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Paedi Quick Notes

Preterm Problems

Respiratory Distress Syndrome

• Common < 28 weeks
• Lack of surfactant due to immature lung, preventable if anticipated prenatally and mother given
• Treat with respiratory support and surfactant therapy via tracheal tube or catheter

• Complication of RDS, particularly if ventilated, but can also occur in normal neonates
• Treat with chest drain

Apnea, Bradycardia, Desaturation

• Mostly due to immature central respiratory control and will resume breathing with gentle
• Need to exclude other causes: anemia, infection, electrolyte disturbances, seizures, heart failure,
aspiration from GER

Temperature Control
• Thin skin, little fat, and high surface area to mass ratio means easy heat loss
• Overhead heater and ambient humidity in incubator to treat

Patent Ductus Arteriosus

• Ranges from no symptoms to heart failure with murmur
• If symptomatic, closure by NSAIDS (ibuprofen), followed by surgical ligation if fails

• IgG mostly transferred in third trimester, if born too early, they won’t have maternal IgG and is
prone to infection

Necrotising enterocolitis
• In first few weeks, irritable and feeding difficulties, with vomiting (bile stained maybe), blood in
stool, abdominal distention
• X-ray show distended bowels with intramural gas, if perforate will see free gas under diaphragm
• Treat by parenteral nutrition, Ab, surgery if perforated. Circulatory and ventilatory support usually

Brain Injury
• Assessed by US
• Germinal matrix most prone to haemorrhage when ischemia occur due to perinatal asphyxia,
RDS, or pneumothorax
• Haemorrhage may be confined to the matrix or rupture into ventricle causing IVH
• Large IVH may lead to hydrocephalus, treated initially with spinal/ventricular tap and later with
VP shunt
• Periventricular white matter damage can occur with ischemia and inflammation even without
hemorrhage, and if so may only be an echo-dense “flare”, cystic lesions on US 2-4 weeks later
means definite loss of white matter
• Bilateral cysts is called PVL and is linked spastic diplegia and cognitive impairment

Retinopathy of Prematurity
• The in-utero oxygen environment is needed for normal eye development, premature exposure to
the high oxygen external environment (risk increased by high conc. oxygen therapy) causes
fibrovascular proliferation near retina, and when fibrous tissue contract it leads to retinal
detachment and blindness
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• Treatment with laser therapy

Bronchopulmonary dysplasia
• Defined as infants who still have oxygen requirement at 36 weeks
• Damage to lung mainly due to delayed maturation, but exacerbated by ventilation trauma,
oxygen toxicity, and infection
• Death may occur with subsequent infection, pulmonary hypertension
• CXR show patchy fibrosis +/- cysts
• Treatment is ventilatory support (weaning from mechanical -> CPAP -> high flow nasal cannula -
> ambient oxygen) and corticosteroid for infants highest risk of neurodevelopment damage

• Infants < 36 weeks cannot suck and swallow and needs other way of feeding, enteral preferable
(e.g. NG tube)
• The feed is still breast milk if possible supplemented with phosphate, calcium, proteins and
• If very low birthweight or sick, use PRN via peripheral or central line
• Osteopenia of prematurity prevented by calcium, phosphate, vit D supplements
• Iron mostly transferred in 3rd trimester, iron supplements are started at several weeks of age and
continued after discharge


• This is encephalopathy resulting from the deposition of unconjugated bilirubin in basal ganglia
and brainstem nuclei
• Presents with irritability, hypertonia (opisthotonos), seizure, coma
• Later develop choreoathetoid CP, learning difficulties, sensorineural deafness

Jaundice < 24 hours of age

• Hemolysis (rhesus, ABO, G6PD, spherocytosis)
• Congenital infection (conjugated)

• If untreated, rhesus presents with anemia, hydrops, and HSmegaly
• Rhesus is usually D-antigen, preventable by prophylactic anti-D immunoglobulin for rhesus
negative mothers
• ABO usually mild, positive Coombs
• G6PD in middle east, east asia, and africa
• Spherocytosis usually a family history

Congenital Infections
• Look for other signs

Jaundice 2 days - 2 weeks

• Physiological jaundice
• Breast milk jaundice
• Dehydration
• Infection (particularly UTI)
• Bruising
• Polycythaemia (venous hematocrit > 0.65)
• Hemolysis (particularly G6PD)
• Crigler-Najjar

Physiological Jaundice
• > 50% of neonates are visibly jaundiced, unconjugated, diagnosis by exclusion
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• Short infant red cell life span (70 days), physiological breakdown of high Hb conc at birth, and
inefficient hepatic bilirubin metabolism in first few days predispose to jaundice

Breast milk jaundice

• Unconjugated
• Suspected due to increased enterohepatic circulation

• Unconjugated
• > 10% loss of BW, usually from delayed breastfeeding

• Unconjugated as well, from hemolysis, reduced hepatic function, poor intake, increased
• Particularly UTI

Evaluation and Treatment of Jaundice

• Jaundice progresses from head to limbs, easier to see when skin pressed, check with TCB and
finally confirm with blood
• Check for risk factors:
• Sepsis
• Dehydration
• Hemolysis
• ABO, rhesus, G6PD, blood film
• Take serial measurements of bilirubin on gestation specific chart, phototherapy (450nm) and
exchange transfusion if needed

Respiratory Distress in Term Infants

• Transient tachypnoea of newborn
Less common
• Meconium aspiration
• Pneumothorax
• Pneumonia
• Persistent pulmonary hypertension of newborn
• Milk aspiration
• Diaphragmatic hernia
• Tracheo-esophageal fistula
• Pulmonary hypoplasia
• Airway obstruction (e.g. choanal atresia)
• Pulmonary hemorrhage
• Congenital heart
• HIE, neonatal encephalopathy
• Severe anemia
• Metabolic acidosis

Meconium aspiration
• Incidence increases by birth age
• Key diagnostic point is seeing meconium in amniotic fluid, and CXR
• CXR shows hyperinflated lungs, and patchy consolidation and collapse
• Treat with ventilatory support, usually mechanical ventilation needed

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• Risk factors are prolonged rupture of membranes leading to chorioamnionitis and low birth
• Board spectrum antibiotics used empirically

• Occurs spontaneously in 2% of babies, but usually asymptomatic

Milk aspiration
• More common with preterm infants, respiratory distress, and neurological damage

Persistent pulmonary hypertension of the new born

• Primary, or secondary to birth asphyxia, meconium aspiration, RDS, sepsis
• Causes a life threatening right to left shunt with cyanosis and SOB
• X-ray is clear except pulmonary oligemia, and then you do an echo to exclude congenital heart
and look for signs of pulmonary hypertension such as raised pulmonary pressure and TR
• Respiratory (usually mechanical) and circulatory support needed. Inhaled nitric oxide or sildenafil
for vasodilation.

Diaphragmatic hernia
• Rare, and many are diagnosed antenatally
• Usually hernia at left posterolateral foramen
• Bowel sounds heard at lung field, absent breath sounds, apex displaced to the right
• Diagnosis by C/AXR
• If suspected, stabilise patient and do NG suction, then do surgery
• Pulmonary hypoplasia is common and mortality is high


• Early onset < 48 hours usually infection from birth canal or chorioamnionitis, risk factor being
premature or prolonged rupture of amniotic membrane, or maternal fever (chorioamnionitis)
• Late onset usually nosocomial

• CBCdc
• Microbiological investigations
• Blood culture
• Urine culture, multistix
• < 1 week reflects high grade sepsis rather than isolated UTI
• Lumbar puncture
• Gram stain, culture, cell count, glucose/protein

• Early onset: cover gramP (e.g. listeria, group B strep) with amoxicillin, cover gramN with
aminoglycoside like gentamycin
• Late onset: cover gramP (strep in particularly) with flucloxacillin, cover gramN with gentamycin

Group B Strep
• Causes both early and late infections
• Early infections usually pneumonia, but can meningitis and sepsis
• Late infections occur up to 3 months after the strep colonises baby skin or mucous
membranes, usually meningitis but can focal like osteomyelitis, septic arthritis
• Screening at 35-38 weeks and prophylactic intrapartum IV antibiotics if positive
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• Causes a mild, influenza like illness in mother and passes to fetus through placenta, leading to
abortion, preterm delivery, neonatal/fetal sepsis
• Meconium staining of liquor amnii in preterm infants is characteristic, widespread rash,
septicaemia, pneumonia, and meningitis

Gram-Negative Infections
• Early onset from birth canal, chorioamnionitis
• Late onset usually environmental, but occasionally translocation from intestines

• Sticky eyes common in neonates starting on 3rd-4th day of life, just clean with water or saline
• Red eyes with purulent discharge indicates infection
• Usually due to staph/strep, treat with topical eye ointment e.g. chloramphenicol or neomycin
• If along with swelling of eyelids within first 48 hours, might be gonococcal, gram stain, culture,
and start empirical IV cephalosporin, clean eyes frequently
• Chlamydia trachomatis usually at 1-2 weeks (but also possible at birth), identified with IF
staining, treat with oral erythromycin, also check mother and partner and treat

• Transmitted when pass through birth canal or ascending infection
• Risk from primary infection high (40%) so C section indicated, but recurrent infection risk low
• Presents in first 4 weeks with herpetic lesions on skin/eye, or with encephalitis and disseminated
• Treat with aciclovir, maternal treatment before delivery also effective

Hep B
• Vaccinate infants whose mother is positive after birth and antibody response checked later
• If HBeAg positive as well give Ig at birth and within 24 hours after birth


• IUGR, preterm, DM mothers, large-for-dates, hypothermic, polycythemic, or ill for any reason is
at risk
• Symptoms are irritability, lethargy, drowsiness, seizures, apnea
• No agreed definition of hypoglycaemia, but try to keep infant above 2.6 mmol/L
• If low should be confirmed by lab, two low values or one very low < 1.6 is indication to start IV
dextrose (10-20%)
• High conc dextrose give via central line to avoid extravasation leading to necrosis and reactive
• If still cannot fix, start glucagon

Neonatal Seizures

Vascular: HIE, malformations, intracranial hemorrhage/infarction
Infection/inflammatory: sepsis, meningitis, encephalitis, congenital infections
Metabolic: hypoglycemia, hypo/hyperNa, hypoCa, hypoMg, IEM, pyridoxine dependency,
Iatrogenic/idiopathic: drug withdrawal (maternal opiates)

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Perinatal Stroke
• Usually MCA ischemia, other causes are hemorrhage, venous thrombosis in dural sinus
• Present with seizures at 12-48 hours in term infant (focal or generalised), but no other
abnormalities (in contrast to HIE)
• Diagnosis confirmed MRI
• 50% develop motor disability (usually hemiplegia) and cognitive dysfunction, larger lesions
results in epilepsy

Craniofacial disorders

Cleft lip
• For lip, Left : Right : Bilateral = 6 : 3 : 1
• Surgery at 3 months for lip

Cleft palate
• May lead to feeding problems, if observed, orthodontic advice and dental prosthesis needed
• Secretory otits media common and should be followed up on
• Surgery at 6-12 months, avoid adenoidectomy as will exacerbate feeding and voicing problem
• Holistic approach with plastic and ENT surgeons, pedi, orthodontist, audiologist, speech therapist

Pierre Robin Sequence

• Triad of micrognathia, glossoptosis, cleft palate
• Difficulty feeding and cyanotic episdes due to glossoptosis, leading to growth faltering in the first
few months, infant lies prone to prevent glossoptosis
• Persistent obstruction treat with nasopharyngeal airway, eventually micrognathia resolves
spontaneously completely, and cleft palate can be repaired

Gastrointestinal Disorders

Esophageal Atresia
• Usually with tracheo-esophageal fistula
• Associated with polyhydramnios, detected by absent stomach bubble on antenatal US
• If suspected, confirmed by passing feeding tube and check with XR to see if reaches stomach
• Presents with persistent salivation and drooling from mouth, cough and choke when fed, and
have cyanotic episodes

Principles of BO
• Bile stained vomiting is BO until proven otherwise

• May be detected on antenatal US
• Presents with persistent vomiting (may be bile stained), and no passage of stool after meconium
(or even meconium may not be passed)
• High lesions present soon after birth, low lesions present after days
• Causes are duodenal stenosis/atresia (downs), jejunal/ileum stenosis atresia, meconium ileus
(CF), malrotation with volvulus, meconium plug
• Structural problems are treated surgically after electrolytes abnormalities are corrected,
meconium ileus first treated with gastrografin enema and then surgery if fails, meconium plug
usually passes spontaneously

• Hirschsprung disease (asso. downs): no meconium passed in first 48 hours, and later abdomen
distends, 15% presents as acute enterocolitis
• Rectal atresia: high lesions associated with vesico/urethrorectal vestiula in boys, vesico/
vaginorectal fistula in girls, treat with surgery

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• Often diagnosed antenatally
• In exomphalos (omaphocele), contents herniate through umbilical ring covered by amniotic
membrane and peritoneum. Associated with other malformations.
• In gastrochisis, contents protrude through defect in abdominal wall with no covering.
• Gastroschisis has high risk of dehydration and protein loss, cover with clear occlusive wrap, NG
tube aspiration, IV fluids, and then surgery

Genetic Disorders

Down’s Syndrome (trisomy 21)

• Incidence is 1 in 650, increases with maternal age (for nondisjunction)
• Recurrence is 1 in 200 if < 35 yr, > 35 yr similar to age related risk (1 in 385 in 35yr, 110 in 40yr)
• Result from nondisjunction (94%), translocation (5%), or mosaicism (1%)
• If translocation, parental chromosomes analysis needs to be carried out
• Risk of recurrence is 10-15% if mother has translocation, 2.5% if father has
• If 21:21 translocation, all off spring ahve downs
• If neither have translocation, risk of recurrence less than 1%
• All mothers screened for nuchal thickening on US and markers in blood prenatally, if suspected,
amniocentesis to check fetal karyotype. NIPT also possible.
• Features are:
• Head: round face, flat nasal bridge, upslanted palpebral fissures, epicanthic folds, brushfield
spots in iris, small mouth and protruding tongue, small ears, flat occiput and third fontanelle
• Trunk: short neck, short stature
• Limbs: single palmar crease, clinodactyly, sandal gap
• Cardiovascular: congenital heart (AVSD)
• GI: duodenal atresia, hirschsprung, celiac disease
• Neurological: hypotonia, epilepsy, early-onset alzheimers
• Developmental: delayed motor milestones, variable learning difficulties
• Special senses: cataracts, squints, myopia, secretory otitis media causing hearing loss
• Respiratory: OSA
• Musculoskeletal: acquired hip dislocation, atlantoaxial instability
• Neoplasm: increased leukaemia and solid tumours risk
• Infection: increased susceptibility

Edwards Syndrome (trisomy 18)

• Low birthweight
• Prominent occiput
• Small mouth and chin
• Short sternum
• Flexed, overlapping fingers
• Rocker-bottom feet
• Cardiac/renal malformations

Patau Syndrome (trisomy 13)

• Structural defect of brain
• Scalp defects
• Small eyes
• Micropththalmia and other eye defects
• Cleft lip/palate
• Polydactyly
• Cardiac/renal malformations

Edwards and Patau Syndrome

• Most baby die in infancy
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• Many are detected by antenatal ultrasound and confirmed by amniocentesis, NIPT also possible
• Recurrence risk low unless translocation

Turner Syndrome (45X)

• 95% cases results in early miscarriage
• 50% are 45X, others have short arm deletion, isochromosome with two long arms, and other
structural defects in X. 45X, 46XY mosaicism increase risk of gonadoblastoma
• Can be detected by antenatal US with edema of neck, hands, or feet, or a cystic hygroma
• Treat with growth hormone, and estrogen replacement at puberty
• Features are:
• Trunk: short stature, neck webbing, widely spaced nipples, pigmented moles
• Limbs: lymphedema in neonates hands/feet, spoon-shaped nails, cubits valgus
• Cardiac: coarctation of aorta
• Endocrine: hypothyroidism, delayed puberty, ovarian dysgenesis
• Renal: renal anomalies
• Infection: recurrent otits media

Klinefelter syndrome (47, XXY)

• Recurrence risk very low
• Features:
• Infertility
• Hypogonadism with small testes
• Gynecomastia
• Tall stature

Autosomal dominant disorders

• Huntington
• Marfan
• NF
• Noonan
• Tuberous sclerosis
• Achondroplasia
• Myotonic dystrophy
• Osteogenesis imperfecta
• FH

Autosomal recessive disorders

• CF
• Friedreich ataxia
• Galactosemia
• Sickle cell
• Thalassaemia
• Tay-sachs disease

X-linked recessive disorders

• Color blindness (red-green)
• Fragile X
• G6PD
• Hemophilia A, B
• Hunter syndrome (MPS II)

Fragile X syndrome
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• Moderate-severe learning difficulty
• Macrocephaly
• Macroorchidism (postpubertal)
• Characteristic facies (lung face, large everted ears, prominent mandible, broad forehead)
• Other features: mitral valve prolapse, joint laxity, scoliosis, autism, hyperactivitiy

Noonan Syndrome
• Characteristic facies
• Mild learning difficulties
• Short webbed neck with trident hair line
• Pectus excavatum
• Short stature
• Congenital heart disease (PS, ASD)

Newborn Lesions

Peripheral cyanosis of hand and feet

• Resolves in one day

Traumatic cyanosis
• Petechiae and blue discolouration over head but tongue not affected

Subconjunctival haemorrhage
• Document to avoid confusion

Epstein pearls
• Along midline of palate

Epulis and ranula

• Cysts on gums (epulis) and floor of mouth (ranula)

Breast enlargement
• Due to in utero hormones

White vaginal discharge or small withdrawal bleed

• Due to in utero hormones

Capillary hemangioma
• aka Strawberry nevus, usually not present at birth, appear at 1st month of life, increase in size
until 3-15 months of age, then gradually regress
• Small lesions do not need treatment, or just propanolol to speed regression
• Large lesions or those that interfere with vision or airway treated with oral propranolol
• Complications are ulceration and hemorrhage

Port-wine stain
• Usually present on head or neck
• Grows with the infant and does not regress
• If along distribution of CN V, may be associated with Sturge Weber, Klippel Trenaunay syndrome
• Treated with laser therapy

Natal teeth of front lower incisors

• Remove if loose to prevent aspiration

Extra digits
• Plastic surgery removal

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Midline abnormality of spine or skull
• Needs further investigation

Palpable and enlarged bladder

• Sign of obstruction and needs an US
• In males may be posterior urethral valves

Positional Talipes
• Passively correctable, dorsiflex the foot can touch front of lower leg

Talipes equinovarus
• Not correctable


Basic DDx
• Infection
• Acute abdomen and IO
• Other GI disease
• Allergic conditions

Infants DDx
• Overfeeding
• Infections
• GE
• URTI/otitis media/pertussis
• Meningitis
• Food allergy and food intolerance
• IO
• Structural problems
• Pyloric stenosis
• Atresia
• Duplication cysts
• Intussusception
• Strangulated inguinal hernia
• Malrotation
• Volvulus
• Hirschsprung disease
• Eosinophilic esophagitis
• Renal failure

Preschool DDx
• Infection
• Appendicitis
• IO
• Intussusception
• Malrotation
• Volvulus
• Adhesions
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• Foreign body (bezoar)
• Celiac disease
• Raised ICP
• Renal failure
• Testicular torsion

School age and adolescents Dix

• Infection
GI causes
• Appendicitis
• Celiac
Neurological causes
• Migraine
• Raised ICP
• Alcohol/drug/medications
• Pregnancy
• Testicular torsion
• Renal failure
• Bulimia/anorexia nervosa
• Cyclical vomiting syndrome

• Extremely common due to LES immaturity, nearly all resolves by 12 months
• Diagnosed clinically, but if not sure, can do 24-hr esophageal pH/impedance monitoring,
endoscopy with biopsies, contrast study to exclude anatomical abnormalities
• GERD is diagnosed when significant, usually in neurological problems (CP)
• Complications of GERD:
• Faltering growth
• Esophagitis (hematemesis, iron deficiency anemia)
• Pulmonary aspiration (recurrent pneumonia, apnea in preterm infants)
• Sandifer syndrome (dystonic neck posturing)
• If uncomplicated, treat with inert thickening agents (carobel), smaller more frequent feed
• If significant, treat with H2 receptor antagonist (Rantidine) or PPi (omeprazole), surgery if
unresponsive or stricture develops with Nissen fundoplication

Pyloric stenosis
• Presents 2-8 weeks of age
• More common in boys and firstborn, family history
• Projectile vomiting, faltering growth, dehydration, hypochloremic metabolic alkalosis
• Gastric peristalsis may be visible, olive mass palpable in RUQ (after emptying with NG tube), US
to confirm diagnosis
• Manage by correcting dehydration and electrolytes followed by surgery (pyloromyotomy)

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Acute Abdominal Pain

• Appendicitis
• IO
• Peritonitis
• Meckel diverticulitis
• Pancreatitis
• Trauma
• Non-specific abdominal pain and mesenteric adenitis
• Gastrointestinal
• GE
• Constipation
• Renal
• Renal calculus
• Hydronephrosis
• Hepatic:
• Hepatitis
• Gynecological:
• Pubertal females menstrual pain
• Hematological
• Psychological
• Lead poisoning
• Acute porphyria
• Idiopathic
• Lower lobe pneumonia
• Testicular torsion
• Hip and spine

Acute appendicitis
• > 3 years old
• Vomiting, anorexia, periumbilical -> LUQ pain, fever
• In preschool children fecalith more common and can be seen in CXR
• Ultrasound support clinical diagnosis and demonstrate complications
• Appendicectomy is treatment in uncomplicated cases, may choose conservative management
with IV antibiotics first, and later do appendicectomy
• If signs of complications (e.g. generalised peritonitis) like perforation, abscess, etc, treat with
antibiotics, fluid resuscitation before surgery

Non-specific abdominal pain and mesenteric adenitis

• Non-specific pain resolves in 24-48 hours, less severe in appendicitis, and RLQ pain variable,
often following URTI with cervical lymphadenopathy
• In some these abdominal signs do not resolve and appendicectomy is performed
• Mesenteric adenitis is diagnosed at laparoscopy if appendix is normal but large mesenteric
nodes are seen

• Most common cause of IO in infants after neonatal period, peak 3 months - 2 years

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• Usually no cause found, but suspected is viral infection leading to peyer’s patches
lymphadenopathy forming a lead point
• Usually ileum pass into cecum
• Complication is venous obstruction, leading to hemorrhage, perforation, and necrosis
• Severe colicky pain, refuse feeds, vomiting, redcurrant jelly stool, sausage shaped mass may be
• Abdominal distension and shock
• X-ray and US good to confirm diagnosis and ceck response to treatment
• If complicated, need surgery. If uncomplicated, radiologist can do arectal air insufflation first, 75%
successful, if not need surgery.
• Recurrence < 5%

Meckel Diverticulum
• 2% have it, it is a remnant of the ileal vitello-intestinal duct, which may contain ectopic gastric
mucosa or pancreatic tissue
• Most are asymptomatic, but may present with severe rectal bleeding or IO (volvulus,
intussusception, diverticulitis)
• Technetium scan demonstrate increased uptake by ectopic gastric mucosa in 70% of case,
treatment by surgical resection

• Predisposes to voluvlus
• Obstruction usually in first few days but can be later occasionally
• Urgent laparotomy is needed


• Viral, usually rotavirus, others like adenovirus, norovirus, coronavirus also possible
• Bacterial, most commonly campylobacter jejuni, others like shigella, E coli, salmonella also
• Protozoan, like giardia and cryptosporidium

• Investigations needed only if septic, blood in stool, or immunocompromised, recent foreign travel,
diarrhea not improved by day 7
• Check RFT, glucose, stool culture, blood culture
• Resuscitate and antibiotics given if there is suspected sepsis, extraintestinal spread, salmonella
< 6 months old, malnourished or immunocompromised, or specific infections (clostridium difficile,
cholera, shigellosis, giardiasis

Celiac Disease

• Immune response to gliadin of gluten, in 1% of population

• Classic presentation at 8-24 months after introduction of wheat-containing weaning foods
• Faltering growth, abdominal distention, buttock wasting, abnormal stools, general irritability
• Now usually present with mild, non-specific GI symptoms + anemia + growth faltering in later
• Serological supports diagnosis: anti-tTG, EMA, but confirmation is by intestinal biopsy followed
by resolution of symptoms and catch up growth upon gluten withdrawal

Inflammatory Bowel Disease

Crohn’s Disease
• Growth failure, delayed puberty
• Fever, lethargy, weight loss
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• Abdominal pain, diarrhea, weight loss triad
• Extra intestinal manifestation:
• Oral lesions and perianal skin tags
• Uveitis
• Arthralgia
• Erythema nodosum
• Diganosis by endoscopy and histology
• Remission induced by polymeric diet in 75% of cases, steroids if ineffective
• Maintain remission by immunosuppressant medications (AZA, methotrexate)
• Anti TNF like infliximab if above fails
• Long term supplemental enteral nutrition to correct growth failure (overnight NG tube,
gastrostomy feeds)
• Surgery for complications or refractory to medical treatment

Ulcerative Colitis
• Bleeding, diarrhea, colicky pain
• Extra intestinal manifestations are erythema nodusum and arthritis
• Weight loss and growth failure less common
• Diagnosis by endoscopy and histological features
• 90% have pancolitis
• In mild disease, aminosalicylates (mesalazine) for induction and maintenance.
• In moderate disease with rectum and sigmoid colon involvement, manage with topical steroids
• More aggressive disease need systemic steroids for induction and immunomodulatory (AZA) +/-
low dose steroids for maintenance
• Severe fulminating disease is a medical emergency and need IV fluids, IV steroids, if fails,
cyclosporin is used
• Colectomy for severe fulminating disease (toxic megacolon), or for unctrolled chronic disease
• Regular colonscopic screening 10 years from diagnosis due to increased risk of adenoCA

• Infants average 4 stools per day, drop to 2 by 1 year, after that 1 a day
• Definition is infrequent passage of dry, hardened feces, accompanied by straining or pain and
bleeding associated with hard stool
• Usually no cause is found, but causes are:
• Psychological (anxiety, poor toilet habits)
• Dehydration and reduced fluid intake
• GI causes — celiac disease, anal fissure, anorectal abnormalities (e.g. hirschsprung)
• Hypercalcemia
• Hypothyroidism
• Lower spinal chord disease
• Treatment is first with disimpaction and then maintenance treatment
• Disimpaction — polyethylene glycol 3350 + electrolytes (Movicol Pediatric plain) is given with
escalating dose over 1-2 weeks until impaction resolve, if this is inadequate, add a stimulant
laxative like SENNA, if movicol not tolerated, substitute with osmotic laxative like lactulose
• Maintenance — low dose Movicol +/- stimulant for minimum of 6 months, reducing the dose
• Dietary advice — sufficient fluid, balanced diet
• Behaviour advice — sit on toilet after meal times

Hirschsprung disease
• Lack of ganglion cells in myenteric and submucosal plexus
• Lesions extend from rectum for a variable distance proximally, 75% rectosigmoid, 10% entire
• Presentation usually in neonatal period with failure to pass meconium within first 24 hours, and
subsequent IO with abdominal distension and bile stained vomiting
• Rectal examination show narrowed segment and withdrawal releases stool and flatus
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• Less common presentation with life threatening hirschsprung enterocolitis in neonates, or chronic
constipation and growth failure in later childhood
• Diagnosis by suction rectal biopsy, anorectal manometry or barium studies help give an idea of
the segment involved but not reliable for diagnosis
• Management is surgery (colostomy + anastomoses)

Food Allergy and Intolerance

IgE mediated allergy

• Usually IgE mediated, presents as urticaria, face swelling, or anaphylaxis
• Diagnosis is by history (symptoms occurring 15minutes-2hours after ingestion) and skin-prick/IgE
antibodies test, if in doubt a double blind food challenge can be used
• If no cardiorespiratory symptoms it is mild, if yes it is severe
• Written self management plans and adequate training needs to be given to child and family
• Mild reactions treated with antihistamines
• Severe reactions treated with IM adrenaline in EpiPen, which the child should carry at all times

Non-IgE mediated
• GI symptoms hours after ingestion like diarrhoea, vomiting, abdominal pain + eczema
• More severe presentation may be with proctitis or food protein-induced enterocolitis syndrome
(repeated vomiting until shocked)
• Skin prick is negative
• Diagnosis is clinical, but may be supported by endoscopy and intestinal biopsy showing
eosinophilic infiltration, if in doubt double blind food test can be done

Food Intolerance
• Non-immune mediated hypersensitivity
• E.g. temporary lactose intolerance following infection


Common Cold
• Usually rhinovirus, coronavirus, and RSV
• Symptomatic treatment with paracetamol

• Viral usually adenovirus, enterovirus, rhinovirus
• Bacterial common in older children by group A strep

• Viral usually EBV (IM triad, pharyngitis/tonsillitis, fever, lymphadenopathy)
• Bacterial group A strep
• Bacterial has more constitutional disturbances like headache, apathy, abdo pain, cervical
lymphadenopathy, white tonsilar exudate, etc
• IM usually more membranous exudate, but not reliable
• Treat with antibiotics (penicillin or erythromycin) if severe (avoid amoxicillin as can cause rash in
• Admission needed if cannot eat or drink, with IV fluids and analgesia

Scarlet fever
• By group A strep
• Fever followed by headache and tonsillitis in days
• Sandpaper maculopapular rash develops on trunk and spread sparing palm/soles and face
• Face is flushed with perioral paleness
• Treat with penicillin or erythromycin

Page 15 of 30
Acute Otitis Media
• Most common 6-12 months because young children have short horizontal and poor functioning
eustachian tubes
• Examination of tympanic membrane show bright red and bulging with loss of light reflection +/-
• Viral causes are RSV and rhinovirus
• Bacteria are pneumococcus, Haemophilus, Moraxella
• Complications are mastoiditis and meningitis
• Symptomatic treatment + antibiotics (amoxicillin) if child unwell after 2-3 days

Otitis Media with Effusion

• Caused by recurrent ear infections, common in 2-7 years
• Conductive hearing loss
• Eardrum dull and retracted, often with fluid level visible
• Treat with ventilation tubes (grommets), but benefits don’t last beyond 12 months
• If recur about grommet extrusion, reinsert grommets with adenoidectomy

• Usually viral, but may be secondary bactieral infection
• Antibiotics and analgesia for treatment


Infective causes:
• Croup
• Epiglottitis
• Bacterial tracheitis
• Measles
• Diptheria
• Lymphadenopathy (IM, TB, malignancy)
• Quinsy
Other medical causes:
• Anaphylaxis (acute laryngeal angioedema)
• Hypocalcemia
Physical and traumatic causes:
• Foreign body
• Trauma
• Inhalation of smoke and hot fumes

• Usually parainfluenza
• Common from 6 months to 6 years
• Coryzal symptoms followed by barking cough, stridor
• If mild, can treat at home with antipyretics and oral dexamethasone
• If moderate (symptoms present at rest but no significant distress) - severe (significant distress),
observe and give oral dexamethasone + nebulised adrenaline
• If impending respiratory failure (cyanosis, decreased consciousness), IV/IM dexamethasone,
nebulised adrenaline, consider intubation with ENT surgeon and anes guy

Acute epiglottis
• Hemophilus type B, life threatening emergency
• Onset over hours, with a silent and still child with drooping saliva
Page 16 of 30
• Intubate with ENT surg and anes guy under GA and admit to ICU
• IV antibiotics e.g. cefuroxime, prophylaxis with rifampicin to close contacts

Bacterial Tracheitis
• Usually staph aureus
• High fever, rapidly progressive airway obstruction copious thick airway secretion
• Treat with IV antibiotics, intubation and ventilation as required

Chronic Stridor
• Structural (laryngomalacia, subglottic stenosis)
• External compression (lymph nodes, mass)


• Asthma
• Bronchiolitis
• Atypical pneumonia
• Foreign body
• Aspiration
• Anaphylaxis
• Usually RSV
• 90% aged 1-9 months
• Coryzal symptoms precede cough and stridor
• Perform pulse oximetry in all children, CXR and blood gases if respiratory failure suspected
• Admission indicated for apnea, persistent spO2 < 90%, inadequate oral intake (< 50-75% usual),
severe SOB with grunting, marked recession, resp > 70 breaths/min
• Treat with oxygen, IV/NG fluids, should recover in 2 weeks
• If severe resp support may be needed, e.g. bronchopulmonary dysplasia, but monoclonal
antibody to RSV (palivizumab monthly by IM) can be used as prophylaxis

• Investigations — skin prick, PEFR, spirometry, response to bronchodilator (FEV 1 > 12%
improvement is asthma)

Acute Management
Admission required if high dose SABA is not enough, is becoming exhausted, still have marked
reduction in predicted FEV1 or peak flow < 50%, or SpO2 < 92%

CXR only if unusual features (asymmetry suggesting pneumothorax, collapse), or signs of severe
infection. Blood gas only in life threatening or refractory cases, usually normal unless in extremis.

If moderate, SABA via spacer +/- mask, and oral prednisolone.

If severe, add oxygen, SABA/nebulised salbutamol, oral pred/IV hydrocortisone. Consider inhaled
ipratropium,IV salbutamol, aminophylline, Mg.

If life threatening, nebulised salbutamol, oral pred/IV hydro, nebulised ipratropium. Also consider
the things above. Admit PICU.

Chronic Management
Step up approach:
1. Inhaled SABA (ventolin) as needed
2. Preventer therapy with ICS (200 ug/day, or 400ug/day in adolescents+). LTRA in < 5 yo if ICS
cannot be used. Monitor height weight.
Page 17 of 30
3. < 5 years, LTRA. If poor response add ICS to 200. > 5 years, LABA. If partial or poor response
then ICS 400 (800 if ado+). Stop LABA if poor response, and consider LTRA or SR
4. < 5 years, refer to resp pedi. 5-12 years, ICS 800. Ado+ ICS 1600, consider LTRA, SR
5. Maintain current ICS dose. Add oral steroids, refer to resp pedi.

In general, > 2 days per week of SABA use requires step up. If 3 months good control, can step


• Whooping cough by bordetella pertussis
• After week of coryza (catarrhal phase), develop a paroxysmal cough followed by inspiratory
whoop (or apnea in an infant) and may lead to post-tussis vomiting (paroxysmal phase) and
cyanotic attacks, this phase lasts up to 3 months, then gradually resolves over weeks to months
(convalescent phase)
• Admit to hospital, NPA to PCR/culture and identify organism, lymphocytosis on CBC
• Isolate the patient and treat with macrolide (only effective if started in catarrhal phase)
• Close contacts need macrolide prophylaxis
• Immunisation by DTP vaccine, but not 100% effective

• Newborn — genital flora such as group B strep, gram-ve enterococci and bacilli
• Infants and young children — respiratory viruses particularly RSV, pneumococcus, hemophilus,
pertussis, chlamydia also possible, staph aureus rare but serious
• Children over 5 years — mycoplasma, pneumococcus, chlamydia pneumoniae
• At all ages consider TB
• CXR to confirm diagnosis, sputum culture/NPA for micriobiological diagnosis
• Admission for <92% SpO2, recurrent apnea, poor intake
• Treat with oxygen, analgesia, IV fluids, newborns need broad spectrum antibiotics, older children
<5 years oldcan treat with amoxicillin (augmentin if unresponsive), for children over 5 years,
amoxicillin or erythromycin
• Pleural effusion needs drainage, persistent fever despite 48 hours of antibiotics suggests pleural
• Those with lobar collapse or atelectasis need followup 4-6 weeks after with X-ray to check lung

Recurrent Cough

Cystic Fibrosis

• Autosomal recessive, mostly in caucasians, average life expentancy 30s currently, projected 40s
for current newborns
• CFTR mutation, most commonly deltaF508

• Immunoreactive trypsinogen (IRT) raised in newborns and can be tested in heel prick test,
followed by mutation screening, lastly confirm with sweat test
• Ultimately, 95% die of respiratory failure
• Diagnosis by sweat test for elevated chloride, if unsure or confirmed but phenotype unknown, do
a genetic sequencing

Page 18 of 30
Clinical Features
• Meconium ileus
• Prolonged NNJ
• Growth faltering
• Recurrent chest infections
• Malabsorption, steatorrhea (due to pancreatic exocrine insufficiency, reflected by fecal elastase)
Young Child
• Bronchiectasis
• Rectal prolapse
• Nasal polyp
• Sinusitis
Older child and adolescent
• Allergic bronchopulmonary aspergillosis
• DM
• Cirrhosis and portal hypertension
• Distal intestinal obstruction (meconium ileus equivalent)
• Pneumothorax or recurrent hemoptysis
• Sterility in males (congenital bilateral absence of vas deferens)

• Regular physiotherapy and child/parent taught how to clear secretions using percussion and
postural drainage, controlled deep breathing exercises in older children, physical exercise
• Regarding chest infections:
• Continuous prophylactic oral antibiotics (flucloxacillin) witha dditional rescue antibiotics for
increase in respiratory symptoms or decline in lung function
• Persisting symptoms or signs need IV antibiotics for 14 days via PICC, parents are taught how
to give IV antibiotics at home, severe CF also need regular IV antibiotics with Portacath
• Chronic pseudomonas infection treated by daily nebulised antipseudomonal antibiotics (e.g.
• Patients not advised to socialise with other people with CF
• Nebulised DNase or hypertonic saline to decrease viscosity of sputum
• Macrolide antibiotic azithromycin decreases respiratory exacerbation by immunomodulatory
• Bilateral sequential lung transplantation is the only therapeutic treatment for end-stage CF lung
Pancreatic insufficiency:
• Oral enteric-coated pancreatic replacement therapy taken with all meals
• Fat-soluble vitamin supplements
• High calorie diet 150% of normal, provided by overnight gastrostomy feeding
Hepatic disease:
• One third of adolescent patients have hepatomegaly or evidence of liver disease
• Regular ursodeoxycholic acid to improve bile flow
• Cirrhosis, portal hypertension, liver failure rare, failure treated by transplant and is very
• Distal intestinal obstruction syndrome cleared by combination of oral laxatives

Heart Murmurs

Innocent Murmur
• 3S3N
• Asymptomatic
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• Soft, blowing, systolic
• Left sternal border
• Normal heart sounds
• No thrills
• No radiation

• If congenital heart is suspected, do CXR and ECG, followed by Echo

Heart Failure

Neonates (obstructed duct dependent systemic circulation)
• Hypoplastic left heart syndrome
• Critical AS
• Severe coarctation of aorta
• Interruption of aortic arch
Infants (high pulmonary blood flow, L->R shunts)
• Large PDA
Older children and adolescents
• Eisenmenger
• Rheumatic heart
• Cardiomyopathy


• Peripheral cyanosis occur when child is cold, polycythemia, or in any form of stress
• Persistent central cyanosis in otherwise well infant is nearly always sign of structure heart

Newborn Cyanosis + SOB > 60 DDx

• Respiratory (RDS, persistent pulmonary hypertension of newborn, meconium aspiration,
pulmonary hypoplasia, etc)
• Cardiac (cyanotic heart)
• Infection (sepsis, particularly group B strep)
• IEM (with metabolic acidosis and shock)

Left-to-right Shunts

• Murmurs may not be very apparent until several weeks due to pulmonary pressure still being
• PDA murmur may be systolic at birth

• Secundum ASD (80%) or Primum ASD/partial AVSD
• Partial AVSD opening is lower and hence involves AV valves, also associated with cleft mitral
valve which tends to MR
• Murmur — ejection systolic ULSB from increases PV flow, fixed and widely split S2
• Partial AVSD murmur — apical PSM from AR
• Commonly asymptomatic, but can present with recurrent chest infections and arrhythmias from
• CXR show increased pulmonary markings, cardiomegaly
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• ECG in secundum associated with partial RBBB and right axis deviation due to right ventricular
• ECG in Partial AVSD with superior QRS axis with negative aVF
• Patients with right ventricular dilatation needs treatment, by occlusion device by cardiac
• Partial AVSD needs surgery at 3-5 years old

• May be perimembranous. muscular, or supracristal
• Small VSD are smaller than aortic valve ~3mm, asymptomatic except for the PSM at LLSB and
quiet P2, these lesions will close spontaneously, but maintain good dental hygiene while still
• Large VSDs are same size or larger than aortic valve, present with heart failure and faltering
growth after 1 week, and reccurent chest infections
• The PSM murmur may be soft or not present, an apical mid-diastolic murmur (increased flow
through mitral valve) and loud P2 may be heard
• ECG shw biventricular hypertrophy
• CXR show increased markings, enlarged pulmonary arteries, cardiomegaly, and pulmonary
• Treatment for heart failure is diuretics with captopril (ACEi), additional calories, surgery at 3-6

• Continuous machinery mumur below clavicle, bounding pulse
• Usually asymptomatic but large lesion can cause heart failure
• CXR ECG normal unless heart failure then will be like VSD
• Occlusion device via cardiac catheter at 1 year of age, or surgical ligation will fails

Right-to-left shunts

• Presents with cyanosis SpO2 ≤ 94% in first week
• Hyperoxia test — give infant 100% oxygen in headbox or ventilator for 10 minutes, if PaO2
remains < 15 kPa, then it is persistent pulmonary hypertension or congenital heart, if not then
probably a lung disease, blood gas analysis needed for PaO2 as oximetry not accurate at this
• Cyanosis neonate treated by attending to ABC, then start prostaglandin infusion while observe
for potential side-effects like apnea, jitteriness and seizures, flushing, vasodilatation and

Teratology of Fallot
• Large VSD, overriding aorta, subpulmonary stenosis, right ventricular hypertrophy
• Diagnosed antenatally for identification of the murmur in first 2 months, or present with cyanosis
in first few days, prone to hypercyanotic spells
• Show clubbing in older children, systolic ejection murmur at LSB from day 1
• CXR show small boot shaped heart, pulmonary artery bay, right sided aortic arch, decreased
pulmonary markings
• ECG normal at birth, RVH when older
• Infants who are cyanosed in neonatal period are treated with modified Blalock-Taussig shunt
(pulmonary artery subclavian artery connection) or balloon dilatation of right ventricular outflow
• Hypercyanotic spells usually self limiting followed by sleep, if > 15 min, treat with analgesics
(morphine), IV propranolol, IV fluids, bicarbonate (to correct acidsos), muscle paralysis and
artificial ventilation
• Surgical corrrection at 6 months

Page 21 of 30
Transposition of Great Arteries
• Fatal unless have other defects (usually present) like VSD, ASD, PDA
• Cyanosis usually on day 2 when ductal closure occurs
• Murmur is a loud single second heart sound, usually no murmur or systolic murmur from
stenosis/increased flow to the pulmonary outflow tract (left)
• CXR show narrow upper mediastinum with “egg on side” appearance of heart, increased
pulmonary vascular markings
• Management is prostaglandin infusion to open the PDA, balloon artial septostomy (pull open the
ASD with balloon) in 20%, definitive surgery by arterial switch in first few days of life

Eisenmenger Syndrome
• Shunt reversal usually at 10-15 years, death in 40/50s
• Medication to retard pulmonary hypertension like inhaled NO, IV magnesium, PDEi sidenafil until
transplant needed

Common Mixing

Complete AVSD
• Associated with Downs
• Pulmonary hypertension present
• Cyanosis at birth or heart failure at 2-3 weeks
• No murmur, detected on echo screening with Downs baby or antenatal ultrasound
• Superior axis on ECG
• Treat heart failure with diuretics + captopril, surgical repair at 3-6 months

Tricuspid Atresia
• Accompanied with VSD and ASD, triscupid valve does not exist, right ventricle small and
• Cyanosis in newborn if duct dependent, or become cyanosed and SOb later
• Early palliation with Blalock Taussig Shunt in severely cyanosed children, pulmonary artery
banding operation if breathless
• Completely corrective surgery not possible with most as right ventricle is hypolastic, palliation
with surgery connecting SVC to PA after 6 months (Glenn operation) and connect IVC to PA at 3-
5 years (Fontan operation)

Outflow Obstruction in Well Child

Aortic Stenosis
• Usually associated with MS and coarctation of aorta
• Usually asymptomatic with murmur, severe cases present with syncope, chest pain on exertion,
reduced exercise tolerance
• In neonates, critical stenosis leads to duct dependent circulation and present with severe heart
failure SOB
• CXR show prominent left ventricle with post-stenotic dilatation of ascending aorta
• ECG show LVH
• Symptomatic patients or resting pressure gradient > 64mmHg need balloon valvotomy
• Eventually, aortic valve replacement will be needed

Pulmonary Stenosis
• Partially fused pulmonary valve leaflets
• Most asymptomatic, critical patients present with neonatal cyanosis in first few days
• CXR poststenotic dilatation of PA
• ECG show RVH
• If gradient > 64 mmHg, transcather balloon dilatation is needed

Adult type coarctation of aorta

Page 22 of 30
• Gradually becomes more severe over the years, not duct depent
• Is asymptomatic except for systemic hypertension and RF delay
• CXR show rib-notching (collaterals) and 3 sign (site of coarctation) in descending aorta
• ECG show LVH
• If severe, treat with stent insertion by cardiac catheter, if not surgery

Outflow Obstruction in Sick Infant

• Usually very sick with heart failure and shock
• Manage with ABC and prostaglandin, early surgery

Coarctation of the aorta

• Closure of arterial duct tissue leads to contraction which narrows the aorta as well
• Present with acute circulatory collapse at 2 days when duct close, leading to metabolic acidosis
• Absent femoral pulses
• CXR show cardiomegaly
• ECG normal
• Management is urgent surgical repair

Interruption of aortic arch

• No connection between proximal aorta and distal to arterial duct, so CO is dependent on PDA,
VSD usually present
• Present with heart failure and shock in neonates
• Absent femoral pulse and left brachial pulse
• Urgent surgery within first few days
• Associated with DiGeorge syndrome

Hypoplastic left heart syndrome

• Detected antenatally by US, if not, they are the sickest out of all conditions here
• Weakness or abbsence of all peripheral pulses in contrast to weak femoral pulse
• Treatment is by Norwood procedure, followed by Glenn or hemi-Fontan at 6 months, and Fontan
at 3 years

Cardiac Arrhythmias

• Most common childhood arrhythmia, usually due to re-entrant circuits
• 250-300 beats/min, in neonates and young children can lead to heart failure and pulmonary
• ECG CXR Echo needed
• Treat with circulatory/respiratory support, vagal stimulating manoeuvres (e.g. carotid sinus
massage, cold pack to face), IV adenosine (induces AV blockage)
• Electrical cardioversion with synchronized direct current shock if adenosine fails
• Maintenance therapy with flecainide or sotalol
• Digoxin can be used alone with no delta wave, + propanolol if yes
• 90% don’t have second attack, so stop treatment at 1 year old, those with WPW needs to be
reassessed in teenage and may need atrial pacing
• Those who relapse or are at risk are treated with percutaneous RFA or cryoablation of accessory

Long QT Syndrome
• Increase risk of developing VT leading to LOC on exertion in late childhood
• Inheritance is AD

Page 23 of 30
• Common in adolescents

Neurally Mediated
• In response to stressors, e.g. standing up too quickly (orthostatic intolerance), sight of blood,
unexpected pain
• Usually prodrome of dizziness and light head feeling and abnormal vision, associated with
nausea, sweating, pallor

Cardiac Syncope
• May be arrhythmic, e.g. SVT, VT from long QT
• May be structural, e.g. AS, HOCM
• Features of cardiac syncope are symptoms on exercise, family history of sudden death, and
• Check BP, and cardiovascular exam, ECG QT interval

Urinary Tract Infection

• Half have structural abnormalities
• Pyelonephritis leads to scarring, and if bilateral may lead to hypertension and chronic kidney

Clinical Features
• Infants non specific — fever, vomiting, lethargy/irritability, poor feeding/faltering growth, jaundice,
septicaemia, offensive urine, febrile seizures
• Children — dysuria, frequency, urgency, abdominal/loin pain, fever +/- chills rigors, lethargy and
anorexia, vomiting and diarrhea, hematuria, offensive/cloudy urine, febrile seizures, recurrence
of enuresis

Collection of samples
• In child in nappies, can use a clean-catch sample (preferred) or use an adhesive plastic bag (but
contamination from skin)
• If urgent samples, urethral catheter or suprapubic aspiration under US
• In older child, use midstream sample
• All samples should undergo MCS, multistix
• Urine culture more than 10^5 CFU per mL gives 90% chance of infection, rises to 95% if
• In catheter or suprapubic aspirate, 1 organism per mL is diagnostic

• Enteric flora — E coli, klebsiella, proteus, pseudomonas, strep fecalis
• Pseudomonas particularly associated with structural abnormalities and indwelling catheters

Risk Factors
• Infrequent voiding
• Incomplete micturition
• Obstruction from constipation
• Neuropathic blader
• Vesicoureteric reflux
• Vulvitis

Vesicoureteric reflux
• Developmental abnormality, ureter displaced laterally and enter directly into the bladder rather
than at angle, with shortened or absent intramural cause
Page 24 of 30
• Mild cases only reflux into ureter, severe cases causes intrarenal reflux, hydronephrosis, and
renal scarring following UTI
• Mild cases usually resolve with age

• Extensive investigations only recommended for recurrent or atypical UTI characterised by
• Severely ill, sepsis
• Poor urine flow
• Abdo, bladder mass
• Raised creatinine (evidence of renal failure)
• Failure to respond to antibiotics in 48 hours
• Infection with atypical (non-E coli) organisms
• First prove the urinary infection
• If nitrate positive, leukocyte esterase positive — treat as UTI, send for MCS if risk of severe
disease or if recurrent
• If nitrate positive, leukocyte esterase negative — start antibiotics, diagnosis rely on MCS
• If nitrate negative, leukocyte esterase positive — start antibiotics if good clinical evidence of
UTi, diagnosis rely on MCS
• If both negative, look for other causes
• Imaging is first with ultrasound, if abnormal:
• < 1 year, follow by MCUG DMSA
• MCUG basically a fluoroscopy of the bladder and urethral, contrast introduced to bladder via
catheter, demonstrates VUR and urethral obstruction
• DMSA is a uptake scan, scarred and non functioning areas are demonstrated (UTI false
positive < 2 months)
• 1-3 year, follow by DMSA
• > 3 year or normal, no further investigtions

• < 3 months, admit to hospital and give IV augmentin for at least 5-7 days, then start prophylactic
antibiotics (usually trimethoprim)
• > 3 months or upper UTI (urine positive + fever ≥ 38, or urine positive + loin pain), treat with oral
antibiotics (e.g. trimethoprim) or IV augmentin 2-4 days followed by oral antibiotics for 7-10 days
• Cystitis/lower UTI treat with oral trimethoprim for 3 days
• Other points:
• Consider antibiotics under 2-3 years with congenital abnormalities or upper UTI
• Treat constipation if present
• Counselling points:
• High fluid intake
• Regular voiding + double voiding
• Good perineal hygiene
• Follow-up needed for recurrent UTI, renal scaring, or reflux
• Dipstix with any nonspecific illness + MCS
• Urinalysis for proteinemia (track chronic kidney disease)
• Long term, low dose antibiotic prophylaxis
• Circumcision
• Anti-VUR surgery if progression of scarring with ongoing VUR
• BP checked annually if renal defects present
• Regular assessment of renal growth and RFT if bilateral defects


• Daytime continence usually occurs by 4 years old, nighttime by 5-7 years old

Primary Daytime Enuresis

Page 25 of 30
• Lack of bladder control over 3-5 years, usually accompanied with nighttime enuresis
• Etiology is functional (lack of attention, etc), anatomical (ectopic ureter, constipation), neuropathic
bladder, infective (UTI)
• In ectopic ureter there is constant dribbling, in neuropathic bladder S2, S3, S4 sensory loss may
be present, anal tone and gait abnormalities
• Investigation — urine MCS for UTI, US + urodynamic studies for anatomical cause, X-ray/MRI
spine for neuropathic bladder
• Treat secondary causes, primary benefit from star charts, bladder training, and pelvic floor
exercise. Portable alar with pad in pants can be used if lack of attention of bladder sensation.
Anticholinergics (oxybutynin) if all else fails.

Secondary Enuresis
• Loss of previously achieved continence due to:
• Emotional upset
• Osmotic diuresis (i.e. DM, chronic renal disease) and DI
• Investigations — urine MCS, multistix for glycosuria, proteinuria, osmolality of early morning
urine (water deprivation test if abnormalities detected)

Nocturnal Enuresis
• Present in 6% of 5 years old (usually not treated until 5 years old), 1.5% of 10 year old, genetic
• Organic causes as with secondary enuresis
• Investigations only indicated if signs of secondary enuresis, e.g. recent onset, other disease
• Counselling
• Explain problem is common and no need for shame as no conscious control
• Star chart
• Enuresis alarm (takes weeks to work) — child must get up, go to toilet, then help change
sheets, then go back to sleep
• Relapse in 1/3, just try again
• Desmopressin for 3-6 months if all else fails, or for acute relief


• Transient proteinuria occur during febrile illness or after exercise do not require investigations
• Persistent proteinuria should be quantified by measuring urine protein-to-creatinine ratio in early
morning sample (normal < 20)

• Orthostatic proteinuria
• Nephrotic syndromes
• Steroid resistant nephrotic syndromes
• MN (associated with hepatitis and SLE)
• Increased GFR (e.g. hypertension)
• Reduced renal mass in GFR
• Tubular proteinuria

Nephrotic Syndrome Features

• Periorbital edema
• Scrotal/vulval, leg/ankle edema
• Ascites
Page 26 of 30
• SOB from pleural effusions
• Infections due to loss of Ig in urine

Nephrotic Syndrome Complications

• Hypovolemia — abdominal pain, faint, low urinary Na, high hematocrit, ugent treatment with IV
normal saline, IV 20% albumin with furosemide if severe
• Thrombosis — due to urinary loss of AT III, may be exacerbated by steroids (increase
coagulation factors synthesis)
• Infection (capsulated bacteria) — pneumococcus in particularly, pneumococcal and seasonal flu
vaccine recommended. Chicken poxx and shingles with aciclovir
• Hypercholesterolaemia — correlates inversely with serum albumin

Nephrotic Syndrome Investigations

• Urine dipstick for protein, MCS, Na
• RFT (urea, electrolytes creatinine, albumin)
• Complement C3 C4
• ASOT or anti-DNase B titres and throat swab
• Hepatitis B/C screen
• Malaria screen if travel abroad

Minimal Change Disease

• 90% of nephrotic syndrome is MCD and resolves with corticosteroids
• More common in asian boys and associated with atopy, often precipitated by respiratory infection
• Features are:
• Age between 1-10 years
• No macroscopic hematuria
• Normal BP, complements, renal function
• Management is daily oral prednisolone for 4 weeks, then switch to alternate days for 4 weeks,
then gradually weaning it off, usually takes 11 days to become protein free in urine
• Those who do not respond after 4-6 weeks or have atypical features need renal biopsy (normal
except fusion of podocytes in MCD)
• 1/3 resolves completely, 1/3 have infrequent relapse, 1/3 have frequent relapse and hence
steroid dependent
• If steroid dependent, consider steroid sparing agents like cyclophosphamide and cyclosporin A,
and as last resort rituximab (anti B cell monoclonal antibody)

Steroid-resistant Nephrotic Syndrome

• Refer to nephrologist
• Manage edema with diuretics, salt restriction, ACEi, NSAIDS
• Genetic testing helps management (e.g. CoQ10 supplementation and withdrawal of
immunosuppression if CoQ10 pathway defect)

Congenital Nephrotic Syndrome

• Rare, presents in first 3 months, most commonly AR, in finland and consanguineous families
• High mortality from complications, unilateral nephrectomy may be necessary followed by dialysis
when stage 5 CKD, continued until old enough for transplant


• Urine that is red, or hemoglobin +ve in dipsticks should be confirmed with urine microscopy
• Glomerular hematuria suggested by brown urine and casts, accompanied with proteinuria
• Lower bleeding usually red, occurs at beginning and end of urinary stream (uncommon in
• UTI is most common cause
Page 27 of 30
• Acute GN
• Post-infectious (post strep)
• Vasculitis (HSP or rarely SLE and others)
• IgA nephropathy
• Goodpasture syndrome (very rare)
• Chronic GN
• IgA nephropathy
• Familial nephritis (Alport syndrome)
• Thin basement membrane disease
• Infection
• Trauma
• Stones
• Tumours
• Hypercalciuria (usually idiopathic)
• Hematological disorders
• Sickle cell
• Bleeding disorder
• Renal vein thrombosis

All Patients
• Urine dipstick, MCS, protein, calcium
• KUB ultrasound
• RFT (urea, creatinine, albumin, electrolytes), calcium, phosphate
• Coagulation screen, sickle screen
If suspected glomerular hematuria
• ESR, complement levels, anti-DNA antibodies
• Throat swab and ASOT/anti-DNase B titres
• Hep B hep C screen
• Renal biopsy if indicated
• Hearing test and test mother’s urine for blood (Alport syndrome)

Indication for Renal Biopsy

• Significant persistent (after few days) proteinuria
• Recurrent macroscopic hematuria
• Abnormal RFT
• Complement levels persistently abnormal

Acute Nephritis Background

• Causes proteinuria, hematuria, oliguria leading to HT which may lead to seizures, and also
edema (initially periorbital characteristically)
• Management is correct water/electrolyte balance +/- diuretics
• If suspected RPGN (occurs with any GN but uncommon post strep), do renal biopsy,
immunosuppression, plasma exchange since it will progress to CKD if untreated

Post-Strep and other post-infectious GN

• Diagnosed by evidence of strep infection with low C3 levels that return to normal after 3-4 weeks
• Good long term prognosis

• IgA vasculitis following URTI, peak age 3-10 years
Page 28 of 30
• Diagnosis is clinical
• Presents with:
• Fever
• Rash on extensor surfaces and buttocks, trunk usually spared. Initially urticarial, but rapidly
becoming maculopauplar and purpuric and characteristically palpable, may recur over several
weeks (rash is keystone of diagnosis)
• Joint paint (66%) of nees and ankles with periarticular edema (usually resolves before rash
• Colicky abdominal pain, if severe can be treated with corticosteroids
• In some cases more serious GI complications like GI bleed, intussusception, ileus, protein-
losing enteropathy maybe occur. Other complications like orchitis, CNS involvement are rare.
• Renal involvement common, 80% have microscopic or macroscopic hematuria with mild
proteinuria (usually not nephrotic range but possible)
• May progress to CKD, risk factors are heavy proteinuria, edema, hypertension, deteriorating
renal function. If these are present, do a renal biopsy to determine if treatment is needed
(with steroids usually, occasionally cyclophosphamide, IVIG)
• All patients should be followed up for a year to detect persisting hematuria or proteinuria (5-
• Patients with persistent renal involvement or required treatment require long term follow up,
as HT and CKD may develop after an interval of several years
Other Vasculitis
• Polyartereitis nodosa, microscopic polyarteritis, Wegener granulomatosis
• Fever, malaise, weight loss, skin rash, arthropathy, +/- respiratory involvement in wegener
• ANCa is present and diagnostic
• Renal arteriography will daignose polyarteritis nodsa by presence of aneurysms
• These are serious and rapidly progressive
• Treat with corticosteroids, plasma exchange, IV cyclophosphamide continued for many months

IgA Nephropathy
• Similar to HSP, follows URTI, management is the same, but pathology only restricted to kidneys

Familial nephritis
• Most common is Alport syndrome, X-linked recessive
• Diagnosis is clinical supported by biopsy
• Associated with nerve deafness and ocular defects, mother may have hematuria
• Progresses to end stage CKD by early adult life in males
• Requires long term follow up to detect proteinuria and CKD
• DDx is thin basement membrane disease (another familial nephritis), which also needs follow up

• Adolescent girls and young women, common in asia
• Presence of multiple autoantibodies (particularly anti dsDNA), C3 C4 low particularly when active
• Hematuria and proteinuria are indications for renal biopsy
• Immunosuppression is always necessary


• Defined as > 95%tile for height, age, sex
• Risk factor is obesity
• Symptomatic hypertension usually secondary

• Renal parenchymal disease (nephritic syndrome, CKD)
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• Renovascular disease (renal artery stenosis, usually congenital)
• PKD (AR and AD, AR rarer and more serious, diffuse cysts bilaterally)
• Renal tumours
• Coarctation of aorta
• Catecholamine excess (pheochromocytoma, neuroblastoma)
• Cushing syndrome (or iatrogenic)
• Hyperthyroidism
Essential hypertension

• Vomiting, headaches, facial palsy, hypertensive retinopathy, convulsions, proteinuria
• Faltering growth and cardiac failure in infants
• Pheochromocytoma cause paroxysmal palpitations and sweating

• Antihypertensives
• Children with family history encouraged to restrict salt intake, avoid obesity, regular
measurement of BP

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