Neonatal jaundice Flashcards
According to NICE guidelines, what is the assessment process?
Visual inspection, checks at birth, bilirubin level measurement, risk factors for kernicterus, assessment for underlying disease
Assessment for baby under 24 hours old with suspected or obvious jaundice?
Measure and record the serum bilirubin level urgently (within 2 hours). Continue to measure the serum bilirubin level every 6 hours until the level is both: below the treatment threshold stable and/or falling.
Assessment for baby over 24 hours old with suspected or obvious jaundice?
Measure and record the bilirubin level urgently (within 6 hours
Treatment
Phototherapy (short breaks- 30 mins, daily weighing, monitor temp), exchange transfusion, intravenous immunogoblin
What is the physiology of bilirubin?
Bilirubin is mainly produced from the breakdown of red blood cells (Hb). Red cell breakdown produces unconjugated (or ‘indirect’) bilirubin, which circulates mostly bound to albumin although some is ‘free’ and hence able to enter the brain. Unconjugated bilirubin is metabolised in the liver to produce conjugated (or ‘direct’) bilirubin which then passes into the gut and is converted to urobilinogen and excreted in urine and faeces
What neonatal factors causes physiological jaundice?
Increased HB release (neonatal RBC have shorter life span than adult therefore higher turnover) (polycythaemia- haematocrit of 50-60%- more RBCs= more breakdown) Reduced bilirubin activity (liver enzyme that conjugates bilirubin is only 1% active in 1st week of life ) Increased enterohepatic circulation (increased reabsorption of bilirubin from GI tract)
What is jaundice?
Yellow colouration of the skin and sclerae caused by the accumulation of bilirubin (hyperbilirubinaemia) in the skin and mucous membranes Also in gums Physiological- 2-5 days Pathological- within 24hours of birth
What is prolonged jaundice?
Jaundice persisting beyond the first 14 days Prolonged jaundice is generally harmless, but can be an indication of serious liver disease
What causes pathological jaundice?
Production: Increased haemolysis of red cells Prematurity Decreased albumin binding capacity/Competition for albumin binding sites Lack of or reduction in enzymes and carrier proteins Lack of oxygen and glucose Hepatitis or liver damage slow the rate of transport Congenital biliary atresia Slow bowel motility
Why might there be an increased haemolysis of red blood cells and therefore increase in bilirubin production?
Rhesus isoimmunisation or ABO incompatibility RBC defects: Congenital spherocytosis (shortage of red blood cells) , G-6-PD deficiency Sepsis and /or DIC (Disseminated intravascular coagulation is a condition in which blood clots form throughout the body blocking small blood vessels) Bruising and cephalhaematoma or internal haemorrhage Polycythemia–twin to twin or materno-fetal transfusion (delayed cord clamping)–SFD infants–Infants of diabetic mothers
Why might prematurity cause jaundice?
Immaturity of the liver Low energy stores Poor feeding Lower levels of SBR will cause brain damage in preterm babies – there are specific SBR threshold charts for preterm babies
Why might there be decreased albumin capacity?
Hypoxia and acidosis Infection Prematurity Hypoglycaemia
Why might there be competition for albumin binding sites?
Free fatty acids - starvation and cold stress Drugs - sulphonamides, cephalosporins/ diazepam I.V. (Sodium benzoate)/- frusemide and other thiazide diuretics/- heparin
Why might there be a lack of or reduction in enzymes and carrier proteins?
Congenital disorders Prematurity
Why might there be a lack of oxygen and glucose?
Prolonged stress in utero or any stress in SFD infants Hypoxia at birth
Why might hepatitis or liver damage slow the rate of transport?
Metabolic disorders eg: galactosaemia Infection