmus, glaucoma, OSA
Tracheo-esophageal fistula refractive error Internalizing sx (eg: social wdrawal
Hirschsprung Sleep related upper airway & depression)
obstruction (eg: OSA) Risk of Alzheimer/ dementia
Feeding prob – resolve after few Leukemia Shorter life expectancy
weeks Atlanto-axial instability
Hypothyroidism
Vision Over/underwt
Cong cataract (3%) Seizure disorder (6%)
Glaucoma Short stature

Hypotonia & jt laxity

Cong hypothyroidism (1%)
Cong hip dislocation

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THE TEST ☺

Screening test Diagnostic test

Blood test (quad screening, at 16 weeks of POG)
“HIgh” – high in HCG & inhibin A, low in AFP &
unconjugated bilirubin
Usg (nuchal translucency, at 11 – 14 weeks of POG)
Chorionic villus sampling (placenta) - after 10 weeks
(earlier? - limb reduction)
Amniocentesis (amniotic) - after 15 weeks (earlier? –
miscarriage)

After birth –
Initial diagnosis → baby’s appearance (craniofacial
features)
Karyotyping

MANAGEMENT (multidisciplinary)

**if expect newborn w DS, don’t start feeding stat as may have duodenal atresia & feeding prob

Careful examination to look for compli

Even cannot cure, improve medical mx & early intervention – need periodic evaluation of speech, cognitive &
motor fxn

Health surveillance & monitoring

Medication for seizure, thyroid, DM

Surgery - heart, intestine

Physical therapy – more focus on motor dev (eg: hypotonia)

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Speech therapy – trouble speaking (small mouth, large tongue)

Occupational therapy – self-care skill (feeding, dressing, grooming), fine & gross motor skill (sitting, crawling), skill
related to school performance, play & leisure skill

PROGNOSIS

>85% survive to 1 year of age

At least 50% live longer than 50y (d/o compli & severity of retardation)

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 BRONCHIOLITIS
Acute inflammation of bronchioles, resulting in
wheezing & airway obstruction
PNEUMONIA PERTUSSIS
(WHOOPING COUGH/ 100 DAYS COUGH)
Bronchopneumonia = febrile illness w cough, RD + evidence of
localized/ generalized patchy infiltrates.
Lobar pneumonia = similar to BP, except physical findings &
radiographs indicate lobar consolidation.

Age 1 months – 6 months Any age 3 months – 3 years

Culprit Respiratory syncytial virus (RSV) Newborn GBS, E. coli, Enterobacteriaceae, Klebsiella, Bordetella pertussis
Rhinovirus 1-3 months Chlamydia trachomatis (gram –ve coccobacilli)
Adenovirus Preschool Strepto pneumoniae, Hib, staph aureus
Parainfluenza virus Less common - GAS, pseudomonas, Moraxella
catarrhalis
Cyclical periodicity w annual peak occur – in Nov, School age Chlamydia pneumoniae
Dec & Jan Mycoplasma pneumoniae

Others RISK FACTOR Fever

Preterm baby Cough (persist for > 2 weeks)
Low birth weight baby Vomit btwn each episodes
Young maternal age
Low 5-min APGAR score 3 PHASES
Maternal tobacco/ passive smoking Catarrhal – coryza
Not being breastfeed Paroxysmal (last 3 – 6 weeks) –
High altitude Sudden cough, followed by inspi whoop
Cough worst at night & culminate in vomiting
During paroxysm, child goes red & blue in
face (facial congestion), mucus flow from
ASSESS SEVERITY (RR) mouth & nose. Epistaxis & subconjunctival
< 2 months - > 60 bpm H’ge after vigorous coughing
2 – 12 months - > 50 bpm
12 m – 5 y/o - > 40 bpm Convalescent - sx ↓ but persist

CF Mild coryza Fever (high grade)

Low grade fever + cough Running nose
Tachypnea, Chest wall recession Difficulty breathing
Wheezing, Respiratory distress Preceded w URTI
Hyperinflated chest Cough, lethargy, poor feeding, unwell child
On ascult – fine crepitation +/- rhonchi

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 GPE
Tachypnea, nasal flaring, chest recession
↓ expansion
Bronchial breathing, ↓ breath sound
End inspiratory coarse crackles
↑ fremitus
Dull on percussion (consolidation)

Ix CXR – Hyperinflated lung, Lobar or Segmental
collapse/ consolidation
Not routine to do CXR in bronchio, but recommend
in children w severe respi distress, unusual CF, u/l
cardiac or chronic respi disorder & also admission to
intensive care
Blood gas analysis – for infant w severe respi distress
or who are tiring & may enter respi failure
No indicated to do routine FBD & bact testing
(urine/blood) in typical acute bronchiolitis.
Mx Supportive
Need careful assessment of respi status &
oxygenation. Always maintain SPO2 > 93% - give
supp humidified oxygen
IVF & continue feeding.
Neb 3% NaCl - ↑ mucus clearance
Neb salbutamol
Staphylococcal infection – rapid deteriorate!
CXR – multilobar consolidation, cavitation, pneumatocele,
spontaneous P-T, empyema, pleural effusion.
Mx – high dose Cloxacillin (200 mg/kg/day)
Klebsiella – usually presented w eye discharge, so do swab ok
& also ask for high risk behavior.
CXR – consolidation, air bronchogram, parapneumonic effusion. Culture NP swab
Unable to diff bact or virus FBC – ↑ WBC (L > 15 x 10^9/L)
FBC – WBC (Neutrophil – bact, Lymphocyte – viral/ severe
overwhelming infection)
Blood CnS (10 – 30%) – do in severe pneumonia or if poor
CRITERIA HOSPITALIZATION
response to 1st line AB < 3 months (whatever severity)
RFT – ↓ urea (poor feeding) Fever >38.5’c, refuse to feed & vomiting
Pleural fluid analysis – only if there’s pleural effusion Fast breathing +/- cyanosis
Serology test (> 5 y/o) – if suspect atypical pneumonia (MCLM) Assc systemic manifestation
*acute phase serum titre > 1 : 160 or paired sample taken 2 – 4 Fail prev AB therapy
weeks apart w 4 fold rise – good indicator for Mycoplasma Recurrent pneumonia
pneumoniae Severe U/L disorder (eg: immunodef)
Inpatient mx – AB - Macrolide “CAE”
AB – B-lactam (eg: benzylpenicillin), cephalosporin (eg:
cefuroxime), carbapenem, AG) p/s: don’t give to infant → fertile
(consider 2nd line AB when no sign of recovery or pt remain toxic & hypertrophic pyloric stenosis
ill w spiking temp for 48-72 hours)
p/s: atypical pneumonia? – give macrolide “ACE” Vaccine DTaP – 2, 3, 5, 18 months
Severe CAP? – parenteral AB (2nd/3rd cephalosporin + macrolide)
Maintain SpO2 > 95%
IV fluid – avoid overhydrating as in severe pneumonia, there’s ADH
secretion
PCM – just reduce discomfort from sx, but not abolish sx
Chest physiotherapy – remove tracheobronchial secretions
Not recommend cough medication as it cause suppression of
cough & may interfere w airway clearance.
Pneumococcal vaccine

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 Outpatient mx –
Mild pneumonia – fast breathing but no chest recession
So, prescribe oral AB, educate parents about fever mx, prevent
dehydration & identify sign of deterioration.
F/u in 2 days for reassessment or earlier if condi worse.

Compli [usually recover w/i 2 weeks] “PEL CAKS” Pneumonia

Parapneumonic effusion Bronchiectasis
Empyema Convulsion
Lung abscess death
Collapse lung
ARDS
Kidney failure
Septicemia

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 *stridor = high pitch respi sound produced by rapid, turbulent flow of air through narrowed segment of respi tract

CROUP (ACUTE LTB) ACUTE EPIGLOTITIS BACT TRACHEITIS RETROPHARYNGEAL ABSCESS

*clinical Dx (4D – drooling, dysphagia, dysphonia, distress) (PSEUDOMEMBRANOUS CROUP)
Tracheal wall become edematous w Rapid progressive infection of epiglottis & Rapid progressive obstruction *PE infant – bulging of post
profuse secretion, causing narrowing of contiguous structure that may cause L-T *more toxic than croup pharyngeal wall, cervical LN
airway airway obstruction
Location Subglottic Supraglottic Subglottic Post pharynx
Culprit Parainfluenza virus (PIV)** Hemophilus influenza B (Hib) Staph aureus (secondary) Staph aureus
RSV Staph aureus Moraxella catarrhalis GAS
Influenza virus A & B Hib H. influenza
Adenovirus p/s: AVOID EXAMINE THE THROAT Pneumococcus Klebsiella
Age 6 months – 6 years 3 – 6 years <1 y/o, 5 – 7 y/o < 3-4 y/o (boys > girls)
Onset Viral prodrome – has URTI/ coryza Sudden (abrupt) Viral prodrome – has URTI/ coryza Recent ENT infection
gradual (1 – 7 days) 4 – 12 hours acute (1 – 2 days) (eg: OM)
(usually in fall or early winter)
App Well looking Toxic & unwell Well to toxic

Position Comfortable in different positions Tripod position Neck hyperextend Refuse to move neck
(sitting fwd w mouth open) Torticollis – toward affected side
(lessen extension)
Fever Fever (low grade) Fever (high grade) Moderate to high Present
Stridor Loud stridor Soft stridor Mild inspi stridor Present
(when excited, at rest or both) (“musical/ whistle”)
Cough Has (seal-like, barking) Minimal/ absent Brassy cough
Speech HOV Unable to speak HOV Muffled voice
Muffled voice (“hot potato voice”)
Secretion Can swallow Unable to swallow Copious thick secretion (drooling) Drooling
Drooling of saliva

X-ray PA view Lat view Steeple sign Widen pre-vertebral space

Steeple sign (narrowing trachea) Thumb sign (swollen – thickened epi) Irregular tracheal lining
Subglottic narrowing
VC edema

Lat view: ballooning hypopharynx

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 Laryngo- Red, edematous subglottic Large cherry red, swollen epiglottis Purulent tracheal secretion Incision for drainage & culture
scopy Crusting pseudomembrane **do in OT CT scan – diff btwn retro, para
(quinsy), lat abscess
FBC Normal WBC ↑ WBC ↑ WBC
Other Ix Pulse oximetry Blood cns (after stabilized)
ABG no helpful as blood parameter
remain normal until late stage.
Mx Oxygen Immediate refer to hosp & Inform ENT, anest, Refer to hosp immediately Oral AB (clindamycin +
*INDICATION – severe croup, spo2 < paeds Give neb O2 100% cephalosporin)
93%) IV AB (vancomycin & 3rd I & D - in respi distress child
Intubate/ tracheotomy - Ventilator support cephalosporin)
Steroid (dexa) – reduce edema & anti- until edema subside COMPLICATION
infla effect *rapid progressive obstruction - Aspiration pneumonia
AB for 7-10days need intubation Erosion of carotid sheath
Neb adrenaline 0.5 ml/kg *max 5 ml (Ceftriaxone/ cefotaxime/ meropenem) (not respond to croup rx) Upper airway obstruction
*prevent : vaccine (HIB)
Intubate/ ventilate
*do in OT, standby for tracheostomy

Stridor at rest + recession (intercostal, subcostal, sternal)

Stridor w excitement/ at rest, w no respi
distress Stridor at rest + recession + ↓ air entry + alter mental lvl

CRITERIA FOR ADMISSION FOR CROUP

< 6 months
Mod – severe croup
Poor oral intake
Toxic, sick appearance
Apnea/ tachycardia
Lives long distance from hosp (lack reliable transport)

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UPPER RESPIRATORY TRACT INFECTION (URTI)

CLINICAL FEATURES

Nasal discharge/ blockage

Fever

Cough

Febrile convulsion

AEBA

Painful throat

Earache

Difficult feeding (nose are blocked & obstruct

breathing

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 COMMON COLD (CORYZA) SORE THROAT (PHARYNGITIS) TONSILLITIS ACUTE OM ACUTE SINUSITIS
Culprit Rhinovirus** Viral infection** GABHS & EBV Bacteria Strep pneumonia**
Coronavirus (adenovirus, enterovirus, Pneumococcus**
RSV rhinovirus) H. influenza, 4 TYPE OF SINUS
Moraxella catarrhalis Frontal – 7 y/o
Bact infection (older age Ethmoidal – at birth
group) - group A b-hemolytic Virus – resolve spontaneously Maxillary – 4 y/o
(GABHS) RSV, Rhinovirus Sphenoid – 5 y/o
CF Fever Inflamed of pharynx & soft Age: 6 – 12 months → Pain, swelling, tenderness
Clear nasal discharge palate Eustachian tube (short, over cheek
Nasal blockage Still bact ? horizontal, function poorly)
Local LN enlarge & tender -headache, apathy, abd pain, Why not frontal sinus?
white tonsil exudate, cervical Fever , Pain in ear (rubbing/ (uncommon)
Has centor score for GABHS LN enlarge pulling ear) -as frontal sinus not dev until
“A FAST” Tympanic membrane bright late childhood (7y/o)
≤ 1 – no need culture or AB red & bulging
(viral) Acute perforation of eardrum Why maxillary more
2 – 3 – AB only if culture +ve w pus (visible in ext canal) common?
≥ 4 – empirical AB + culture -Has hole ?
COMPLI -
Mastoiditis, Meningitis
Ix Nil AB to strep Ag (ASOA > 200ml) Otoscope bigger size, to see:- Sinus expirate culture
-bright red, bulging of TM Rigid nasal endoscopy
Throat swab culture (normally - air fluid (pus) present
not done) - otorrhea (if TM perforate)
- loss of normal light reflection
Mx Self-limiting NS nose drop Admit if cannot take solid/ liq *most cases resolve AB
-increase fluid intake/ cont PCM for fever Oral food → IV fluid +/- analgesic spontaneously! Analgesia
BF Penicillin for 10days
- NS nose drop AB for 10 days (penicillin/ Pain : PCM
erythromycin) *prevent *Regular analgesia
Fever/ pain → PCM rheumatic fever
[AVOID amoxicillin – *AB : just shorten the
*don’t give antiviral/ AB/ maculopapular rash] duration of pain but not for
anti-histamine reduce hearing loss
Recurrent → OME (cause
speech & learning diff)

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ASTHMA

= Reversible chronic infla airway dis l/t increase airway responsiveness that l/t recurrent episode of coughing,
wheezing, breathlessness & chest tightness esp at night or early morning

DIAGNOSIS: > 20% improvement in PEFR or > 12% improvement in FEV1 post-bronchodilator

Sign of allergic rhinitis –

Allergic shiner (dark circle under eyes)
Cobble stone in conjunctiva
Salute sign
Swollen turbinate

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 INDICATION TO REFER CHILDREN <5 Y/O
FTT
Neonatal or very early onset of sx esp assc w FTT
Vomiting w respi sx
Continuous wheezing
Fail to response to controller medication
No ascc of sx w typical trigger (eg: URTI)
Focal/ cardiovascular sign or finger clubbing
Hypoxemia outside context of viral illness

FEATURES SUGGESTIVE OF ASTHMA IN CHILDREN <5 YEARS OLD

Cough Recurrent/ persistent non-productive cough that worsen at night or accompanied by

wheezing or SOB.
Cough occurring in the absence of respi infections, usually w laughing, crying or
exposure to tobacco smoke
Wheezing Recurrent wheezing during sleep or with triggers such as activity, laughing, crying or
exposure to tobacco smoke or air pollution
Reduced xtvt Not running, playing, or laughing at the same intensity as other children.
Diff/ heavy breathing or SOB occurring w exercise, laughing or playing
Past or fam hx of allergy dis or hx of asthma in 1st degree relative
Therapeutic trial with Clinical improvement during 2-3 months of controller treatment & worsening when
low dose inhaled steroid treatment is stopped.

EVALUATE FOR NEWLY DIAGNOSED ASTHMA

INTERMITTENT MILD MODERATE SEVERE

PERSISTENT PERSISTENT PERSISTENT
Daytime sx < 1x /week >1x/ week Daily Daily
Nocturnal sx < 1x / months >2x / months >1x / week Daily
Exercise induced sx No Has Has Daily
Exacerbation Brief >1x / month >2x / month Freq (>2x/ month)
Affect sleep & xtvt Not affect Affect Affect Affect
Lung fxn Normal >80% 60 – 80% < 60%
(PEFR/ FEV1)

p/s: assess asthma control after initiation of rx as well as RF for poor outcome. During visit, address rx issue
(inhaler technique, adherence & S/E) & co-morbidity (eg: rhinosinusitis, GERD, obese, OSA etc)

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HOW TO ASSESS ASTHMA CONTROL? – GINA “DNAR”

MONITOR EACH VISIT

Asthma control b/o - Interval sx, Frequency &
severity of acute exacerbation, Morbidity 2’ to
asthma, QOL, PEFR or FEV1 monitoring

Compliance - Frequency & technique

Asthma education - Understanding asthma in

childhood, Re-emphasize compliance to therapy,
Written asthma action plan

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PREVENTION *Identify & avoid the trigger

Enviro allergen –

• House dust mites, animal dander, insects like cockroach, mould & pollen, cigarrete smoking

• Useful measures: damp dusting, frequent laundering of bedding w hot water, encase pillow/mattresses
with plastic/vinyl covers, remove carpets from bedrooms, freq vacuuming, remove pets from the
household.

Respi tract infection**

Food allergy

Exercise *even it’s recognized trigger, but don’t limit the

xtvt. Take B2-agonist prior to strenuous exercise.

COMPLICATION – Pneumonia, Pneumothorax, Lung

collapse (atelectasis), Status asthmaticus, cardiac asthma

TREATMENT OF CHRONIC ASTHMA

Step up: assess pt after 1 month of initiation of rx. If control not adequate → consider step-up

Step down: assess pt every 3 months (2x) & if control sustained at least for 4-6 months, then consider gradual rx
reduction

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 Ventolin

Bricanyl

Atrovent

Seretide

Symbicort

Others-
Combivent = salbutamol/ ipratropium
Berodual = fenoterol/ ipratropium
Foster = formoterol/ beclomethasone
Spiriva = tiotropium bromide

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ACUTE ASTHMA

Life threatening asthma – “PA CHEST”

CRITERIA FOR ADMISSION Poor respi effort, paradoxical thoraco-abd
movement
Severe acute asthma Alter mental status – drowsy, confused
Fail of those w mild-moderate acute asthma to respond to neb B2-agonist Cyanosis & < 92%
Hypotension, bradycardia
Relapse w/I 4 hours of neb B2-agonist Exhaustion (cannot speak)
Silent chest
Fail to respond to standard home rx
Threatened PERF (cannot perform)

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 S/E salbutamol –
hypokalemia, palpitation, tremor, headache

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FOOTNOTES ON MX AEBA ^^

Monitor pulse, color, PEFR, ABG & O2 saturation. Close monitoring at least 4 hours

Hydration – give fluid maintenance

Use aminophylline in ICU due to its potential toxicity

IV MgSO4 use in severe exacerbation unresponsive to initial rx.

Avoid chest physiotherapy as may increase pt discomfort

Only give AB if suspect bact infection

Avoid sedative & mucolytics

CXR only helpful to detect complication (eg: pneumothorax, pneumonia, lung collapse)

Efficacy of prednisolone in 1st year of life is poor

On discharge, give pt action plan to assist parents to prevent/ terminate asthma attack. The plan inc:-

How to recognize worsening asthma

How to treat worsening asthma

How & when to seek for medical attention

*salbutamol MDI vs nebulizer

< 6 y/o : 6 x 100 mcg puff = 2.5 mg Salbutamol nebules.

> 6 y/o: 12 x 100 mcg puff = 5.0 mg Salbutamol nebules.

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DIPHTHERIA *life threatening!

MOT Transmission through respi droplet (sneezing or coughing) - “airborne droplet”

Contaminated personal items, household items

Culprit Corynebacterium diphtheriae

-gram +ve bacilli
- non-spore forming
- non-acid fast
- non-motile
Classification Nasal diphtheria
(site) Pharyngeal & tonsillar diphtheria
Laryngeal or laryngotracheal diphtheria
Cutaneous diphtheria

Produces toxin (exotoxin)

1.inhibits cellular protein synthesis
2. responsible for local tissues destruction & pseudomembrane formation – in larynx, trachea,
bronchia (may obstruct the airway )
3. affect heart (myocarditis), nerve (neuritis – soft palate paralyse) & kidney (non-oliguric AKI,
proteinuria), low plat

RF Children, adult not properly immunized

People who live in crowded/ unsanitary condition
Anyone who travels to diphtheria endemic area

Onset 2 – 5 days (gradually)

CF Begin insidiously w sore throat
Thick gray membrane covering throat & tonsils →”wash-leather” elevated greyish-green membrane
on tonsil. Well-defined edge, firm & adherent

Sore throat & HOV

Swollen of neck (bull neck) & tender LN enlargement
Difficulty breathing or rapid breathing
Nasal discharge
Fever (not high) but app toxic

Ix FBC – ↑ WBC - neutrophil dominant, ↓ plat

CnS (swab from nose, pharynx, nasopharynx)
*special tellurite enriched culture media (Loffler’s or Tindale’s)
Urinalysis – Proteinuria

Mx All suspected & confirmed pt must be placed under strict isolation until bacteriological clearance
Strict droplet precaution & hand hygiene – observe by healthcare workers
Take specimen for culture from nose, throat, any mucosal membrane (tissue). Do before give AB

Definitive Mx (diphtheria antitoxin – derived from horse serum)

Single dose of IV infusion of diphtheria anti-toxin (even before know culture result)
Antibiotic – IV penicillin/ IM procaine penicillin (2 weeks) / IV or oral erythromycin (2 weeks)

Immunize before discharge.

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Compli Blocking of airway
Damage to heart muscle - Myocarditis (mortality 50%)
Damage to nerve - Peripheral neuropathy
Loss ability to move – paralysis
Lung infection – respi failure/ pneumonia
Kidney - non-oliguric AKI

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 RESPIRATORY CHANGES

Prior to birth –
↑ Pul arterial resistance, causing pul vessel are collapsed.
Lungs & passageways have small amount of fluid, but no
air. Lung volume too small to allow complete output of RA
through lung circuit, so as blood in Rt side of heart > lung
volume, can cause back-pressure of lung. There’s enough
blood flow to allow growth & development, but not for gas
transfer.
How blood want to leave the RA, esp to bypass the lung? –
He’s the great planner
So, there’s 2 ways –
Ductus arteriosus – connect the trunk of pulmonary artery
to prox descending aorta.
Foramen ovale – hole btwn RA & LA

Blood supply – “AVA”

2 umbilical artery – return deoxygenated blood, wastes &
CO2 to placenta
1 umbilical vein – bring oxygenated blood & nutrient to
fetus

During delivery
Clamping of umbilical vessel at birth causing ↑ systemic
BP & relaxation of pul vasculature. Placental connection is SURFACTANT (type-II pneumocyte)
lost Start at end of 6th month & usually by 8th month
enough for normal respi fxn
At birth (so prem baby has little/ no surfactant when born)
1st breath is caused by contraction of diaphragmatic & ↑ by cortisol & thyroxine
intercostal muscle. Air coming in, forced the fluid out & ↓ by insulin
inflate bronchi, bronchioles & most of alveoli.
Pressure change in respi system takes blood into pul Fxn – ↓ alveolar tension, so help alveolar expansion
circulation. (prevent atelectasis)
The foramen ovale (btwn atria of heart) close, so does the
ductus arteriosus (btwn pul trunk & aorta)

FETAL NEWBORN
Gas exchange Placenta Lungs
RV, LV circuit Parallel Series
Pul circulation Vasoconstricted Dilated
Fetal myocardium Less Good
(contractility, compliance)
Dominant ventricle Right Left
Change in structure Umbilical vein – lig teres
Umbilical artery – med umbilical lig
Ductus venosus – lig venosusm
Ductus arteriosus – lig arteriosus
Foramen ovale – fossa ovalis

30
 TRANSIENT TACHYPNE OF NEWBORN RESPIRATORY DISTRESS MECONIUM ASPIRATION
(TTN)/ “Wet lung syndrome” SYNDROME (RDS) / SYNDROME (MAS)
“Hyaline membrane disease”
Causes Delayed resorption of fetal lung fluid → Surfactant deficiency → poor lung Meconium is sterile but causes
accumulation of fluid in peribronchial compliance due to high alveolar airway obstruction, chemical
lymphatics and vascular spaces → surface tension → atelectasis →↓ inflammation, and surfactant
tachypnea surface area for gas exchange → inactivation leading to chemical
hypoxia + acidosis → respiratory pneumonitis
distress
Delivery Usually term & late preterm Preterm Term & post-term
Onset Immediate to within 2 hours of birth Immediate Immediate
RF Maternal DM Maternal DM Meconium-stained AF
Maternal asthma Preterm delivery Post-term delivery
Male sex Male sex
Macrosomia (> 4.5 kg) LBW
Elective Cesarean section (w/o labor) Acidosis, sepsis
Late preterm delivery Hypothermia
2nd born twin
C- sec w/o labor (↓ cortisol)
CF Tachypnea within 1st few hours of life ± Respiratory distress within first few Respiratory distress within hours of
retractions, grunting, nasal flaring hours of life, worsens over next 24- birth
Often NO hypoxia or cyanosis 72 h Small airway obstruction, chemical
Hypoxia pneumonitis tachypnea, barrel
Cyanosis chest with audible crackles
Hypoxia
CXR Perihilar infiltrates Homogenous infiltrates, Air Hyperinflation
“Wet silhouette”; fluid in fissures bronchograms (microtelectasis) Patchy atelectasis
Hyperexpansion ↓ lung volumes (hypoexpansion) Patchy and coarse infiltrates
May resemble pneumonia (GBS) 10-20% have pneumothorax
Why expiratory If severe, “white-out” with no
grunting in RD?
differentiation of cardiac border
Like “balloon
never use”
Diffuse
Baby try to exhale ground glass
against epiglottis app
(attempt to
preserve lung fxn)

Mx Supportive Resuscitation Resuscitation

Oxygen if hypoxic
Ventilator support (e.g. CPAP)
IV fluids and NG tube feeds if too
tachypneic to feed orally
Prevention Where possible, avoidance of elective
Cesarean delivery, particularly before 38
week GA
Oxygen, Ventilation
Surfactant (↓ alveolar surface
tension, improves lung compliance,
and maintains functional residual
capacity)
Avoid hypothermia
Prenatal corticosteroids if risk of
preterm delivery <34 weeks.
Monitor lecitihin:sphingomyelin
ratio w amniocentesis, L/S 2:1
indicates lung maturity
Prevent preterm w tocolytic agent
Oxygen
Ventilatory support
Surfactant
Inhaled nitric oxide
Extracorporeal membrane
oxygenation for PPHN
If infant is depressed at birth,
intubate and suction below vocal
cords
Avoidance of factors associated
with in utero passage of meconium
(e.g. post term delivery)

31
Complication Hypoxemia In severe prematurity +/- prolonged Hypoxemia
Hypercapnea ventilation, increased risk of Hypercapnea
Acidosis bronchopulmonary dysplasia Acidosis
PPHN PPHN
Pneumothorax
Pneumomediastinum
Chemical pneumonitis
Secondary surfactant inhibition
Respiratory failure
Prognosis Recovery usually expected in 24-72 h Dependent on GA at birth and Dependent on severity, mortality
severity of underlying lung disease; up to 20%
long-term risks of chronic lung
disease

32
NEONATAL HYPOGLYCEMIA (plasma glucose level > 2.6mmol/L after 1st 4 hours of life)

Maternal BG > 8 mmol/L during labor reflect neonatal jaundice

Neonatal DXT 1.7mmol within 1-2 HOL is considered normal, then increase to more stable level
>2.5mmol by 12 HOL.

If suspect neonatal hypoglycemia, immediately do plasma (RBS)/ blood (glucometer/ dextrostix) glucose!
RBS tend to be 10 – 18% higher than whole blood value d/t higher water content of plasma.

TARGET PLASMA GLUCOSE LEVEL

Clinical hypoglycaemia = plasma glucose concentration low enough to cause CF of impaired brain fxn.
• term/ preterm? – > 2.6mmol/L
• term infants < 4h old, well, asx & tolerate feeding? – PG > 1.5mmol/L is acceptable & repeat glucose is > 2.6
mmol/L.
• Infants > 48 hours old, keep > 3.3mmol/L
• Infants w suspected congenital hypoglycaemia disorder or symptomatic infants? – PG > 3.9mmol/L.

SCREENING
Only measure BG concentration in term babies w clinical manifestation or who known at risk of hypo.
Infants who are at risk of hypo & need glucose screening –
• Symptoms of hypoglycemia CLINICAL SIGN OF HYPOGLYCEMIA
• LGA (even without maternal diabetes) (some hypo are asx, so important to
• Perinatal stress monitor in all high risk cases)
• Birth asphyxia/ischemia - caesarean delivery for fetal distress • Jitteriness • Cyanosis • Seizures
• Maternal preeclampsia/eclampsia or hypertension • Apnoeic episodes • Tachypnoea
• IUGR (small for gestational age) • Weak or high-pitched cry • Floppiness
• MAS, erythroblastosis fetalis, polycythemia, hypothermia or lethargy • Poor feeding • Eye-rolling
• Premature (inc late preterm infants) or postmature delivery
• Family history of a genetic form of hypoglycemia
• Congenital syndromes, abn physical features (eg: midline facial malformations, microphallus)

MANAGEMENT
At birth, screen of risk infant –
Well infant who at risk? – immediate feeding (initial feeding give w/I 1 hour of birth), if needed, give supp
feeding until establish BF. Initial BG done 30 mins after 1st feed.
Sick infant? – check BG on admission & set up IV dextrose 10% drip 60 ml/kg/day

COMPLICATION – mental retard, seizure, dev delay, cerebral palsy, cognitive impair, visual prob, microcephaly

33
 Mx for recurrent persistent hypoglycemia –
• PO Diazoxide 5-20mg/kg/day in 3 divided doses
• Chlorothiazide 5-10mg/kg/day divided into 2
doses or Hydrochlothiazide 1-2mg/kg/dose BD
• SC Octreotide (synthetic somatostatin) 5-35
μg/kg/day BD/TDS or as infusion

34
NEONATAL JAUNDICE **normal term newborn produce 6-10 mg/kg/day of bilirubin

= baby become clinically jaundice when bilirubin lvl > 85 umol/L (5 mg/dl)

(1 g of Hb = 34 mg of bilirubin)

History
• Age of onset.
• Previous infants with NNJ, kernicterus, neonatal
death, G6PD deficiency.
•Mother’s blood group (from antenatal history).
• Gestation: the incidence of hyperbilirubinaemia
increases with prematurity.
• Presence of abnormal symptoms such as apnoea,
difficulty in feeding, feed intolerance and
temperature instability.

Physical examination
• General condition, gestation and weight, signs of
sepsis, hydration status.
• Signs of acute bilirubin encephalopathy (ABE)
should be assessed for in all babies with severe NNJ
(see BIND score)
• Pallor, plethora, cephalhaematoma,
subaponeurotic haemorrhage.
• Signs of intrauterine infection e.g. petechiae,
hepatosplenomegaly.
• Cephalo-caudal progression of severity of
jaundice.

Polycythemia –
Infant of diabetic mother
Twin-twin transfusion syndrome
Delayed cord clamping
Maternofetal transfusion
Small for dates infant

How to know about is it

obstruction or hepatitis?
Admit & observe for stool color
for 3 days.
High GGT + pale color – biliary
atresia
HIDA scan – for biliary atresia
(normal uptake, reduce excretion)
& hepatitis (reduce uptake,
normal excretion)

35
PHYSIOLOGICAL JAUNDICE

= due to excessive bilirubin production (higher Hb content & shorter RBC life span in newborn babies) & poor
bilirubin clearance (liver immaturity)

50% newborn infant become visibly jaundice – app day 2-4, resolve after 1-2 week

Not assc w u/l dis & usually benign

Breastmilk jaundice – there’s glucuronyl transferase inhibitor in breastmilk

Breastfeeding jaundice – lack of milk production, so poor enterohepatic circulation (dehydration)

METHOD TO DETECT JAUNDICE

1. Visual assessment (kramer’s rule) – visually assessed every opportunity

= blanch the skin w slight finger pressure & note the u/l color of skin. (do in well-lighted room)

Jaundice visible when bilirubin lvl are about 86-120 umol/L (5-7 mg/dl) & progress from head to toe.

If clinically jaundiced, check w transcutaneous bilirubinometer (TcB) or blood sample (serum bilirubin)

KRAMER’S RULE

= describe relationship btwn serum

bilirubin & progression of skin
discoloration

36
 2. Transcutaneous bilirubinometer (TCB) – used if jaundice is detected
3. Total serum bilirubin – if TCB lvl > 200 umol/L (12 mg/dl)

COMPONENT OF ASSESSMENT – important to identify the RF &

severity, assess general condition of baby & observe sign of
bilirubin toxicity.

1. Excessive wt loss

Assess the adequacy of breastfeeding, weight & hydration status

of all babies during 1st week of life.

Babies w weight loss >7% of birth weight should be referred for

further evaluation and closely monitored for jaundice.

2. Assessment of ABE - use BIND score

3. Blood test
(G6PD screening – need to be reviewed w/I
24 hours)

37
If jaundice persists beyond 14 days in term babies & 21 days in preterm babies, further evaluation for
prolonged jaundice is needed.

38
MANAGEMENT (Avoid sunlight exposure to reduce jaundice as risk of dehydration & sunburn)

*poor milk intake & dehydration will exacerbate jaundice!

1. Phototherapy (gradually bilirubin clearance)

How? – convert soluble bilirubin to more soluble form, excreted in bile or urine

Type: fluorescent tubes, Light Emitting Diode (LED), fibreoptic & halogen bulbs

When? - total serum bilirubin reaches the phototherapy threshold for neonatal jaundice

p/s: once on PTx, need to take serum bilirubin (don’t relay on visual ok )

CARE OF BABIES DURING PHOTOTHERAPY

Avoid sunlight exposure

Continue the breastfeeding

Expose adequately (cover eyes – prevent retinal damage)

Side effect of ptx –
Monitor temp, hydration status regularly - prevent overheating/ wt loss Fever, dehydration (so, do frequent feeding or
Ensure adequate hydration/ UO increase IVF by 20%)
Retinal damage (so, cover eyes)
Turn off photolights & remove eyepads during feeding & blood taking Mutation in gonads (cover gonads too)
Hypocalcemia
Watery diarrhea – d/t bile pigment in gut
Bronze baby syndrome – C/I in conjugated
jaundice (hepatitis)

2. Exchange transfusion (rapidly bilirubin clearance) (can read about protocol of EF in

CPG – appendix 4, m/s 41)

= indicated for severe hyperbilirubinemia (need to monitor closely & rx w intensive PTx)
(Babies undergoing ET should be closely monitored)

Volume to be exchanged is 2x the infant’s total blood volume (2x80mls/kg).

Use (preferably irradiated) Fresh Whole Blood preferably < 5 days old or reconstituted
Packed Red Blood Cells and FFP in a ratio of 3:1.

METHOD: via femoral vein, umbilical artery/ vein, peripheral artery (radial artery),
peripheral vein

39
Indication –

Double volume exchange – to reduce s. bilirubin & also reduce risk of brain damage, >> NH3, remove bact roxin &
also correct L-T electrolyte & fluid in acute renal failure.

Partial ET – to correct polycythemia & also to correct severe anemia.

So, how to prevent severe NNJ then?

All babies that discharged < 2 days after birth – f/u w/I 24 hours of discharge (either in ambulatory setting or at
home)

For babies w severe NNJ admit for rx, need early f/u to detect rebound jaundice after discharge.

Use predischarged screening (clinical RF assessment/ predischarge bilirubin lvl) to prevent severe NNJ in late
preterm & preterm babies

Admit all G6PD deficient babies & monitor for NNJ during 1st 5 days of life. If there’s clinically jaundice, do TSB.

Term G6PD babies w birth wt > 2.5kg & TSB < 160 umol/L (9 mg/dl) may discharged earlier on 4 th day of life & f/u
closely.

FOLLOW UP

•Babies w ABE should have long-term f/u to monitor for neurodevelopmental sequelae.

• Term & late preterm babies w TSB >20 mg/dL (342 μmol/L) or exchange transfusions should have Auditory
Brainstem Response (ABR) testing done within the 1st 3 months of life. If the ABR is abnormal, the baby should be
referred soon to the audiologist for early intervention & neurodevelopmental follow-up should be continued.

• Healthy term & late preterm babies with non-haemolytic hyperbilirubinemia and TSB < 25 mg/dl (428 umol/L)
may f/u at 1’ care lvl (KK lah )

• Preterm baby w jaundice f/u for neurodev sequalae as per f/u plans for all preterm babies.

40
NEUROLOGIC SEQUELE – assess by BIND score

= When bilirubin become dangerously elevated, albumin become saturated. So, circulating bilirubin cross BBB
causing apoptosis & necrosis.

41
SEIZURE = Clinical event in which there’s sudden disturbance of neurological function caused by abn/ excessive neuronal
discharge. Can be epileptic or non-epileptic

EPILEPSY NON-EPILEPTIC
• Idiopathic (70–80%) • Febrile seizures
• Secondary • Meningitis/encephalitis
– Cerebral dysgenesis/ malformation • Metabolic – Hypoglycaemia, Hypocalcaemia/
– Cerebral vascular occlusion hypomagnesaemia, Hypo/ hypernatraemia
– Cerebral damage (eg: cong infection, HIE, • Head trauma
intraventricular H’ge/ ischaemia) • Poisons/toxins.

• Cerebral tumour
• Neurodegenerative disorders
• Neurocutaneous syndromes
Disrupt brain’s normal function Does not disrupt brain’s normal function
l/t some loss of consciousness/ impaired senses No LOC / impaired sense

FEBRILE SEIZURE

= seizure accompanied by fever in absence of intracranial pathology or metabolic derangement, usually in children btwn 3m – 6
y/o. (fever? – so need to find source of infection (eg: URTI, OM, AGE, post-vaccine fever)

SIMPLE FEBRILE SEIZURE COMPLEX FEBRILE SEIZURE

Duration < 15 mins >15 mins
Generalized tonic clonic Focal seizure (preserve conscious lvl)
Freq 1 episode only (not recur during febrile eps) Multiple seizure during febrile episode
Post ictal Return to baseline May not return to normal (residual motor neuro
deficit – Todd’s paralysis)
*affect arm/leg, 1 side, last ~15hours, subside after 2
days
Not cause brain damage. IQ not affected - same in 4-12% risk for subsequent epilepsy
child who did not have febrile fit
1-2% risk to dev epilepsy.

INVESTIGATION - d/o clinical assessment of individual case

FBC, RFT, blood sugar, LP, urinalysis, CXR, blood cns etc

Lumbar puncture (L3 – L5)

INDICATION CONTRAINDICATION
CF of intracranial infection Bleeding tendency
Persistent lethargy after 6 hours of seizure ↑ ICP
Age < 12 months esp if child not receive Hib & Infection at needle insertion site
pneumococcal immunization Cardiac – respi compromise
Fail AB therapy Hemo unstable
Unequal eye reflex/ pupil
GSC <8
Abnormal posture
Papilloedema
Immediately after seizure

42
 [Not all children need to hospitalize.]
So, actually why do we need to admit? – to exclude intracranial
pathology esp infection, Fear of recurrent seizures, to investigate &
treat the cause of fever besides meningitis/encephalitis, to allay
parental anxiety, esp if they are staying far from hospital.
MANAGEMENT

Control fever by avoid excessive clothing, use antipyretic drug (syrup/ rectal PCM 15 mg/kg 6 hourly)

Counsel the parents on benign nature of condition.

Advise parents on first aid measures during seizure

Children w high risk of recurrent febrile seizure inc those w febrile SE need to supplied w rectal diazepam (dose: 0.5 mg/kg).
advise parent on how to administer if seizure > 5 mins.

CAUSES OF SEIZURE “VITAMIN O”

Vascular – stroke, vasculitis
Infection – meningitis, encephalitis, cerebral malaria
Trauma
AV malform – cavernous malform
Metabolic - ↓ Na, Ca, Mg, hypoglycemia. Reye’s
syndrome
Idiopathic
Neoplasm
NCS – NF, tuberous sclerosis, sturge-weber
syndrome
Others – drug overdose, hydrocephalus, multiple
sclerosis

43
STATUS EPILEPTICUS

44
HISTORY TAKING

Pre Age of child

Any warning before the fit? – abd pain, fear, unpleasant sensation (TRO epilepsy)
What was the child doing
Asleep or awake?
Any trigger? (breath holding spells & vasovagal events are often confused w seizure)
Was child well? Any feer?
Travel hx or sick contact
To exc CNS infection (eg: meningitis, encephalitis)
Exc acute systemic metabolic abn that may produce convulsions
Hx of previous afebrile seizures
Ictal Duration of spell? How many episodes? How often?
Was the child responding during the spell or was consciousness impaired?
Did child remember the spell
Repetitive behavior during spell (eg: lip smacking etc)
Describe the body movement
Was there any perioral cyanosis?
What was the child’s skin color during the event
Did the patient lose continence (bowel/ urinary)
Gaze deviation, eye rolling
Post How did the patient feel after the spell?
Did the child seem drowsy, confused and tired after the spell?
How long did it take for the child to get back to baseline condition?
Any transient limbs weakness
Others Trauma
Prev hx of seizure, febrile seizure
Birth hx – maturity, cong defect, H’ge, birth trauma
Detail developmental hx
Immunization hx
Current medication (eg: buspirone can lower seizure threshold)
Fam hx of seizure/ epilepsy

PHYSICAL EXAMINATION

• Vital sign, temp

• Anthropometry – wt, ht, HC

• Neuro : sign of increase ICP, cranial nerves, Motor, sensory, cerebellar, reflexes

• meningeal sign : Kernig, Brudzinski

• Signs of trauma

• Skin exam – neurocutaneous stigmata

• Sources of infection – ears, throat, abdo, resp, CVS

45
MENINGITIS *serious life-threatening ! – high morbidity.

Meningitis = Inflammation of meninges covering the brain.

Aseptic meningitis = Viral meningitis

Partially treated Meningitis = Give AB prior to LP [role of dexa is zero!]

CAUSES

Viral (eg: entrovirus, EBV, HSV, CMV, adenovirus) - self resolving

Bact – may have severe consequence

Non-infectious: malignancy, autoimmune dis

RISK FACTOR

Genetic, Acquired/ congenital immunodeficiency

Hg-pathy (eg: SCD, asplenia, crowding, basilar skull fracture)

Recent/ current infection

46
47
MANAGEMENT

Antibiotic & give dexa before or w 1st AB (0.15 mg/kg 6 hourly for 4 days or 0.4 mg/kg 12 hourly for 2 days)
→ ↓ sequele bact meningitis.
p/s: & also give steroid if CSF tubin & pt not receive prior AB

Supportive measure

Monitor vital sign 4 hourly & monitor input/ output If persistent fever in a patient on
NBM if unconsciousness treatment for meningitis, consider:
• Thrombophlebitis & injection site (eg: IM
Judicious fluid management with careful monitoring to ensure adequate abscess)
circulating volume • Intercurrent infection (eg: pneumonia,
UTI or nosocomial infection)
If fontanel still open, note HC daily. Consider cranial usg/ CT scan if suspect • Resistant organisms. Inappropriate
effusion or hydrocephalus antibiotics or inadequate dosage.
• Subdural effusion, empyema or brain
Seizure chart abscess.
• Antibiotic fever
Daily neuro assessment

Observe for 24 hours after stopping therapy. If no compli, can discharge

COMPLICATION “ABCD CROSS”

Cerebral Abscess – temp will continue to fluctuate. Confirmed on CT scan. Need to drain the abscess

Blindness

CN palsy (local vasculitis)

Deafness (hearing loss) – infla damage to cochlear hair.

Concentration & memory prob/ cerebral herniation

Repeated episode/ epilepsy - local cerebral infarction

Optic nerve atrophy

Stroke

SIADH – need to be careful in fluid mx! If SIAD occur, then reduce to 2/3 fluid maintainer for initial 24 hours

Subdural effusion (esp Hemo influenza & pneumococcal meningitis) – confirmed by CT scan. Resolve
spontaneously, but may need prolonged AB rx

Spastic paraparesis

Hydrocephalus

48
INDICATION

CT SCAN BRAIN (W/O CONTRAST) SUBDURAL DRAINAGE

• Prolonged depression of consciousness • Prolonged • Rapid increase in HC with no hydrocephalus.
focal or late seizures. • Focal neurological signs.
• Focal neurological abnormalities. • Increased ICP
• Enlarging HC • Suspected subdural empyema.
• Suspected subdural effusion or empyema

FOLLOW UP (need long term f/u) PROGNOSIS

• Note development of child at home & in school. • Age: worse in younger patients.
• Note HC • Duration of illness prior to effective antibiotics
• Ask for any occurrence of fits or any behavioural treatment.
abnormalities. • Causative organism: more complications with H.
• Assess vision, hearing and speech. influenzae, S. pneumoniae.
• Request for early formal hearing assessment in cases • Presence of focal signs.
of proven meningitis.
• Until child shown to have normal development
(usually until 4 years old).

49
50
MACROCEPHALY (LARGE HEAD) = head circumference above 98th centile.

CAUSES

Brain Fluid Blood Bone

Cerebral tumor Hydrocephalus IVH Thalassemia
NF-1 Subdural effusion Chronic SDH Ricket
Cyst
GM, WM (alexander dis)

MONRO KELLIE HYPOTHESIS ANTERIOR FONTANEL

Close at 9 – 18 months
Vol of brain + vol of blood + vol of fluid = 0
(PF → 2 – 3 months)
p/s: any increase volume in one of these – other 2 must compensate it. Pulsatile
Btwn Sagittal & coronary
Cerebral blood flow is autoregulated, as long as cerebral perfusion pressure is in range of 60 – Larger than PF
160 mmHg Sunken → dehydration
Bulging → meningitis
if CPP < 60 mmHg - ↓ CBF

51
 CEREBROSPINAL FLUID
Normal CSF production – 20ml/hour
Normal CSF volume – infant: 50ml, adult: 150ml
Normal interventricular pressure – maximum 180mmH20
Production: choroid plexus (lat ventricle)
Absorption: subarachnoid villi
HYDROCEPHALUS

= obstruction to the CSF flow causing dilatation of ventricular system proximal to site of obstruction.

52
CLINICAL FEATURES “ABCDEF IU”

Accelerated head enlargement – ↑ occipital-frontal circumference

Bulging AF – wide open

Cranial suture separated – cracked pot sign

Dilated scalp vein – increased collateral venous drainage

Eye’s downward (“sunset eye”) – abducen nerve palsy

Forehead broad

Irritability, lethargy, poor appetite, projectile vomiting

UMNL : brisk reflex, spastic, clonus, Babinski +ve

Cranial percussion – macewen sign/ cracked pot sound (as suture separate)

INVESTIGATION

CT/ MRI scan

Usg of intracranial (if AF still open) - ventriculomegaly, size and location of lesions

Skull x-ray – suture separate, erosion of post clinoid process, beaten silver app

ICP monitoring can be used to ix NPH & also to test response to shunt

MANAGEMENT

Symptomatic relief – acetazolamide

Rx the causes (eg: obstruction – excision of mass, post fossa decompression for chiari)

Endoscopic – endoscopic 3rd ventriculostomy (ETV) +/- choroid plexus cauterization

Shunt - ventriculoperitoneal (VP), Ventriculoatrial (VA), Ventriculopleural (VPI)

COMPLICATION OF HYDROCEPHALUS

Shunt compli – malfunction, infection, over/underdrainage, shunt infection

Shunt can be malfunction as blockage or infection w coagulase -ve staphylococci.

Overdrainage of fluid can cause low pressure severe intermittent headache, &
relieve by lying down.

Mx by insert regulatory valve

Cerebral palsy, Epilepsy, Dev delay, Mental retard, impair IQ

53
54
 HENOCH-SCHÖNLEIN PURPURA (HSP) / IgA VASCULITIS/ PURPURA RHEUMATICA/ ANAPHYLACTOID PURPURA

Most common vasculitis in children – affect small vessel

Boys > girls (3 – 15 years). Peak during winter months HS type 3 (immune complex mediated)

CAUSES
*exact cause unknown
75% have hx of URTI,
pharyngeal infection, GI
infection
Infection - GAS, hepatitis,
H. pylori
Drug ingestion – ampicillin,
erythromycin
Vaccination – measle
Insect bite

JOINT –
SKIN – Kidney – AGN, Arthritis/ arthralgia
Rash - non-thrombocytopenic nephrotic Site: wt bearing jt (hip, knee & ankle)
purpura syndrome
(palpable & non-blanching) Usually transient/ migratory, typically
Site: symmetrically distributed, oligoarticular (1-4 jt) & non-deforming.
GIT –
below waist (buttock & extensor Often prominent periarticular swelling &
Mild: nausea, vomiting, abd pain, transient
surface of arm & leg, ankle) tenderness.
paralytic ileus
*the trunk is spared, unless No jt effusion, erythema or warmth.
Severe: GIB (melena/ hematemesis), bowel
induced by trauma Have considerable pain & limitation of motion
ischemia & necrosis, intussusception, bowel
perforation Younger children w lower extremity inv refuse
The rash often begins w to ambulate (eg: walk)
erythematous, macular, or
urticarial wheals. It precedes the app of purpura, though usually
Others - (rare in lung & CNS)
The initial rash may coalesce & by no more than 1/2 days
Scrotum – pain, tenderness, swelling
evolve into typical ecchymoses,
CNS – headache, seizure, encephalopathy
petechiae & palpable purpura.

May be itchy, but rarely painful

Skin lesion lasted for 3 – 10 days

“HSP”
Hematuria
Skin – palpable purpura, non-blanching
Pain – abd & joiny
55
INVESTIGATION

Serum IgA ↑↑

FBC – all normal inc platelet. Mildly ↑ WBC

RFT – ↑ creatinine (kidney impair)

ESR ↑

Urinalysis – hematuria

Skin/ renal biopsy → IgA deposition

24h urine protein/ urine protein-creatinine ratio → TRO nephrotic syndrome

Coag – normal

ASOT – prev infection

No ANCA form

MANAGEMENT *self-limiting

Supportive – oral hydration, rest, symptomatic pain relief

Treat accordingly –

Jt pain Ibuprofen, PCM

Severe abd pain Oral prednisolone
IV CS if has nausea, vomiting
Renal involvement Refer to nephrologist!
IV CS (pulse dosing), Oral CS, Oral cyclophosphamide
*steroid → prevent immune system from causing further damage to blood vessel

COMPLICATION *usually rare. But if any, more common in adult

KIDNEY GIT LUNG CNS

AGN Intussusception Pul H’ge Seizure
Nephrotic syndrome GIB Pleural effusion Ataxia
Renal failure Bowel infarction/ Cerebral H’ge
H’gic cystitis perforation Chorea
Duodenal obstruction Cortical blindness
Intestinal stricture

56
 FOLLOW UP PROGNOSIS FOR HSP NEPHRITIS
If initial UFEME normal/ only microscopic hematuria, Progression to ESRD:
monitor BP & UFEME :- • 2-3% of those w initial renal involvement, 15-30% w
• Weekly for the first month after disease onset more severe renal dis
• Fortnightly from weeks 5-12
• Single reviews at 6 & 12 months Children at risk for progression:
• Nephrotic syndrome
If normal UFEME at 12 months, no need further • Renal insufficiency
follow-up.

CHILDREN ADULT
Purpura Limb (dependant area) Limbs, torso
Abd pain Present Present
Arthritis/ arthralgia Knee, ankle, elbow, shoulder Wrist, MCP, PIP, MTP
Renal involvement Uncommon Common
Edema Scalp, face, arm, hand, feet, Absent
scrotum
Course Benign More fulminant
Familial Rare Absent

DIFFERENTIAL DIAGNOSIS

ITP IgA RHEUMATIC FEVER SLE

NEPHROPATHY
Points Rash – petechial Renal biopsy similar w Deposition of IgA on Predominance
supporting HSP findings biopsy deposition of IgA on
↑ ASOT biopsy

Points against No jt, abdominal Age : 20 – 40 y/o Rash : erythema Adult

pain No rash marginatum Has ANA, ANCA,
Plat : HSP normal, No jt/ abdominal pain complement lvl
ITP ↓

57
IMMUNE THROMBOCYTIC PURPURA (ITP) * Peak: 2 – 10 years

= Self-limiting disorder, presenting w isolated thrombocytopenia (< 100 x 10^9/ L) in absence of u/l causes

PATHOGENESIS

Autoimmune disorder c/b autoantibody mediated immunologic destruction of normal platelets (mainly occurring
in spleen), in response to unknown stimulus.

Spectrum of bleeding –
CLINICAL FEATURES
Petechia/ purpura
Hx of viral infection in preceding 2 – 4weeks
Mucosal bleed
No LN/ hepato-splenomegaly (epistaxis, gum bleed, gross hematuria)

Platelet will normalize in few days to 6 months (average 3 weeks) Life threatening (eg: ICH)

INVESTIGATION *ITP = diagnosis of exclusion! INDICATION for BMA –

B4 start steroid
FBC – only ↓ platelet. Otherwise, normal Hg & WBC Fail respond to IVIG therapy
Persistent ↓ platelet > 6 months
PBS – reduced, larger platelet. No abnormal cell. Thrombocytopenia recur after initial response to rx
BM aspirate (if uncertain dx): large platelet, ↑ megakaryote Atypical features – organomegaly, abn blood
count, suspicious PBS
CoAg profile – INR high. PT & APTT normal

ANA/ DNA-Ab – to exclude SLE

Abnormalities that might indicate an alternate diagnosis rather than ITP are –
• Fever or bone or joint pain • A family history of low platelets or easy bruising
• Risk factors for HIV • Skeletal or soft-tissue morphologic abnormalities • Non-
petechial rash • Lymphadenopathy • Abnormal Hb, WBC count, or morphology not
typical of ITP

58
MANAGEMENT (rx direct at clinical status of pt, not plat count)

Mostly self-limiting & resolve spontaneously. Not all children w acute ITP need to admit. As 70% achieve platelet >
50 x 10^9/L by end of 3rd week w/o rx.

So, when to admit? – Advise –

Severe life-threatening bleeding (eg: ICH), regardless platelet count • Precaution w physical xtvt esp small children.
• Avoid contact sports.
Platelet < 20 x10^9/L & bleeding • Seek immediate medical attention if significant
bleed.
Platelet < 20 x10^9/L w/o bleeding but not access to health care • Avoid aspirin /NSAIDs.
Lack of confidence in homecare

↑ risk to get ICH

Platelet < 20 x10^9/L
No need to rx, just observe & monitor Hx of head trauma
plat, in – Give rx, if –
L-T bleeding episode (eg: ICH) regardless Use aspirin
Platelet > 20 x10^9/L w/o bleeding Cerebral AV malformation
Platelet > 30 x10^9/L w only cutaneous plat count
purpura Platelet < 20 x10^9/L & mucosal bleeding
p/s : repeat FBC w/i 7-10 days – ensure Platelet < 10 x10^9/L & any bleeding
no evolving marrow disorder)

Choice of treatment –

Oral prednisolone (2 mg/kg/day) for 14 days, then taper off over 5 days (regardless of response)

Oral prednisolone (4 mg/kg/day) for 3 - 4 days

p/s: don’t continue steroid if no response or there’s rapid relapse after wdrawal

IV Immunoglobulin (IVIG) 0.8 g/kg/dose for a single dose, round up to the nearest bottle to avoid wastage. (S/E –
fever, flushing, headache, nausea, aseptic meningitis & possible blood borne infection (eg: hepatitis)

EMERGENCY TREATMENT

IV methylprednisolone (30 mg/kg/ day) for 3 days Splenectomy?

IVIG (0.8 – 1 g/kg) as single dose Consider if L-T bleeding & severe lifestyle
restriction, still no/ transient success w
Methylpredni + IVIG – in L-T condition IVIG, pulse steroid, anti-D Ig
Pre – vaccine (pneumococcal,
Platelet transfusion (8 – 12 unit/m2 BSA), as plat will be consumed by H’ge meningococcal, hemophilus)
to form blood clot & will reduce further circulating plat p/s - pneumococcal booster given every 5
years
Emergency splenectomy if others fail (prefer laparoscopic) Post – lifelong penicillin prophylaxis (oral
/ IM)
Neurosurgical intervention maybe indicated in ICH
*upto 70% pt achieve complete remission
post-splenectomy

59
CHRONIC ITP = Persistent thrombocytopenia after 6 months of onset

MANAGEMENT

Counselling & educate the pt & caretakers:-

Regarding natural hx of dis

How to detect problems

Possible complication (ICH, immunosuppressive cx (eg: severe varicella)

Parents must aware when & how to seek early medical attention

Asx children can be left w/o therapy & kept under observation w continued precautions during physical xtvt.

Symptomatic children? – need short course of rx as acute ITP to tide them over ‘relapse’ period or during surgical
procedure

1st line 2nd line

Oral prednisolone Steroid pulse: oral dexa (1 mg/kg) on 4 consecutive days every 4 weeks for 4 months
IVIG
Intermittent anti Rh(D) Ig rx for those Rh D +ve.
(45 – 50 ug/kg). may cause drop in Hb lvl.

*in refractory dis → consider rituximab & cyclosporine

ITP TTP DIC

Pathogenesis Anti-plat antibodies Endothelial defect Thrombin excess
Clinical condi Not ill Ill-app Ill-app
Peripheral smear Large platelet Schistocytes Schistocytes
Platelet ↓↓↓↓ ↓↓ ↓
Hg Normal ↓ ↓
MAHA No Yes Yes
Hemolysis labs Normal Abnormal Abnormal
Creatinine Normal Normal/ mildly ↑ Normal/ ↑
PT/ APTT/ INR Normal Normal ↑
Fibrinogen Normal Normal ↓
D-dimer Normal Normal/ ↑ ↑
Management Supportive Supportive Supportive
Steroid Plasma exchange
IVIG Steroid
Splenectomy

60
 By shahirashuhadajailani
(Telegram: budak medik) 

THALASSEMIA *autosomal recessive *hypochromic, microcytic anemia

= Heterogeneous group of inheritance disorder, c/b reduction or absence of synthesis of

normal globin chain (alpha/ beta) *Structure ok, quantity ↓

*all pt w MCH <27pg should be screened for thalassemia.

TYPE OF THALASSEMIA

Hb synthesis – alpha (deletion of chromo 16) & beta (mutation at chromo 11)

Severity – minor, intermedia, major

Genetic – homozygous (affected), heterozygous (not affected)

61
 Jaundice –
Liver cirrhosis
HA – hypersplenism
CLINICAL FEATURES BT - hepatitis

1. Anemia, jaundice, gallstone, hepato-splenomegaly

2. Skeletal changes

Facial deformity Frontal bossing

(Chipmunk facies) Maxillary overgrowth – “jumbling” of upper incisor
Malocclusion of teeth
Chronic sinusitis - Delayed pneumatisation of sinus
Depression nasal bridge
Impaired hearing (S/E desferioxamine)
Bone changes Cortical thinning
Increase porosity of long bone (OP)
Premature fusion of epiphyses – short stature
Paravertebral masses Broad expansion of ribs at vertebral attachment
Paraparesis

Fe overload (hemochromatosis) – why? – repeated transfusion, ineffective erythropoiesis

Arrhythmia

Bronze skin

CM, cirrhosis / fibrosis of liver

DM, delayed puberty

Hypogonadism, hypothyroid

INVESTIGATION

1. FBC - ↓ Hb, ↓ MCH, MCV, MCHC, uniform RDW, ↑ Reticulocyte, ↑ WBC, Normal platelet
2. PBS – Hypochromic microcytic, Aniso-poikilocytosis, Target cell (bleb)
3. Fe study - ↑ Fe, ferritin, transferrin, ↓ TIBC
4. Serum bilirubin (unconjugated) ↑
5. Hg analysis & genetic testing – Hb electrophoresis (↓ or absent HbA, ↑ levels of HbA2, & ↑ HbF) / High
performance liquid chromatography (HILC)/ DNA analysis
6. X-ray of skull, hand

SKULL HAND
Thinning of cortex Thinning of cortex
“Hair on end” app Rectangular app
Widening diploic space Widening of medullary
cavity w coarse trabecular
pattern

7. Liver biopsy - To measure liver Fe concentration (LIC)

62
MANAGEMENT

1. Blood transfusion (Hb decline 1 g/dl/week)

S/E: Fe overload (usually after 10 – 20 BT). So, how to monitor?- serum ferritin > 1000 ug/L

63
 2. Iron chelation agent (Aim: maintain s. ferritin < 1000 ug/L)

DESFERRIOXAMINE (DFO) / DESFERAL DEFERIPRONE (DFP) / KELFER/ DEFERASIROX (DFX) /

FERRIPROX EXJADE
*give with vit C (augment Fe excretion) > 2 y/o

WHEN TO START?
I. After 10 – 20 transfusion
ii. child > 2-3 years old
iii. serum ferritin > 1000 ug/L

Dose 20 – 40 mg/kg/day by SC continuous infusion Oral - 75 – 100 mg/kg/day, TDS 20 – 30 mg/kg OD in liq
using portable pump over 8-10 hours daily, 5-7 dispersible tablet
nights/week *can combine w desferal – using
low dose 50 mg/kg/day
S/E Local skin rxn – inadequately diluted desferal/ GI prob - nausea, vomiting, Transient skin rash
infection diarrhea, abd pain GI prob
Arthritis Reversible ↑ in serum
Yersinia infection – fever, abd pain, diarrhea Zn def creatinine (need monthly
*Mx : stop DFO, Rx w co-trimoxazole/ AG/ 3rd Hepatotoxicity RFT monitoring)
cephalosporin Thrombocytopenia

DFO toxicity (if high dose >50 mg/kg/day in low Idiopathic Agranulocytosis
serum ferritin) – *may need weekly FBC monitoring.
Eye – BOV, VF defect, night blindness (rev) *stop if neutropenic <1500/mm3
Ear – high tone deafness (irrev)
Skeletal – pseudo rickets, metaphyseal changed,
vertebral growth retardation

3. Splenectomy *delayed as long as possible (> 5 y/o)

Indication Evidence of hypersplenism - pancytopenia (recurrent infection)

Blood consumption volume of RBC > 1.5x normal @ > 200-220 ml/kg/ year in pt >5 y/o to
maintain average Hb lvl.
Prevention Give vaccine (pneumococcal & Hib) 4-6 weeks before surgery
Give oral penicillin for life after splenectomy
Thrombocytosis > 800k/mm3 post-op? - Low dose aspirin (75 mg daily)

4. BM transplant

5. Diet - Avoid food high Fe content (eg: red meat, Fe fortified cereals, Fe supplement), Take ↓ Fe absorption (eg:
tea coffee, milk, vit E, zinc)

64
65
 By shahirashuhadajailani
(Telegram: budak medik) 
HAEMOPHILIA (term in CPG: PWH – person w hemophilia)

= group of blood disorder that defect In clotting mechanism

*X-linked recessive inheritance (only boy affected, girls maybe carrier)

CAUSES - liver disease (synthesis clotting factor), < vit K (clotting factor 2, 7, 9, 10), auto-immunity against clotting
factor, DIC

CLOTTING DEFECT

A** B C
(Classic haemophilia) (Christmas haemophilia) (Autosomal recessive)
F8 F9 F11
Mx : desmopressin

CLINICAL FEATURES (5H – Hemarthrosis, Hematoma, Hematochezia, Hematuria, Head h’ge)

Bleeding in neonatal period – umbilical cord, ICH (assisted delivery), bleeding post circumcision, prolonged oozing
from heel stick/ venipuncture

Easy bruising when crawling and walking – fall over (esp 9-12 months (toddler)

66
Hemarthrosis– at large jt (swollen, painful)  may l/t crippling arthritis

Large hematoma following immunization (IM injection)

Bleeding may occur spontaneously or after trauma, operation, or after tooth

extraction

Consider serious if occur in jt (hemarthrosis), muscle esp deep compartment

(ilipsoas, calf, forearm) & mucous membrane in moth, gums, nose, genitourinary
tract

L-T if occur in neck/ throat, intracranial, GIT

INVESTIGATION

FBC – ↓ Hb (bleeding), plat normal

CoAg : APTT ↑, PT normal (as INR normal)

Specific factor 8/9 assay

Even if APTT normal - do von-willebrand screen

*once child is dx w hemophilia, check viral status at dx & then yearly!

Others - Hepatitis/ HIV serology, RFT, LFT (AST/ ALT),

Dx of carrier status for genetic counselling

I. Mother of newly dx son w hemophilia

Ii. Female siblings of boys w hemophilia

Iii. Daughter of man w hemophilia

MANAGEMENT

1. Prophylactic (expensive & need central venous access)

67
 2. Definitive – replace the missing factor

TYPE OF BLEED F8 DOSE (U/kg) F9 DOSE (U/kg) Aim % of factor DURATION Rx

Haemarthrosis 20 40 30 – 40% 2 – 3 days
Soft tissue/ 30 – 40 60 - 80 40 – 50% 4 – 5 days
muscle bleed
ICH / surgery 50 100 100% 7 – 10 days

Calculated formula 0.5 x 1.4 x *in young child, infuse F8 by slow IV push at rate
(ANOTHER OPTION) (% rise required) x (% rise required) x <100 U/mins
(weight in kg) (weight in kg)
*avoid give FFP, cryoprecipitate  ↑
Duration of giving 8 – 12 hours 12 – 24 hours transmission

*all haemophiliacs should be immunized *handle vein w care. NEVER perform cut-down
against hep B (SC route) unless in emergency as it destroy the vein.

3. Supportive (“RiD PRICE S”)

Relieve pain (analgesia) – avoid IM injection.

Use PCM +/- opiod. Don’t use aspirin/ NSAID (affect plat fxn)

Rapid pain relief in haemarthrosis once infuse missing factor concentrate

Dental care. As dental carries – regular source of bleeding

Protect, Rest, Ice, Compression, Elevation

Haemophilia society – give medic-alert bracelet/ chain

Avoid contact sport & drug promoting bleeding (eg: aspirin)

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COMPLICATION

Inhibitors (adverse rxn to CF treatment)

As body think the factor as F/B, so destroy it by inhibitor. (Ab directed against the exogenous F8/9
neutralizing the clotting xtvt)

Suspect when lack of response to replacement therapy despite high dose.

Can occur any age, usually after 10-20 exposure days.

Mx – “bypassing” the deficient clotting factor *difficult! Need consultation w hematologist 

1.recombinant activated F7 (rfVIIa / novoseven)

2. F8 inhibitor bypass xtvt (FEIBA)

3. immune tolerance induction

Jt destruction

Recurrent hemarthrosis in same jt will destroy the jt causing OA/ deformity

Mx : prompt & adequate factor replacement

Muscle atrophy, Compartment syndrome

Transfusion-transmitted infection (eg: HIV, hepatitis) : need immunization & regular screening

Vascular access

Peripheral vein – diff to canulate

Central venous access may have infected or thrombosed

HAEMOPHILIA A HAEMOPHILIA B VON WILLEBRAND DIS

Inheritance X-linked X-linked Autosomal dominant
Factor deficiency 8 9 VWF
Bleeding site Muscle, jt Muscle, jt Mucous
Surgical Skin
Platelet count Normal Normal or low
PT Normal Normal
APTT Prolonged Normal or prolonged
Bleeding time Normal Normal or prolonged
Thrombin time Normal Normal
F8:C Low Normal Normal or low
F9 Normal Low Normal
VWF Normal Low
vWF multimers Normal Variable
RiCof xtvt Normal Low
Plat aggregation in Normal Low
response to ristocetin
Treatment DDAVP Recombinant IX DDAVP
Recombinant VIII VWF concentrate

69
Paed’s protocol 
HAEMARTHROSES
(JOINT HAEMORRHAGES)
Most spontaneous haemarthroses
respond to a single infusion of
factor concentrate.
..>Aim for a level of 30 % to 40%.
If swelling or spasm is present,
treatment to level of 50% is
required &
infusion may have to be repeated at
12-24 hours interval until pain
subsides.
Minor haemarthroses
may not require immobilization,
-elastic bandage or slings
-& ice may help in pain relief.
In severe haemarthroses
-Splint in position of comfort.
-Rest.
-Early physiotherapy.
INTRACRANIAL HAEMORRHAGE
(ICH)
Pre-treatment factor assay level &
inhibitor level before starting tx &
to repeat after 3 days of tx to
ensure adequate levels have been
achieved & no inhibitor has
developed.
For haemophilia A give factor
replacement before suspected
bleed is confirmed by CT scan
• Aim to ↑ Factor VIII level to
100%.
For haemophilia B if monoclonal
factor IX is used a level of 80% is
adequate & if prothrombin complex
concentrate (PCC) is used 50% level
is recommend.
Post treatment factor assay level ( ½
H after infusion ) to ensure required
factor level is achieved ( if the level
is not achieved , consider
development of inhibitors ) &
should be repeated after 3 – 5 days
SURGERY
PRE-OP INVESTIGATIONS
1 .Full Coag profile – PT, PTT
2. Pre-factor assay level & inhibitor
lvl
3. Blood grouping
4. Full antibody screening & full
cross matching if required.
..>Calculate dose ½ hour before
operation, infuse pt w appropriate
F.
..>Preferable level:
- 80-100% for factor VIII
- 70% for monoclonal factor IX
- 50% if prothrombin complex
concentrate (PCC) used
..>Check post transfusion specific
factor level ½ H later if necessary or
after surgery to ensure correct
factor level is achieved.
..>Clotting factor level should be
maintained above 50% during the
operation & 24 hours after surgery.
ILIOPSOAS BLEED
SYMPTOMS:
Pain/discomfort in the lower
abdomen/upper thighs
SIGNS:
Hip flexed, internally-rotated,
unable to extend
• Danger: Hypovolaemia, large
volumes of blood may be lost in the
retroperitoneal space.
MANAGEMENT:
Factor replacement: 50U/kg stat,
followed by 25U/kg bd till
asymptomatic,
then 20U /kg every other day for
10-14 days.
Ultrasound / CT scan to diagnose.
Physiotherapy - when pain subsides.
Repeat U/S to assess progress.
HAEMATURIA
MANAGEMENT
-Bed rest.
-Hydration (1.5 x maintenance).
-Monitor for first 24 hours: UFEME
& Urine C&S.
-If bleeding persists for > 24 hours,
start factor concentrate infusion.
-Perform KUB & Ultrasound of the
kidneys.
Don’t give ANTI-FIBRINOLYTIC
DRUGS (tranexamic acid) because
this may cause formation of clots in
the tubules which may not
recanalize.

Urgent CT scan: ..>Maintain adequate factor levels

If CT scan confirms ICH : maintain -Days 1-3 60-80%
factor -Day 4-7 40-60%
- 80%–100% for Day 1 to Day 7 -Day 8-14 30-50%
- 50% for Day 8 to Day 21.

If CT scan show no evidence of ICH,

Repeat factor assay & check
admit 1 day for observation.
inhibitor level on day 3 to ensure
adequate.
..>Follow up CT scan after 2 weeks

*Post operatively a minimum of 10

to 14 days replacement therapy is
recommended.

70
 DIARRHEAL DISEASE Red flag –
Bloody stool
= sudden change to loose / watery stool, often accompanied by vomiting Fever
Petechia/ purpura
a. consistency change – watery content Sx of severe
b. frequency - > 3 – 4x/ day dehydration
c. wt stool - > 10 g/kg/day Wt loss/ FTT

THE CULPRIT

VIRUS BACTERIA
Rotavirus** E. coli
Adenovirus Shigella & Salmonella (dysentery + blood, pus in
Norvovirus stool, pain + tenesmus)
Astrovirus Campylobacter jejuni (+ severe abd pain)
Calcivirus Cholera & ETEC (profuse, rapidly dehydrating
diarrhea)
Rapid onset More insidious
Stool Watery May mixed w mucous +/- blood (dysentery)
Vomit +++ +/-
Abd pain +/- +++
Anorexia +/- +++

MECHANISM OF DIARRHEA (PATHOPHYSIOLOGY)

Secretory Osmotic Mixed S-O Motility Inflammation

Vibrio cholera, Lactose intolerance, Rotavirus Hypermotility, IBD, celiac dis,
viral gastroenteritis Malabsorption diagnosis of bact dysentery
exclusion

Bloody diarrhea
CLINICAL TYPE (dysentery) –
“CHEESSY”
1. Acute watery diarrhea (< 14 days) → secretory, osmotic Campylobacter jejuni
EHEC, ETEC
*assc w significant fluid loss & rapid dehydration Entamoeba histolytica
Shigella
2. Acute bloody diarrhea (dysentery) – “CHEESSY” Salmonella
3. Chronic/ persistent diarrhea (> 14 days) Yersinia enterocolitica

= assc w chronic enteropathy w impaired mucosal healing & diminished digestive & absorptive capacity, causing
malabsorption & maldigestion

71
so, when pt c/o diarrhea +/- vomiting – then assess state of hydration ask yourself is the child in “SHOCK”? –
most accurate – degree of wt loss during diattheal illness. if yes, go straight to plan C.

Children at risk of dehydration Why infant at risk of dehydration?

If passed >6 diarrhea stool in prev 24h
Vomited >3 in prev 24h
Unable to tolerate/ not been offered extra fluids
Have malnutrition
Infants, esp those <6 m/o or those born w low birth wt
1.have greater surface area to wt ratio causing greater
insensible water loss (300 ml/m2/ day)
2. Higher basal fluid requirement (100-120 ml/ kg per
day)
3. Immature renal tubular reabsorption
4. Cannot obtain fluid for themselves when thirsty

Example of Plan C –
12 kg child is clinically shocked & 10% dehydratied as result of AGE.
Initial therapy – establish ABC.
give FR rapid IV bolus = 20ml x 12 = 240 ml 0.9% NS
Fluid deficit = 10 x 12 x 10 = 1200 ml over 4-6 hours w 0.9% NS
Daily fluid maintenance = [100 x 10] + [50 x 2] = 1100 ml over 24 hours w 0.9% NS D5%
Replace OGL (diarrhea or vomiting) orally whenever possible = 5 – 10ml/kg for each episode

72
 MANAGEMENT for ACUTE DIARRHEA

PLAN A PLAN B PLAN C

Rx diarrhea at home (+ ORS)
3 rules of home treatment –
1. Give extra fluid (as much as child will
take)
Tell the mother –
BF frequently & longer at each feed
Exclusively BF? – give breastmilk + ORS or
cooled boiled water
Not exclusively BF? – give one or more of
ORS, food-based fluid (rice water, cereal
water, soup) or cooled boiled water
It’s especially important to give ORS at
home when the child has been rx w plan
B & C during this visit!
Give mother 8 sachets to use at home.
Teach how to mix & give ORS.
Show how ORS to give in in addition to
usual fluid intake –
<2 years → 50 - 100 ml after loose stool
≥2 years → 100 - 200 ml after loose stool
(it wt available, then give 10 ml/kg of
ORS after each loose stool)
2. Continue feeding
Breastfed infant? – continue nursing on
demand.
Formula fed infants? – continue their
usual formula immediately on
rehydration
Usually no need lactose-free or lactose-
reduced formula.
Children receiving semi-solid/ solid food?
– continue to receive their usual food
during illness
Avoid foods high in simple sugar as
osmotic load may worsen the diarrhea
Rx some dehydration w ORS
ORS over 4-hour period
[formula = child wt (kg) x 75]
Use weight.
If not, use child’s age.
p/s: if child want more ORS than
shown, give more!
Also teach mother to give ORS.
After 4 hours, reassess the child
& classify for dehydration.
Then select appropriate plan to
continue rx (Plan A, B or C).
Begin feeding the child.
If possible, observe the child AT
LEAST 6 HOURS after re-
hydration.
If mother must leave before
complete rx –
Show her to prepare ORS sol at
home
Show her how much ORS to give
to finish 4h rx at home
Give her enough ORS packers to
complete rehydration.
Also give her 8 packet as
recommended in Plan A.
Explain the 3 rules of home rx
(Plan A).
If there’s cholera outbreak in yr
area, give appropriate oral AB
after pt is alert.
Rx severe dehydration quickly (IV/ IO isotonic NS)
Assess & establish ABC quickly.
Start IV / IO fluid immediately!
If pt can drink, then give ORS by mouth while the drip is
being set up
Give initial fluid to resuscitation of shock – 20 ml/kg of
0.9% NS or Hartmann’s sol as rapid IV bolus
(repeat until out of shock or suspect fluid overload)
Please remember to review the pt after each bolus &
consider other causes of shock if child not responsive to
fluid bolus (Eg: septicemia)
Once circulation restores, commence rehydration, provide
maintenance & replace OGL.
Fluid deficit/ rehydration: % x kg x 1000
(use isotonic sol - 0.9% NS or Hartmann over 4-6 hours)
F. maintenance: use 100-50-20/day or 4-2-1/hour
(use 0.9% NS D5%)
OGL: 5-10 ml/kg for each episode
Reassess the hydration status frequently (eg: at 1 – 2
hourly) & adjust the infusion as necessary.
p/s –
More judicious fluid administration rate will be required in
certain situations (eg: child < 6 months, child w comorbid,
child that need careful fluid balance (eg: heart kidney prob,
severe malnutrition), child w severe hypo or
hypernatremia
Start giving more of maintainance fluid as oral feeds (eg:
ORS, about 5 ml/kg/h) as soon as child can drink, usually
after 1-2 hours for older child. the fluid should administer
frequently in small vol (cup & spoon works very well).

3. When to return to clinic/hospital NOTES – ORS ^^ Once child able to feed & not vomiting, can use oral
- Not able to drink / breastfeed Content rehydration as plan A or B & IV drip reduced gradually &
or drink poorly Na & glucose – 75 mmol/L taken off.
- Become sicker Cl - 65 mmol/L
- Develop fever K - 20 mmol/L INVESTIGATION AT ED
- Has blood in the stool Citrate - 10 mmol/L VBG – met acidosis
RFT
How to give?
blood sugar
Look at the back of ORS sachet
Wash hand. Clean the utensil
Put 1 sachet ORS into 250ml boiled water
Give freq small sips from cup/spoon
If child vomit, wait 10 mins, then
continue but more slowly ok
Continue give extra fluid until diarrhea
stop.
73
 p/s: During rehydration therapy, patients need frequent assessments and adjustments of the IVD, watch out
for fluids overload signs; puffy eyes and hepatomegaly

PHARMACOLOGICAL AGENT

Anti-diarrheal (only diosmectite (smecta) → reduce stool output & duration of diarrhea. Acts by restoring integrity
of damaged intestinal epithelium, also capable to bind to selected bacterial pathogens & rotavirus.

Others anti diarrhea not recommended as prevent stool excretion → colonization of org in body →
worsen the condi (eg: kaolin (silicates), loperamide (anti-motility) & diphenoxylate (anti motility).

Anti-microbial – AB not used as a routine. Reliably helpful only in dysentery child or suspect cholera w severe
dehydration
AB indicated in -
Antiemetic – not recommended - shigella dysentery
- suspect cholera (rice watery stool)
Probiotic - the effectiveness is very strain & dose specific. So certain - diarrhea assc w other acute infection (eg: pneumonia, UTI)
probiotic je can be used as adjunct. - for salmonella gastroenteritis in very young baby (<3m),
immunocompromised, systemically ill
Prebiotics – not recommended

Zinc supplement – during acute episode of diarrhea in children ≥ 6 months in area where prevalence of zinc def or
malnutrition is high. Dose - 20 mg/day for 10-14 days

INDICATION FOR ADMISSION TO HOSPITAL INDICATION FOR IV THERAPY

Severe dehydration or shock
Too young (< 3months)
Too ill – lethargy, drowsiness, high fever
Failed ORS rx & need for IV therapy
Uncertainty of Dx
Caregivers not able to provide adequate care at home
Social/ logistical concerns that may prevent return evaluation if
needed
Persistent vomiting or worsening diarrhea
Compli : bloody diarrhea indicating colitis
1. severe dehydration, shock
2. unconscious child
3. failed ORS rx d/t continuing rapid stool loss (> 15-20 ml/kg/h)
4. failed ORS rx d/t freq, severe vomiting, drinking poorly.
5. abd distension w paralytic ileus, usually caused by some anti-
diarrheal drug (Eg: codeine, loperamide) & hypokalemia
6. glucose malabsorption - increase in stool output & large
amount of glucose in the stool when ORS solution is given

COMPLICATION

Dehydration → shock

Electrolyte imbalance

Malnutrition

Extra-intestinal manifestation

Always keep in mind about NON-ENTERIC causes

of vomiting in paeds –
- UTI
- raised ICP
- parenteral vomiting/diarrhea

74
CHRONIC DIARRHEA –

1. TODDLER’S DIARRHEA *Dx of exclusion in thriving child

Most common loose stool in early childhood

Caused by excessive intake of fruit juice that contain non-digestible carbohydrate.

Freq watery stool, but normal growth & weight gain

Stool has undigested food particle.

Excoriated diaper rash

Typically improve tremendously when child’s beverage intake is reduced/ changed

Management – adequate fiber, normal fluid intake, 35-40% fat, discourage >> fruit juice.

2. LACTOSE INTOLERANCE = lack of lactAse

Action of colonic bact on unabsorbed lactose → release acid & gas

Persistent loose stool

Abd distension, Increase flatus

Perianal excoriation

Diagnosed by Benedict’s test → detect presence of reducing sugar (lactose) in stool

Result: blue → brick red

Managements – lactose-free diet, soy formula or lactase containing tablet/capsule/drop (eg: lacteeze, lactoid)

75
76
PAEDIATRIC FLUID & ELECTROLYTE GUIDELINES

p/s: these guidelines apply to children who are unable to tolerate enteral fluids.

safe use of IVF therapy in children need accurate prescribing of fluid & careful monitoring as incorrectly prescribed
or administered fluids are hazardous.

if need IVF therapy – then maintenance fluid requirements should calculate using Holiday Segar formula b/o
weight.

Fluids are given IV for the following reasons –

• Circulatory support in resuscitating vascular collapse.
• Replacement of previous fluid and electrolyte deficit.
• Maintenance of daily fluid requirement.
• Replacement of ongoing losses.
• Severe dehydration with failed nasogastric tube fluid replacement (Eg: on-
going profuse losses, diarrhea or abdominal pain).
• Certain co-morbidities, particularly GIT conditions (e.g. short gut or previous
gut surgery)

FLUID COMPARTMENT
Total body water (TBW) 60% -
Intracellular (40%)
Extracellular (20%) - Intravascular (5%) & Interstitial (15%)

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FLUID RESCUSCITATE

• Fluid deficit sufficient enough to cause impaired tissue

oxygenation (clinical shock) should be corrected with a fluid bolus
of 10-20mls/kg.

• Always reassess circulation - give repeat boluses as necessary.

• Look for cause of circulatory collapse - blood loss, sepsis, etc. This helps decide on the appropriate alternative
resuscitation fluid.

• Fluid boluses of 10mls/kg in selected situations - e.g. DKA, intracranial pathology or trauma.

• If associated cardiac conditions, then use aliquots of 5-10mls/kg

• Avoid low sodium-containing (hypotonic) solutions for resuscitation as this may cause hyponatremia.

• Measure blood glucose: treat hypoglycaemia with 2mls/kg of 10% Dextrose solution.

• Measure Na, K & glucose at the beginning & at least 24 hourly from then on (more frequent testing is indicated
for ill pt or pt w co-morbidities). Rapid results of electrolytes can be obtained from blood gases measurements.

• Consider septic work-up or surgical consult in severely unwell patients with abdominal symptoms (i.e.
gastroenteritis).

Total fluid requirement = fluid deficit + maintainance + ongoing loss

DEFICIT MAINTENANCE ON GOING LOSSES

0.9% NS
% x kg x 1000
Reassess clinical status and weight at
4-6hours, and if satisfactory continue.
= volume of daily fluid intake
0.9% NS + 5% Glucose
+/- KCl 20mmol/L
Holliday & Segar
First 10 kg - 100 ml/kg
Next 10 kg - 50 ml /kg
Each kg > 20kg - 20 ml/kg
(eg: from drains, ileostomy,
profuse diarrhoea)
0.9% NS or
Hartmann’s solution.
Any fluid losses > 0.5ml/kg/hr
needs to be replaced.
Calculation may be b/o each prev
hour or each 4-hour period d/o
the situation.
For example: a 200mls loss over
the previous 4 hours will be
replaced with a rate of 50 ml/hr
for the next 4 hours).

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ELECTROLYTE IMBALANCE

Ph 7.35 – 7.45
PO2 90 – 100 mmHg
PCO2 35 – 45
HCO3 20
- – 28
Na+ 135 – 145 mmol/L
K+ 3.5 – 5
Cl- 95 – 105

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 The daily K requirement is 1-2mmol/kg/day.
Normal values of K are –
• Birth - 2 weeks: 3.7 - 6.0mmol/l
ELECTROLYTE • 2 weeks – 3 months: 3.7 - 5.7mmol/l
• 3 months and above: 3.5 - 5.0mmol/l
1. Potassium (K)

HYPOKALEMIA HYPERKALEMIA
serum K+ < 3.4 mmol/l >5 mmol/L
Causes “DITCHS” “MACHINE”
DKA Medication - eg: oral K supp, K+ sparing diuretics, ACEI,
Drug - diuretic, salbutamol NSAID
Inadequate intake (eg: NPO, anorexia) Acidosis - DKA
Too much water Adrenal insufficiency
Cushing (↑ aldosterone) Cellular dysfxn (eg: burn, trauma injury)
Heavy fluid loss (eg: nausea, vomiting, sweating, NG suction) Hemolysis
Intake ↑
Nephro - acute kidney failure
Excretion impairs

CF “7 L” “MURDP”
1. lethargy (confusion, irritability) Muscle weakness +/- paralysis
2. low, shallow respi (↓ ability of accessory muscle) Urine ↓
3. lethal cardiac dysrhythmia (U wave) Respi distress
4. lots of urine Diarrhea
5. leg cramo ↓ heart contractility
6. limp muscle ECG - tall, peak T wave
7. low BP, HR Reflex (hyper)

Mx Identify & rx u/l condition. Monitor ECG

Rx if < 3 mmol/l or
(1 g KCL clinically Symptomatic & < 3.4 mmol/l Lytic cocktail –
= 13.3 IV calcium
mmol Oral KCL to max of 2 mmol/kg/day in divided doses. Neb salbutamol
KCL) Always give KCL by IV infusion, NEVER by bolus injection. IV Insulin w dextrose
Max conc via peripheral vein is 40 mmol/L IV bicarbonate
Max infusion rate is 0.2 mmol/kg/hour

Compli p/s – Cardiac arrhythmia

HypoK often seen w chloride depletion & met alkalosis. Cardiac arrest
Refractory hypokalaemia may occur w hypomagnesaemia. Progressive muscle weakness
Hypotension

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 Daily Na requirement - 2-3mmol/kg/day
Normal serum Na - 135-145mmol/l.
2. Sodium (Na)

HYPONATREMIA HYPERNATREMIA
serum Na+ < 135mmol/l serum Na+ > 150 mmol/l

p/s – hypoNa encephalopathy is medical emergency! mod hypernatremia = 150-160mmol/l

severe hypernatremia = > 160mmol/l.
Causes Hypovolemic – vomiting, diarrhea, diuresis “6 D” –
Euvolemic – SIADH, hypothyroid, low aldosterone 1. diarrhoea – water loss in excess of Na
Hypervolemic – CHF, cirrhosis 2. dehydration
3. diabetes insipidus – water deficit
4. diuretic
5. dis – kidney, sickle cell
6. docs (iatrogenic)

CF “SALT LOSS” May app sicker than expected for degree of dehydration.
Stupor, confusion, disorientation, coma
Anorexia (nausea, vomiting) Irritability
Lethargy Skin feel ‘doughy’
Tendon reflex ↓ Ataxia, tremor, hyperreflexia
Limp muscle – weakness Seizure
Orthostatic hypotension Reduced awareness, coma
Seizure, headache
Stomach cramping Shock occur late as intravascular vol is relatively preserved.

Mx In shock? – FR w 0.9% NS bolus.

Avoid rapid correction – may cause cerebral edema,
convulsion & death.
Aim to correct deficit over 48-72 hours and ensure the rate
of fall of plasma Na < 12 mmol/L in a 24-hour period
(0.5mmol/l/hour).
Remember to give FM & replace OGL
In acute sx hypoNa in term neonate & children, review the Repeat blood urea & electrolyte every 6 hours until stable.
fluid status, seek immediate expert advice.
Consider taking action as follows – If hyperNa worsen or unchanged, r/v fluid type & consider
• 2 ml/kg bolus (max 100 ml) of 3% NaCl over 10–15 mins. change to hypotonic sol (eg: 0.45% NaCl w dextrose).
• sx still present? - further 2 ml/kg bolus (max 100 ml) of 3% Measure Calcium & glucose as hypernatremia can be
NaCl over next 10–15 mins associated with hypocalcaemia and hyperglycemia, and need
• If sx still present after 2nd bolus, check plasma Na level & to be corrected concurrently.
consider 3rd 2ml/kg bolus (max 100 ml) of 3% NaCl over 10–
15 mins.
• Measure plasma Na concentration at least hourly.
• As sx resolve? - decrease the frequency of plasma Na
measurements b/o the response to rx.
• Do not manage acute hyponatraemic encephalopathy using
fluid restriction alone.
• After hyponatraemia sx have resolved, ensure that the rate
of increase of plasma sodium does not exceed 12 mmol/l in a
24-hr period.

Children w asx hypoNa –

No need 3% NaCl.
If dehydrated, mx w oral fluids or IV rehydration w 0.9% NaCl

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 3. Calcium (Ca)

HYPOCALCEMIA HYPERCALCEMIA
< 7 mg/dl
Causes Hypoparathyroid “SHAMPOO DIRT”
Vit D def Sarcoidosis
Alter vit D metabolism d/t medication usage Hyperthyroid/parathyroid
Dis affecting kidney or liver Alkali-milk syndrome
Hypo/ hyper-Mg Metastasis
Hungry bone syndrome Myeloma
Phosphate infusion Paget dis
Rapid citrated blood transfusion OP
Medications Osteogenesis imperfect

Vit D toxicity
Immobility
RTA
Thiazide
CF “CAT Numbness” Bone, groan, moan, stone
Convulsion
Arrythmia Bone – bone pain
Tetany Moans – psychiatric sx, lethargy, fatigue,
Stridor memory loss
Spasm (muscle cramp) Groan – Muscle weakness, constipation
Numbness in fingers Stone – kidney stone, severe thirst/ polyuria
ECG – long QT interval, torsade de pointes ECG – short QT interval, bradycardia
(VT)

Chvostek’s +ve = twitching of facial muscle

Trousseous’s +ve = carpopedal spasm d/t
inflate BP cuff

METABOLIC ACIDOSIS METABOLIC ALKALOSIS

Seen in a patient w Seen in patients w
-↑ H+ production (eg: DKA) -H+ loss (eg: vomiting)
-↓ H+ loss (eg : kidney failure) - H2CO3 ingestion
- Loss of bicarbonate (eg: vomiting)
“ALKALI”
Non-anion gap High AG (>12) Aldosterone ↑ (hyperaldosteronism)
Hyper alimentation “KLTR” Loop diuretic, thiazide / laxative
Acetazolamide Ketone alKali ingestion (antacid, baking soda, milk)
Renal tubular acidosis (DKA, alcohol, Anti-Coag – citrate
(RTA) starvation) Loss fluid → vomiting, dehydration, GI suctioning
Diarrhea Lactate ↑ NaH2CO3
Uretero-pelvic shunt Toxin – aspirin,
Post hypocapnia salicylates, cyanide, CO
Spironolactone Renal failure (uremia)

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 DENGUE

= ”breakbone” fever – a mosquito borne tropical dis caused by dengue virus

Vector - Aedes aegypti/ albopictus

Virus – flavivirus (ssRNA)

Serotype – DEN 1 – 4 p/s: infected w 1 serotype give lifelong immunity to that serotype, but not other serotype.

Incubation period: 4 -7 days

if SUSPECT OR CONFIRMED dengue, it’s mandatory to do DISEASE NOTIFICATION!

(Notified by telephone w/I 24 hours & followed by written notification w/I 1 week using BNP8)

Hallmark of severe dengue –

increased vascular
permeability (BV become
porous) → plasma leakage
→ ↓ intravascular vol, ↓ BP
→ shock

PROBABLE DENGUE WARNING SIGN

Live in & travel to dengue endemic “ALL LoVES”
area Abdominal pain (intense)
Fever + any 2 :- Liver enlarge (> 2cm)
Nausea, vomiting Lethargy, restlessness
Rash Lab - ↑ HCT (> 40%) w concurrent rapid ↓
Aches & pain in plat count
+ve tourniquet test Vomiting (persistent)
WBC ↓ Effusion – ascites, pleural/pericardial
effusion
Any warning signs (“ALL LoVES”) Significant mucosal bleeding

Tourniquet test (HESS test):

Laboratory confirmed dengue
(important when no sign of plasma
leakage)
inflate BP cuff on upper arm to pt
midway btwn SBP & DBP for 5 mins.
Look at cubital fossa for >20
petechiae (non-blanching) in 2.5 cm2

Dengue serology

i. < 5 days → NSI Ag (after day 5 +ve : sev dengue)

ii. > 5 days → IgM IgG

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FEVER
May suddenly dev high grade
fever, last 2-7 days.
Often accompanied by facial
flushing, rash, generalized body
ache, vomiting, headache
Some may have sore throat,
injected pharynx, conjunctival
infection
Mild H’gic manifestation –
petechiae, mucosal membrane
bleeding
Earliest indicator – progressive
decrease TWBC followed by plat
reduction
PRIORITIES DURING 1ST ENCOUNTER
1. establish whether the pt has dengue or not
2. determine what phase of illness
3. recognize any warning sign/ presence of severe dengue
Most DF pt w/o WS no need to hospitalize, provided they
are alert, no WS or evidence of abn bleeding, oral intake
& urine output are satisfactory, & the caregiver is
educated regarding fever control & avoiding NSAID & is
familiar with the course of illness.
These pt need daily clinical +/- lab assessment until
danger period has passed (see below)
PRIORITIES OF MANAGING HOSPITALIZED PT W DENGUE IN
CRITICAL PHASE
1. Replace plasma loss
2. Early recognition & treatment of H’ge
3. Prevent fluid overload
Fluid therapy in dengue shock has 2 part - initial, rapid fluid
boluses to reverse shock f/b titrated fluid volumes to match
ongoing losses.
but if pt has WS of plasma leakage but not in shock, may not
need rapid fluid bolus.
Hemodynamic state should be used as MAIN driver of IVF
therapy. HCT as a guide. not the other way around.
Limit fluid in febrile phase. if need IVF to correct hydration,
USE ONLY ISOTONIC SOLUTIONS (eg: NS)
CRITICAL RECOVERY/ REABSORPTION
Occur after day 3 of fever or around defervescence After 24-48h of critical phase, usually plasma
indicated by rapid drop in temp, coincide w increase leakage stops followed by reabsorption of
capillary permeability. extravascular fluid.
Last about 24-48 hours. Pt’s general wellbeing improve, appetite
return, GI sx improve, hemo status stable &
Evidence plasma leakage: diuresis ensures.
1.raised HCT
2. hemodynamic instable Some may has classical rash of “isle of white in
3. fluid acc in extravascular space the sea of red” w generalized pruritus.
4. hypoproteinemia
Important to note that HCT lvl stabilize & drop
In less severe pt, these changes are minimal & further d/t hemodilution following
transient. reabsorption of extravascular fluid.
May recover spontaneously or after short period of
fluid/ electrolyte therapy The recovery of plat count is preceded by
recovery of WBC.
In more severe form plasma leakage, pt may dev
compensated/ decompensated shock. Organ dysfxn may worsen (Eg: hepatitis,
Notes the warning sign for high possibility of compli. encephalitis, ICH) as pt enter reabsorption
phase.
Noted the platelet & HCT lvl.
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