Neonatal Flashcards
Methods of fetal blood sampling
- Umbilical vein
- Intrahepatic vein
- Cardiocentesis (last resort)
Methods of confirming fetal blood
- MCV - caution if fetus has been transfused or mother is macrocytic
- Apt Downey (maternal blood goes brown due to alkaline denaturing
- I antigen on maternal RBCs but not fetal
- HCG - best method. Shouldn’t be present in fetal blood
Clotting factor levels in neonates compared to adults
Lower - Protein C, Protein S, AT, Vit K dependent proteins (II, VII, IX, X) - vitamin K deficiency at birth (no intestinal bacteria and immature fetal liver)
Normal - Factor VIII, Factor V and fibrinogen
Higher - Usually VWF
Reasons why neonates are prone to thrombosis
- Reduced physiological inhibitors of haemostasis
- Impaired fibrinolysis
- Small calibre vessels
Pathogenesis of NAIT
Maternal alloantibodies (IgG) against fetal platelet antigens, derived from father during pregnancy or delivery causes destruction of fetal platelets and severe fetal and/or neonatal thrombocytopenia.
- HPA-1a, HPA-4 and HPA-5b (more mild) are the most common antigens. HLA is rarely responsible.
- These antigens are found on platelet GPs e.g. GPIIb/IIIa so there is a functional deficit as well.
Clinical features of NAIT
- ICH in utero or at birth
- Widespread petechiae/purpura
- Severe thrombocytopenia at birth or in first 3 days, typically resolves by 2 weeks
Management of NAIT in newborn
Affected neonates should be treated with HPA-compatible platelets.
Use of HPA-1a(-), HPA5b(-) platelet transfusions is indicated as genotyping/serotyping takes some time and these platelet products are generally available immediately and will be suitable for most cases.
IVIG may also be used.
Ultrasound scan of the head should be performed to look for ICH in severe thrombocytopenia.
Risk factors for severity of NAIT
- Anti-HPA-1a antibody (more severe than anti-HPA-5b)
- Second pregnancy
- Sibling with ICH due to NAIT
Diagnosis of NAIT
- Fetal or neonatal thrombocytopenia
- Maternal platelet antibodies
- PIFT
- PAKLx (HPA and HLA)
- Crossmatch
- HPA-1a phenotype in mother and father
- Genotype mother, father +/- fetus
Causes of neonatal thrombocytopenia
- NAIT
- Maternal ITP
- Congenital infection
- Severe Rh disease
- BM failure (syndromes, congenital leuk)
- Placental insufficiency
- Birth asphyxia
- DIC/TTP
RBC requirements for IUT
O negative, rr, Kell neg
Antigen negative for maternal antibodies. Extended phenotype reduces the risk of development of additional antibodies.
Very high haematocrit (>80%) to reduce the volume transfused (triple spun) fast transfusion
< 5 days old (decreased K+, increased 2,3-DPG to allow for better oxygen dissociation from Hb)
Leucodepleted
Irradiated to prevent TA-GVHD
CMV negative
DAT negative
Transfused within 24 hours of irradiation (decreased K+)
What are F cells?
F cells are RBCs that contain 25% HbF
- May be present in normal adults (up to 1%)
- Increased HbF in pregnancy from 8 weeks, peaks as high as 7% at 32 weeks
What is the principle of the Kleihauer test?
Fetal RBCs contain HbF which is resistant to acid and alkali denaturation compared to HbA in adult RBCs.
When dry blood films are fixed and then immersed in an acid buffer solution, HbA is denatured and eluted, leaving red cell ghosts. Red cells containing HbF are resistant and the haemoglobin can be stained; these fetal cells stand out in a sea of ghost maternal cells
Difficulties encountered in the Kleihauer test leading to false positives and negatives.
Thickness of film - if too thick adult red cells may not elute properly (false pos)
If unfixed slides are stained, all the cells will appear as ghost cells (false neg)
Timing of fixation is critical (5 mins) - over fixation inhibits elution process (false pos)
Timing of elution is critical (20 seconds)
Variations in pH and buffer
Reticulocytes may give false positives (usually less pink)
Methods of reducing iatrogenic blood loss in neonates (6)
- Delayed cord clamping
- Essential tests only (protocols, senior approval)
- Minimise discarded blood from lines and return if able
- POCT - ABG, VBG (require much smaller blood volumes)
- Microcollect tubes (downside is requirement for manual analysis in lab)
- Non-invasive monitoring e.g. bilirubin, C02
Causes of anaemia in childhood (by age)
Premature - decreased EPO, shortened RBC survival, iatrogenic from testing, nutritional
0-3 months - physiological (decreased EPO, shortened RBC lifespan, increased oxygenation) vs pathologic - IBMF, infection, haemolysis, blood loss
3-6 months - commonly haemoglobinopathy
>6 months - iron deficiency
Causes of megaloblastosis of childhood
B12:
1. Dietary (B12 deficient mother, vegan diet in child)
2. Malabsorption or pancreatic insufficiency
3. Congenital - IF deficiency, transcobalamin deficiency, thiamine responsive megaloblastic anaemia, DIDMOAD
Folate:
1. Dietary e.g. goat’s milk diet
2. Drugs e.g. MTX, anticonvulsants
3. Malabsorption
4. Increased requirements e.g. haemolysis
