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Neonatology Chapter 5: Paediatrics 107
https://t.me/med1917
Infection
→ neonatal period = highest risk for serious invasive bacterial infection
Early onset sepsis <48h Late onset sepsis >48h
Source Bacterial: ascend from birth canal
• Invade amniotic fluid & pass into fetal lungs
Viral: via placenta
Organisms
• GBS
• Listeria monocytogenes
• Gram –ve: gonococcus, chlamydiae, E. coli
• HSV, CMV, HIV, hepatitis B, toxoplasmosis
Presentation
• Respiratory distress & apnoea
• Temperature instability
• HR/ RR
• Pallor/jaundice/mottled
Meningitis: bulging fontanelle, hyperextended neck & back (opisthotonos)
Risk factors
• PROM / prolonged ROM (>24h)
• Maternal fever in labour (chorioamnionitis)
• Infected 2nd baby in multiple pregnancy
• Maternal GBS in pregnancy / prev. GBS baby
Investigations
• CXR
• Septic screen (FBC, U&Es, LFTS, blood & urine cultures, CRP, glucose, lactate)
• LP & CSF culture (if signs of meningitis or raised CRP with no known source)
Management
5
Immediate broad-spectrum IV ABX e.g. penicillin & gentamicin + supportive Tx (fluids, O2)
+ senior review
Infection acquired from environment
• Coagulase –ve staphylococcus
• Staphylococcus aureus
• Enterococcus
• GBS
• Gram –ve: gonococcus, chlamydia, klebsiella, E. coli
• Failure to feed / gain weight
• Fatigue, irritability, crying
• Abdo distension / vomiting
• Parenteral nutrition (infected lines)
• Tracheal tubes
• Invasive procedures
• Premature/LBW
0.3% of births
GROUP B STREP
Source: 20% women = carriers → 10%
of these will pass to baby
Presentation: respiratory distress/
pneumonia, sepsis, meningitis
Prevention: screen high risk mothers
→ intrapartum ABX
LISTERIA
Source: unpasteurised milk, soft
cheese, undercooked poultry
Presentation: flu-like illness in mother,
meconium-stained liquor, fetal rash
Complications: miscarriage, preterm
delivery, neonatal sepsis
HSV
Source: active maternal infection →
40% of these will pass to baby
Presentation: herpetic lesions on
skin/eye, encephalitis
Prevention: C-section if active at labour,
aciclovir for flare-ups in pregnancy
HEPATITIS B
Prevention: screen high risk mothers
→ active immunisation: neonatal hep B
vaccination shortly after birth
→ passive immunisation: hep B Igs
given to neonate
→ do not breastfeed
CHLAMYDIA
Timing: 1–2w
Sx: purulent discharge + swollen
eyelids
Tx: PO erythromycin
OPHTHALMIA NEONATORUM
Gonococcus/chlamydia
Timing: within 48h
Sx: purulent discharge + swollen
eyelids
Complications: ulceration → blindness
Tx: IV penicillin/cephalosporin
High risk GBS:
Confirm with vaginal swab/MSU
• Previous GBS baby
• Maternal fever in labour
• Prolonged ROM
• Preterm labour/PPROM
5
NICE (2016, updated 2017) Sepsis [NG51]
108 Chapter 5: Paediatrics Neonatology
https://t.me/med1917
prematurity = <37w
Antenatal steroids given if:
• maternal DM
• threatening labour <34w
→ helps pulmonary maturation
→ reduced risk of IVH & PDA
Periventricular leukomalacia (PVL)
= hypoxia damages white matter surrounding
the ventricles
RFs: preterm, LBW, IVH
Problems of prematurity
6
• Respiratory distress syndrome (RDS) → within 4h of birth
▶ Increased risk of lung infection e.g. RSV, adenovirus (causing bronchiolitis)
▶ Pneumothorax may occur 2° to artificial ventilation
▶ Mx: artificial surfactant, respiratory support
• Apnoea, bradycardia & desaturation
▶ Episodes are common <32w – cessation of breathing for 20–30s
▶ Usually due to immature respiratory control – but need to exclude hypoxia,
infection, anaemia, hypoglycaemia, HF
▶ Mx: gentle physical stimulation, caffeine stimulants, CPAP
• Bronchopulmonary dysplasia / chronic lung disease → still require O2
therapy >36w corrected age
▶ RFs: artificial ventilation, oxygen toxicity, infection
▶ Complications: recurrent infection, pulmonary hypertension
▶ Mx: wean off artificial ventilation onto CPAP, then ambient O2
→corticosteroids may help
• Hypothermia
▶ Due to large surface area to volume ratio, thin skin, little subcutaneous fat,
cannot curl up/shiver
▶ Consequences: energy consumption, hypoxia, hypoglycaemia, no weight
gain
▶ Mx: incubation / plastic wrap
• Infection
→ Major cause of death
▶ IgG transferred across placenta in 3rd trimester – preterm infants have less
▶ Usually nosocomial – catheters, ventilators
• Intraventricular haemorrhage (IVH) → 25% very low BW infants
▶ RF: very low BW, pneumothorax, RDS, perinatal asphyxia, CMV
▶ Sx: apnoea, lethargy, hypotonia coma, bulging fontanelle
▶ Complications: hydrocephalus, PVL, cerebral palsy
▶ Mx: CSF drainage, ventriculoperitoneal shunting
• Necrotising enterocolitis (NEC) → bacterial infection of ischaemic bowel wall
▶ RFs: preterm, very low BW, cow’s milk (not breast milk)
▶ Sx: feed aspiration, vomiting (may be bilious), abdo distension/pain,
freshbloody stools
▶ Complications: shock, bowel perforation, post-surgical strictures
▶ Ix: AXR ± USS
▶ Mx: stop oral feeding, broad-spectrum ABX, parenteral nutrition, artificial
ventilation → surgery if perforated bowel
• Retinopathy of prematurity (ROP) → vascular proliferation at junction of retina
▶ Complications: retinal detachment, fibrosis, blindness
▶ RFs: high conc. O2 therapy, very low BW
▶ Mx: laser therapy → screen high risk infants weekly (<1.5kg or <32w)
• Hypoglycaemia
▶ RFs
• preterm, IUGR (low glycogen stores)
• diabetic mother (islet cell hyperplasia = hyperinsulinaemia)
• LGA, hypothermia, polycythaemia, illness ( demand)
▶ Sx
• irritable/jittery
• lethargic/drowsy/hypotonic
• apnoea
▶ Mx: aim for BG >2.6mmol/L
• early, frequent feeding
• regular BG monitoring
• IV glucose
• seizures
6
NICE (2019) Specialist neonatal respiratory care for babies born preterm [NG124]
Genetics & syndromes
https://t.me/med1917
↳ Syndrome: particular set of multiple anomalies occurs repeatedly
in a consistent pattern due to an underlying mechanism
Chromosomal abnormalities
TRISOMIES → non-disjunction, translocation or mosaicism
DOWN SYNDROME (trisomy 21) ≥50% live over 50y
Physical features
• round face
• small mouth/ears
• hypotonia
• flat nasal bridge
• protruding tongue
• single palmar crease
• epicanthic folds (upper eyelid)
• Brushfield spots (in iris)
• ‘sandal gap’ between toes
Associated abnormalities: screen for these at birth
e.g. ECHO, TFTs, vision & hearing screens
• congenital heart
defects (40%)
• hearing impairments
(otitis media)
• early onset Alzheimer’s
disease
• moderate learning
difficulties
Fig. 5.9 Down syndrome.
• visual impairments
(cataracts, squint)
• epilepsy, coeliac
disease, infections
Chapter 5: Paediatrics 109
→ 2% babies have congenital malformation
→ 5% babies have genetic disorder
Down syndrome affects 1 in 150 live births
Diagnosis of Down syndrome
• antenatal screening: combined/ triple test
• chromosome analysis (blood test): FISH
Maternal age: 20 30 35 40 44 Overall
Prevalence: 1 : 1530 1 : 900 1 : 385 1 : 110 1 : 37 1 : 650
EDWARDS SYNDROME (trisomy 18)
= 1 in 8000
Physical features
• IUGR / low BW
• Prominent occiput, small mouth
• Flexed, overlapping fingers
• Rocker-bottom/clubbed feet
• Cardiac & renal malformations
→most die in infancy
PATAU SYNDROME (trisomy 13)
= 1 in 14,000
Physical features
• Brain defects (microcephaly)
• Small eyes (microphthalmia)
• Cleft lip/palate
• Polydactyly
• Cardiac & renal malformations
→most die in infancy
OTHER CHROMOSOMAL SYNDROMES
TURNER SYNDROME (45,X) = 1 in 2500
Physical features
• Short stature
• Spoon-shaped nails
• Lymphoedema of hands/feet
• Webbed neck
Associated conditions
• Congenital heart defects (aortic coarctation)
• Delayed puberty
• Hypothyroidism
• Ovarian dysgenesis = infertile
• Renal anomalies
Webbed neck
Wide carrying angle
Fig. 5.10 Physical features
of Turner syndrome.
Investigations for Turner syndrome
• Blood karyotyping
• Buccal swab (for Barr body = inactive X
chromosome)
• LH & FSH
• For complications: TFTs, urinalysis
(for glucose etc.)
Tx for Turner syndrome
• Growth hormones
• Oestrogen replacement
→ develop 2° sexual characteristics but still
infertile
110 Chapter 5: Paediatrics Genetics & syndromes
https://t.me/med1917
KLINEFELTER SYNDROME (47,XXY) = 1 in 1000
Physical features
• hypogonadism / small testes = infertile
• gynaecomastia
• lack of chest/facial hair
• tall stature
Tx: testosterone therapy may help
Single gene/Mendelian disorders
AUTOSOMAL DOMINANT = 50% chance child inherits affected allele
TUBEROUS SCLEROSIS = 1 in 6000
Signs Associated conditions
Fig. 5.11
Angiofibromata.
• ‘ash-leaf ’ lesions (hypopigmented)
• shagreen patches (rough patches)
• ungual fibroma (nail tumour)
• angiofibromata (benign
nasopharyngeal tumour in butterfly
distribution over nose)
• benign tumours (brain, skin, heart, eyes, lungs)
• infantile spasms
• autism
• epilepsy
Fig. 5.12 Ash-leaf patch.
Fig. 5.13 Café au lait spots.
ACHONDROPLASIA (DWARFISM) = disorder of bone growth
→ Tx: growth hormones/surgery for spine
Signs Associated conditions
• short stature & limbs/digits
• large head (macrocephaly)
• apnoea • obesity
• lordosis • spinal stenosis
• large forehead & depressed nasal bridge
MARFAN SYNDROME = 1 in 5000 → disorder of connective tissue
(fibrillin-1mutation)
Signs Associated conditions
• tall & thin
• hypermobility
• scoliosis
• AAA, aortic dissection, valve regurgitation
• glaucoma, cataracts, retinal detachment
• lung collapse, asthma, sleep apnoea
• long limbs
• crowded teeth
• sunken chest
NEUROFIBROMATOSIS = 1 in 3000–4000 → skin changes + tumours along nerves
Signs Associated conditions
Type 1:
• café au lait spots
• axillary/groin freckles
• Lisch nodules (benign growth in eye)
• neurofibromas (benign)
• malignant peripheral nerve sheath tumours
• hypertension
• scoliosis
Fig. 5.14 Noonan syndrome.
Type 2: (much rarer)
• hearing loss / balance problems
• juvenile cataracts
CN VIII tumours
• vestibular schwannoma
• bilateral acoustic neuromata
NOONAN SYNDROME = 1 in 1000
Signs Associated conditions
• short stature
• webbed neck
• pectus excavatum
• flat nasal bridge
• mild learning difficulties
• congenital heart disease (pulmonary stenosis, ASD)
• bleeding disorders
• scoliosis
• wide-set eyes
→ similar phenotype to Turner syndrome
Genetics & syndromes Chapter 5: Paediatrics 111
https://t.me/med1917
AUTOSOMAL RECESSIVE = if both parents are carriers, 25% chance child is
affected (all offspring = carriers)
↳ often affect metabolic pathways
↳ risk increased by consanguinity
PHENYLKETONURIA (PKU) = very rare
= congenital enzyme deficiency (phenylalanine hydroxylase) → phenylalanine
accumulation
Symptoms
• very fair hair/skin & eczema
• severe learning difficulties/
behaviour problems
• anxiety/depression
• epilepsy
Diagnosis
• blood phenylalanine levels
(heel-prick test)
Treatment
• phenylalanine-restricted diet
Examples of autosomal recessive conditions
• CF
• SCA
• PKU
• Tay–Sachs
• Friedreich ataxia
• Thalassaemiar
XLINKED RECESSIVE = males are affected, females are carriers (but may show
mild disease)
↳ 50% chance son of female carrier is affected
↳ 50% chance daughter of female carrier is carrier
↳ All daughters of affected males are carriers
↳ Sons of affected males are unaffected
FRAGILE X = very rare
→ due to CGG nucleotide repeats
Signs Associated conditions
• macrocephaly
• large testes (post-puberty)
• long face & broad forehead
• large, everted ears
• prominent mandible
DUCHENNE MUSCULAR DYSTROPHY = 1 in 4000
→ loss of matrix protein dystrophin → abnormal cell signalling
Signs Associated conditions Management
• waddling gait (frequent falls) –
climb stairs / run slowly
• calf pseudohypertrophy – fat
replaces muscle
• Gower sign – must turn prone
to rise
• progressive muscular atrophy
(cannot walk by 10–14y)
• mod/severe learning difficulties (mean IQ 50)
• autism
• hyperactivity
• mitral valve prolapse / joint laxity
• scoliosis
• learning difficulties
• cardiomyopathies
• respiratory failure
• scoliosis
Life expectancy: late 20s
• exercise, stretching
• walking aids
Scoliosis: brace/surgery
Respiratory: CPAP
Parental support groups
Examples of X-linked recessive conditions
• Colour-blindness
• Fragile X
• Haemophilia A/B
• DMD/BMD
• G6PD deficiency
Fig. 5.15 Fragile X.
Diagnosis: clinical signs + markedly
elevated serum CK
XLINKED DOMINANT = very rare → both males & females affected
(malesusually die)
RETT’S SYNDROME – 99% of cases are de novo mutations (1% = X-linked
dominant)
Symptoms: severe speech, learning & coordination problems
• 6–18m: apparently normal development (may be delay in motor skills / signs
of autism)
• >1y: repetitive hand/eye movements (wringing, clapping, blinking, staring),
apraxia, slow growth
Other problems: seizures, scoliosis, muscle weakness, breathing abnormalities
112 Chapter 5: Paediatrics Genetics & syndromes
https://t.me/med1917
OTHER DYSMORPHIC CONDITIONS
PRADER–WILLI SYNDROME = no paternal copy of Chr. 15q11–13 (sporadic)
Signs Associated conditions
Fig. 5.16 Prader–Willi syndrome.
• hypotonia
• neonatal feeding difficulties
• insatiable appetite later in childhood
• narrow forehead
• almond-shaped eyes
• triangular mouth
ANGELMAN SYNDROME = no maternal copy of Chr. 15q11–13 (sporadic)
Signs Associated conditions
• ‘coarse’ facial features
(rounded, heavy, thickened skin)
• microcephaly
• widely spaced teeth & wide mouth
• prominent lower lip
• poor growth in childhood
• developmental delay
• obesity/T2DM
• learning difficulties
• behavioural problems
• intellectual disability
• severe speech impairment
• hyperactivity
• ataxia
• seizures
Fig. 5.17 Angelman syndrome.
Fig. 5.18 Williams syndrome.
RUSSELL–SILVER SYNDROME = slow growth before & after birth PLUS
dysmorphic features
Signs Associated conditions
• LBW / failure to thrive
• head often disproportionate to small body
• triangular face (prominent forehead, narrow chin)
• curved 5th finger
WILLIAMS SYNDROME = may be auto dominant or de novo
Signs Associated conditions
• ‘elfin’ appearance
(wide mouth, small, upturned nose, short)
• outgoing and friendly
• short stature
• delayed development
• learning disabilities
• mild learning disabilities
• hypercalcaemia
• ADHD
• aortic stenosis
Growth and puberty
https://t.me/med1917
Stage of growth % height grown Dependent on*
1. Fetal 30% Placental nutrition, maternal size/health
2. Infantile (<2y) 15% Nutrition, thyroid hormones, genes
3. Childhood 40% Nutrition, thyroid & growth hormones, genes
4. Puberty 15% Sex hormones & growth hormones, genes
*emotions/happiness also impact growth by affecting hormones
Role of hormones
Chapter 5: Paediatrics 113
• Growth hormone: at growth plate & stimulates ILGF to organ size
• Thyroid hormones: act at growth plate
• Sex hormones: cause growth spurt and fusion of growth plates
(oestrogen deficiency = delayed fusion = tall stature)
Measuring growth
• Weight, height**, head circumference
• Plot serial growth measurements on growth chart
• ± Bone age, pubertal stage, BMI
**<2y measure length not height
Short stature
→ height below the 2nd centile (2 SDs below the mean)
CAUSES
• Non-pathological
▶ familial – short parents (consider genetic growth disorder – karyotype Ix)
▶ constitutional delay of growth & puberty – late bone maturation &
growth spurt (genetics, poor diet or exercise)
• Pathological
▶ IUGR / extreme prematurity – may need GH Tx
▶ Chromosomal disorders – Down’s, Turner, Noonan, Russell–Silver
▶ Endocrine – associated with weight (weight > height centile)
▶ Nutritional / chronic illness – associates with weight (weight<height)
e.g. coeliac, Crohn’s, chronic renal failure
INVESTIGATIONS
• Height velocity: 2 measurements, 1y apart
• Height comparison:
1. against weight 2. against expected/mid-parental height (MPH)
Height of father height of mother
MPH2
+7cm forboys
7cmfor girls
Growth hormone = peptide hormone
Indications for urgent specialist referral:
• <0.4th centile or >99.6th centile
• Height markedly discrepant from weight
• Measurements cross centile line after 1y
• Measurements cross 2 centile lines in 1st y
Remember to correct for prematurity:
• subtract no. of weeks premature
• correct up to 1y of age if born ≥32w
• correct up to 2y of age if born <32w
Endocrine causes of short stature
• GH deficiency
▶ 1° deficiency
▶ 2° to hypopituitarism e.g.
craniopharyngioma
▶ Laron syndrome = defective GH receptors
• Excess corticosteroids
▶ Iatrogenic – alternate Tx days to risk
▶ Cushing’s syndrome = rare in children
• Hypothyroidism
• Hx, examination, hormone screen (GH, TFT, cortisol):
▶ dysmorphic features, features of chronic/endocrine illness, birth Hx
Target height: MPH ± 2SDs
(±10cm in boys, 8.5cm in girls)
DDx of tall stature
• Familial
• Endocrine: hyperthyroidism, CAH, GH
• Precocious puberty
• Genetic syndromes: Marfan, Klinefelter
114 Chapter 5: Paediatrics Growth and puberty
https://t.me/med1917
Puberty
Females Males
Tanner I
Child
About ten
Fig. 5.19
Tanner II
years old
Tanner III
First period
Tanner IV
1–2 years after
rst period
Stage 1 = no pubertal signs
precocious puberty is more common in females
*prevent
conserve height potential
growth plate fusion)
(stop premature
Tanner V
Grown up
9–11y: 2° sexual characteristics:
→ breasts then pubic hair
10–12y: growth spurt
11–13y: menarche
If pubic hair but no breast/testicle development,
PRECOCIOUS PUBERTY → development of 2° sexual characteristics <8y in
females and <9y in males
↳ True/central: gonadotropin-dependent (premature activation of
hypothalamic axis)
↳ False/pseudo: gonadotropin-independent (excess sex steroids)
Causes
Females:
• Central = majority (idiopathic/familial) – ask about FHx
• Other = CAH, adrenal tumour, pituitary adenoma
Males:
nearly always pathological
• Central = uncommon
• Mainly tumours: intracranial, adrenal, testicular
Investigations
• FHx, examination, hormone screen
• Growth chart
• X-ray hand – determine bone age
• Orchidometer – >4mm = puberty started
• USS ovaries/uterus – size/endometrial thickness
• MRI – hypothalamic tumours
Management*:
• Central: GnRH analogues
• Pseudo: identify & treat underlying cause of excess sex hormones
10–14y: 2° sexual characteristics:
→ testicles >4ml then pubic hair
12–14y: growth spurt
(after 18m delay)
must Ix for CAH etc.
PREMATURE THELARCHE = early breast development (6m – 2y) but no
other 2° sexual features / growth spur t
↳ of no consequence – do not need to intervene
PREMATURE ADRENARCHE = pubic hair <8y (F) or <9y (M) but no other
2°sexual features / growth spur t
↳ due to early maturation of androgen production in adrenal glands
↳ USS ovaries/uterus + bone age Ix to r/o central precocious puberty or
conditions likeCAH
GYNAECOMASTIA = abnormal breast enlargement in males (in 50% boys
during early adolescence → self-limiting)
↳ Causes: Klinefelter, testicular feminisation, hypo-/hyperthyroidism,
obesity,alcohol
DELAYED PUBERTY → absence of pubertal development by 14y in females
and15y in males
Causes
Constitutional delay in growth & puberty (most)
• short in childhood, long legs compared to back
Other causes
• Hypogonadotropic hypogonadism ( gonadotrophins)
▶ systemic disease: CF, anorexia, Crohn’s, exercise
▶ intracranial tumours / pituitar y damage
▶ syndromes: Kallmann’s
Growth and puberty Chapter 5: Paediatrics 115
https://t.me/med1917
• Hypergonadotropic hypogonadism ( gonadotrophins)
▶ syndromes: Turner’s, Klinefelter’s
▶ steroid hormone enzyme deficiency
Investigations
• FHx, examination, hormone screen (TFT, LH/FSH)
• Growth chart
• X-ray hand – determine bone age
• Pubertal staging: testicular volume/USS
• Karyotyping
Management
• r/o or treat underlying causes
• reassure puberty will occur (Tx not usually needed)
• IM testosterone/oestradiol
Diabetes mellitus
TYPE 1 DIABETES MELLITUS → autoimmune destruction of pancreatic beta
cells = insulin insensitivity
Risk factors
dad with T1DM
• Environmental triggers: enteroviral infections, cow’s milk, overnutrition
Symptoms
• Polydipsia, polyuria, weight loss, lethargy
• ± nocturnal enuresis, infections, signs of DKA
Diagnosis = symptoms PLUS
• Random blood glucose >11.1mmol/L
• Fasting blood glucose >7mmol/L (TFTs, coeliac screen, TPO to r/o other causes)
Management7:
MDT (paediatrician, specialist nurse, dietitian, support groups)
1. Intensive education for child & parents
• Injection of insulin & blood glucose monitoring (finger-prick/continuous
monitoring)
• Diet & exercise: carb counting, low GI carbs, carb-free snacks, adjustment for
activity, alcohol
• ‘Sick-day’ rules: do not stop insulin (monitor glucose every 3–4h, may
need insulin)
• Signs of DKA/hypoglycaemia
2. Insulin
• Subcutaneous pump = continuous infusion of rapid acting (NovoRapid)
• Basal-bolus injection regimen = 2× LA breakfast & night PLUS SA before
each meal
3. Monitoring for complications: annual review
• Growth & pubertal development – risk obesity / delayed puberty
• BP, renal function, eyesight, foot health
• Associated autoimmune conditions: TFTs, coeliac screen, RA
↳
Need to educate school too
DM affects 2 in 1000 children (98% = T1DM)
Target blood glucose:
Pre-prandial: 4–7mmol/L
Post-prandial: 5–9mmol/L
LA = Long-acting SA = Short-acting
Difficulties of glucose control in children
• Sugary foods/eat at odd times
• Infrequent/unreliable monitoring
• Poor family support
• Exercise
• Illness ( insulin need)
DIABETIC KETOACIDOSIS (DKA)
Symptoms
• ‘Pear-drop’ smelling breath
• Abdominal pain
• Vomiting
• Dehydration
7
NICE (2015, updated 2022) Diabetes (type 1 and type 2) in children and young people [NG18]
• Hyperventilation (Kussmaul
breathing)
• Drowsiness/coma
Think sepsis if:
Fever/hypothermia, hypotension,
refractory acidosis, lactic acidosis
116 Chapter 5: Paediatrics Growth and puberty
https://t.me/med1917
Management8: emergency → hospital admission
Investigations
1. ABCDE
2. Fluid resuscitation & ongoing rehydration (cautiously)
• Blood glucose >11.1mmol/L
3. Insulin therapy & potassium
• Blood ketones >3mmol/L
• pH <7.3 or HCO
• U&Es: Na, K, urea, Cr
• ECG: for hypokalaemia
–
<15mmol/L
3
IV fluids*
0.9% saline (10ml/kg over 30min)
then calculate maintenance + deficit needs
*avoid rapid
rehydration as risk
cerebral oedema
Fixed rate high dose insulin
(0.1 units/kg/h)
Causes of hypoglycaemia
• Neonatal hypoglycaemia (common)
• Preterm / maternal DM / sepsis
• Fasting / missed meals / exercise
• exogenous insulin dose
• Tumours (insulinoma)
• Drug-induced: sulphonylureas
• Liver disease / glycogen storage disorder
• Addison’s, CAH, GH deficiency
• Alcohol
Measure blood glucose in any child who:
• Becomes septic / appears seriously ill
• Has a prolonged seizure
• Has an altered state of consciousness
Take care not to overload insulin as is
hypertonic → cerebral oedema
Potassium replacement
+ KCl as insulin causes K+ to fall
Identify & treat underlying cause
**ketones <0.6, alert,
no nausea/vomiting
• switch to SC insulin
• encourage regular feeding & fluids
AND
e.g. ABX if septic
Once stable**
Glucose replacement
+ 5% dextrose when BG <15mmol/L
Closely monitor:
• Fluid input/output
• Blood glucose
• U&Es (K+, Na, Cr, urea)
• Acid–base status
• Neurological state
Fig. 5.20
Complications
• Electrolyte imbalances (Na+, K+) –monitor U&Es
• Cerebral oedema – headache, agitation, GCS, eye palsies
• Aspiration
HYPOGLYCAEMIA = blood glucose <2.6mmol/L
Symptoms
• Sweating, pallor, palpitations/tremor
• Headache / vision changes / confusion
<4.0 in diabetics
<2.0 in asymptomatic, term neonates
• Hypotonia, poor feeding (in infants)
• Drowsiness, seizures, coma
Investigations
• Careful Hx
• Physical examination
• Blood glucose & ketones
• FBC, CRP, U&Es, LFTs, TFTs, blood gases
short/pigmentation suggest hormone issue
hepatomegaly suggests glycogen storage
disease
• Hormones – insulin, C-peptide, GH, cortisol
• Urinalysis – pH, ketones, reducing substances
Management
9
1. Oral fast-acting glucose: sugar y drink / Glucogel
2. IV glucose: 2ml/kg dextrose bolus then 10% dextrose infusion
3. IM glucagon if unconscious / fail to respond
DIABETES INSIPIDUS DI = ADH (antidiuretic hormone) disorder causing
polydipsia and polyuria
• Central DI: insufficient ADH production → responds to desmopressin
• Nephrogenic DI: lack of kidney response to ADH → more common type
in children → no response to desmopressin
8
BSPED (2021) Guideline for the management of children and young people under the age of 18 years
with diabetic ketoacidosis
9
NICE (2015, updated 2022) Diabetes (type 1 and type 2) in children and young people [NG18]
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