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41 Cards in this Set
- Front
- Back
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What is the difference between the direct and indirect coomb's test?
When are they used? |
Direct - detects IgG or complement on the surface of the RBC
Add anti-IgG or anti-complement to the patient's RBCs - test is +ve if RBCs agglutinate Use: haemotlyic disease of newborn; autoimmune haemolytic anaemia, haemolytic transfusion reaction Indirect: Detects antibodies in serum that can recognise antigens on RBCs Mix patient's serum with donor RBCs + Coomb's serum (anti-human IgG antibodies) - test is +ve if RBCs agglutinate Use: cross matching; atypical blood group; blood group antibodies in pregnancy women |
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What is physiological jaundice due to and when does it occur?
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Onset 2-3 days of life, resolution 7-10 days (term baby); 3 weeks (prem)
Due to increased production of bilirubin (due to increased haemolysis due to shorter lifespan of RBCs) + immature neonatal liver - trouble conjugated bilirubin |
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Is there a risk of kernicterus with physiological jaundice?
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No
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What is breastfeeding jaundice? How is it different to breast milk jaundice
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Breast feeding jaundice - occurs within 1st week of life - due to lack of milk production --> dehydration --> exaggerated physiologic jaundice
Breast milk jaundice - Unknown MOA but probably due to an inhibitor of glucuronyl transferase found in breast milk - onset 7 days peak 2-3rd week - lasts 6-8 weeks Cessation of breast is NOT indicated |
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What are the causes of pathological jaundice with unconjugated hyperbilirubinaemia
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Haemolytic:
Spherocytosis, G6PD defcieicny ABO and/or Rh incompatibility, Kelly Duff, etc, splenomegaly, Sepsis Non-haemolytic: Haematoma, polycythaemia, sepsis, hypothyroidism, Gilbert syndrome |
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What are the causes of conjugated hyperbilirubinaemia
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Hepatitis:
Infectious (sepsis, HBV, TORCH) Metabolic: Galactosemia, tyrosinaemia, hypothyroidism, CF Drugs Post hepatic: biliary atresia |
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If a baby presents with jaundice within the first 24 hours of life what do you need to be thinking about
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Usually haemolysis (ABO, Rh, G6PD, spherocytosis) or sepsis
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If the baby presents with jaundice within 48-96 hours what do you need to think about
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Usually physiologic, breastfeeding
BUT still think of: sepsis, haemolytic (G6PD, spherocytocis etc), bruising, cephalhaematoma, GIT obstruction, metabolic disorders, liver enzyme defects |
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If a baby presents with jaundice after 1 week of life what type is it usually
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Conjugated
Gilbert, Crigler-Najjar Inborn errors of metabolism Biliary tract obstruction - atresia Unconjugated: breast milk, hypothyroidism, GIT obstruction,TORCH, UTI, Bacterial sepsis |
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What symptoms will a baby get with kernicterus?
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Up to 15% will have no obvious neurological Sx
Lethargy, hypotonia, poor feeding, high pitched cry, opisthotonic posturing, fever, apnoeas, seizures, coma, death Late sequelae: sensorineural hearing impairment, chorioathetosis (irregular contractions + twisting and writhing), ataxia, learning difficulties |
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What is kernicterus
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Due to the less developed BBB bilirubin more easliy crosses and deposits in the basal ganglia --> neurological problems
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What coexistent factors increase the risk of kernicterus with hyperbilirubinaemia
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sepsis, meningitis, haemolysis, hypoxia, hypothermia, hypoglycaemia, prematurity
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Investigations for neonatal jaundice
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Serum bilirubin (conjugated and unconjugated)
FBC - film and reticulocyte count Blood group (Mum and bub) Coombs (direct antigen test) If acutely unwell - septic screen If unconjugated or presents after day 3 - galactosemia, TFTs, LFTs, Urine metabolic screen, check guthrie card |
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How does phototherapy work in treatment of jaundice
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blue-green light converts unconjugated bilirubin to harmless isomers
NB: only works on unconjugated bilirubin but that is the only one we are worried about in terms of kernicterus |
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What treatments for neonatal jaundice do we have?
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Phototherapy - only for unconjugated
Exchange transfusion - baby's blood is removed in aliquots and replaced with transfused blood Removes bilirubin and antibodies |
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What are the side effects of phototherapy
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Retinal damage
Rash (disappears after light) Loose stools - always give extra fluid Increased temperature |
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Why is phototherapy contraindicated for conjugated hyperbilirubinaemia
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It produces a toxic metabolite which also imparts a bronze hue on the baby's skin
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When is exchange infusion warranted for neonatal jaundice?
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Commonly with haemolytic disease and G6PD
Usually with bilirubin > 340 and likely to exceed that due to haemolysis This is lower with preterm or sick infants |
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Potential side effects of exchange transfusion
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transfusion reaction
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How is bilirubin metabolised?
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RBC --> biliverdin --> bilirubin --> combines with albumin and transported to the liver where it undergoes conjugation with glucuonamide
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Why is hypoglycaemia a problem in babies
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Glucose = essential nutrient for the brain
Hypoglycaemia --> encephalopathy and potential to produce long term neurological injury |
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What is the ideal BGL for neonates
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> 24 hrs = > 2.5
< 24 hrs = > 2 in term babies; > 2.5 in premature or sick babies |
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Symptoms of hypoglycaemia in neonates
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Poor feeding
Jitteriness and irritability Apnoea and cyanosis Hypotonia Convulsions |
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Which babies are at risk of hypoglycaemia?
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Diabetic mother, LGA > 4.5 - increased levels of circulating insulin
Preterm, IUGR/SGA, < 2.5kg - lack of glycogen stores, reduced ability to use alternative fuels - paradoxically hyperinsulinaemic possibly due to IUGR (insulin a growth factor?) Asphyxia, hypothermia - excess utilisation of glycogen stores Starving, poor feeding, vomiting - inadequate provision of substrate Thermal stress, sick baby, infection, metabolic - hypermetabolic state |
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Name some causes of hypoglycaemia
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Liver immaturity --> less gluconeogenesis and ketogenesis
Consumption of glycogen stores during parturition --> impairment of glycogenolysis Hyperinsulinism secondary to transient hyperglycaemia in neonates born to mothers with poor glycaemic control Asphyxia, SGA --> hyperinsulinaemia (cause unknown) |
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Management of neonatal hypoglycaemia
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Regular feeds
IV 10% dextrose Infants born to insulin dependent mothers --> NICU and regular BGL monitoring within 1 hour Others (gestational and non-insulin dependent) can go to postnatal ward |
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Define apnoeas in the newborn
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absence of respiratory gas flow for > 15-20 seconds
central: no chest movement obstructive; chest movement Mixed: combination NB: periodic breathing in which rapid respiration are alternated with apnoeas 10-15 secs are normal in infants |
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What are the causes of apnoeas in the newborn term
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< 24 hours - sepsis
> 24 hours CNS: IVH, seizure, hypoxic injury Infection: sepsis, NEC, meningitis GI: GORD, aspiration Metabolic: hypoglycaemia, hypocalcaemia, hyponatraemia hypo,hypertension, anaemia, hypovolaemia, PDA, heart failure Morphine |
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Signs of intestinal obstruction in the neonate
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Bilious vomiting
Abdominal distension Delayed passage of meconium |
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Name some causes of intestinal obstruction in the newborn
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Duodenal atresia
Jejunoileal atresia Malrotation Meconium ileus Imperforate anus - may have fistula with urinary tract - recurrent UTIs Hirshsprung disease |
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Investigations for intestinal obstruction in neonates
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AXR
Abdo US if pyloric stenosis |
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What relationship is the neonates BSL to the Mum's
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Neonate's is 2/3 Mum's
Maintained by facilitated diffusion across placenta NB: glycogenolysis and gluconeogensis are not active prior to delivery |
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Why do you get a transient fall in BGL during first few hours of birth?
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No glycogenolysis and gluconeogensis active while in utero - these must be switched to immediately
Get transient fall because the counterregulatory hormones (glucagon, GH, adrenaline, and cortisol) take a while to induce endogenous glucose production |
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When should you intervene with BSL?
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< 2.0 if asymptomatic full term neonate or healthy preterm > 35 GA
< 2.5 if preterm neonate < 35 GA, symptomatic neonate, sick neonate requiring NCC support |
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How should you manage babies at risk of hypoglycaemia?
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Feed ASAP after birth (within 2 hours)
continue every 3-4 hours Complementary feed via bottle/OGT Repeat BSL 60 mins after feed |
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How should you manage symptomatic hypoglycaemia
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Transfer to NCC
IV fluids 10% dextrose started 2ml/kg (if give higher amount may have rebound hypoglycaemia) BSL monitoring frequently |
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Why do babies have larger glucose requirements than adults?
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larger brain to body size ratio
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Treatment of persistent hypoglycaemia
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glucagon or hydrocortisone
NB: collect insulin, cortisol, GH, ammonia, lactate, pyruvate, and formal BSL prior to administration of hydrocortisone |
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What is used in the treatment of hyperinsulinism
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diazoxide
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When is the cut off for hypoglycaemia requiring further investigation
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> 7 days duration with appropriate treatment
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Name some pathological causes of hypoglycaemia
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1. Hyperinsulinism
IDDM (transient hyperinsulimism); persistent hyperinsulinemic hypoglycaemia of infancy (beta cell hyperplasia), Beckwith Weideman syndrome (congenital growth disorder) 2. Inborn errors of metabolism glycogen storage disorder, fatty acid oxidation defects, organic acidaemias 3. Other Congenital hypopituitarism, congenital adrenal hypoplasia |
