CHEMPATH: Paediatric clinical chemistry Flashcards
What is the rate of infant death in the first year similar to?
Same as in adults aged 55-64 yo.
Highest in LBW infants
What are the common consitions seen in LBW infants?
- Respiratory distress syndrome (RDS) - Common before 34th week of pregnancy, lack the surfactant protein in the lungs
- Retinopathy of prematurity (ROP) - an abnormal growth of blood vessels in the eye –> vision loss
- Intraventricular haemorrhage (IVH)
- Patent ductus arteriosus (PDA)
- Necrotising enterocolitis (NEC)
What are the features of NEC?
Inflammation of the bowel wall à necrosis and perforation
- bloody stools,
- abdominal distension
- intramural air
What kind of preparation for birth does the foetus undergo in the last trimester of pregnancy?
Laying down stores e.g. fat and glycogen
When do nephrons form? When does urine production begin? When does complement form? When is functional maturity of GFR reached?
Nephrons - 6 weeks
Urine - 10 weeks
Full complement - 36 weeks
GFR functional maturity - 2 yo
What are the differences in infant kidney anatomy compared to adults?
- Glomerulus: large SA:volume ratio (so relatively low GFR for their SA)
- PCT: shorter
- Loop of Henle/DCT: shorter and DCT is relatively unresponsive to aldosterone
What are the consequences of large SA:volume ratio of the infant glomerulus?
- Slow excretion of solute load
- Limited amount of Na+ available for H+ exchange
What are the consequences of short PCT in infant kidneys?
- Lower resorptive capability BUT this is still adequate for the filtered load
- Renal threshold for glycosuria is much lower (i.e. glycosuria will appear at lower plasma glucose levels than in adults)
- Reabsorption of bicarbonate is not as effective –> propensity for acidosis
What are the consequences of short loop of Henle/DCT and reduced aldosterone sensitivity of the infant kidney?
- Short –> reduced concentration ability (max to osmolality of 700mmol/kg vs 1500mmol/kg in adults)
- Unresponsive to aldosterone –> persistent Na loss (1.8mmol/kg/day) –> THEREFORE reduced potassium* excretion
*So upper limit of normal is 6mmol/L in children up to 4yo
Why do ALL infants lose weight in the first 7 days of life? How much loss is normal in a term and preterm infant?
- In utero they have more ECF than adults
- Ex utero they have less pulmonary resistance –> release of ANP –> redistribution of fluid –> weight loss in the first 7 days of life
Loss of 40ml/kg in a term baby and 100ml/kg in a preterm baby
NB: should gain weight by days 7-10
What % of adult body vs preterm vs term infant is composed of water?
Adult = 60%
Term neonate= 75%
Preterm neonate = 85%
Daily requirements of water, K and Na for neonates vs adults of a proportional size.
How often should you monitor sodium levels in preterm infants? When can K+ be supplemented if necessary?
- Plasma Na+ should be measured daily in neonates born <30 weeks
- K+ should only be given once urine output of >1ml/kg/hr has been achieved [normal adult output]
- In adults aldosterone –> increase K+ excretion AND increase Na+ reabsorption
- Since infants have aldosterone insensitivity –> reduced K+ excretion (mild hyperkalaemia) and persistent Na+ losses so at risk of hypernatraemia and so must be monitored and fed often.
Name 3 broad causes of electrolyte disturbances in neonates.
- High insensible water loss
- Drugs
- Growth
Why do infants have high insensible water loss?
- High surface area
- High skin blood flow
- High metabolic/respiratory rate
- High transepidermal fluid loss (skin is not keratinised in premature infants, occurs >28 weeks)
Which drugs commonly given to infants cause electrolyte disturbances?
- Bicarbonate (for acidosis) BUT Na bicarb contains high sodium
- Antibiotics BUT contains high sodium content (sodium salts)
- Caffeine/theophylline (for apnoea) BUT increases renal sodium loss
- Indomethacin (for PDA) BUT causes oliguria
Name 3 causes of hypernatraemia in an infant >2 weeks old. How should the cause be investigated?
- Dehydration
- Salt poisoning*
- Osmoregulatory dysfunction
Ix: Routine measurement of urea, creatinine and electrolytes on paired urine and plasma on admission may differentiate the rare causes but keep salt poisoning at back of your mind.
Name a congenital disorder which can cause hyponatraemia in an infant.
CAH (congenital adrenal hyperplasia)
How does CAH cause hyponatraemia? How does CAH cause ambiguous genitalia in female infants?
Most common cause is 21-hydroxylase (21-OH) deficiency –> reduced cortisol / aldosterone –> salt loss –> hyponatraemia
The lack of 21-OH –> accumulation of 17-OH progesterone and 17-OH pregnenolone instead which are precursors for androgens
What are the clinical features of CAH?
- Hyponatraemia/hyperkalaemia with volume depletion (lack of aldosterone) –> salt-losing crisis
- [Hypoglycaemia (lack of cortisol) is uncommon]
- Ambiguous genitalia in female neonates (not obvious in male neonates – present with salt-losing crisis and may die)
- Growth acceleration due to extra androgens
What is the trend for Hb after birth?
Decreases up to about 30 days as infant starts making HbA
List 3 reasons for neonatal conjugated hyperbilirubinaemia.
- High level of bilirubin synthesis (from rbc breakdown)
- Low rate of transport into the liver
- Enhanced enterohepatic circulation
What factors make even small rises in free/unconjugated bilirubin dangerous in infants? How much conjugated bilirubin can most infants bind?
- They have low albumin (lower in prematurity) at about 34g/L - each 1g/L of albumin binds 10micromol/L of bilirubin so limit of 340micromol/L before free bilirubin is released into the bloodstream
- They have a leakier BBB so free bilirubin will cross more easily and cause kernicterus
How are bilirubin thresholds for no treatment/phototherapy/exchange transfusion determined in infants?
NICE guidelines have charts
Preterm charts for each week available
