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MK SR INDEX CASES CHILD HEALTH > Neonatal Jaundice > Flashcards

Neonatal Jaundice Flashcards

1
Q

Where does haemopoesis occur in the foetus vs post natally?

A
  • Fetal life Main site is liver

* Post natal Bone marrow

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2
Q

Describe phases of Haemoglobin production in fetus and newborn

A

Embryonic phase
• Embryonic Hb (produced between 4-8 weeks gestation)

Fetal phase
• Hb F main Hb in fetal life • α2 γ2
• Higher affinity for oxygen

At birth
• HbF, Hb A and HbA2
• gradually replaced by HbA & HBA2 by end of yr 1.

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3
Q

At 1 year of age, fetal Hb should be low. What is the significance of increased HbF?

A

Increased HbF is an indicator of inherited Hb disorders

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4
Q

How do Hb levels change at birth?

A

At birth Hb is high (14-21.5g/dl)

falls over the first few weeks, nadir around 2-3 months of age
(~10g/dl)

Preterm infants may have a steeper falls at an earlier age
6.5 - 9g/dL at 4-8 weeks of age

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5
Q

Why do pre-term infants require vitamin supplementation?

A
  • The stores of iron, folic acid and vitamin B12 adequate at birth
  • However they are inadequate in pre term birth and have to be replenished.
  • Stores of iron, folic acid & vitamin B12 are adequate but may get depleted at early age in preterms
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6
Q

Cause of anaemia can be categorised by which three categories?

A

Impaired red cell production: Red cell aplasia, Ineffective erythropoiesis (Iron deficiency, chronic inflammation)

Increased red cell destruction: auto-immune haemolysis, haemoglobinopathies, red cell membranes diseases

Blood loss: Fetomaternal bleeding, Haemorrhage, Bleeding disorders

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7
Q

Presentation in iron deficiency anaemia in infants

A
  • Tire easily, feed slowly
  • History of blood loss or malabsorption
  • May appear pale
  • May have ‘pica’ - Inappropriate eating of non food materials
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8
Q

Differential for microcytic hypo chromic anaemia in children

A

Iron deficiency anaemia

Β or α thalassemia trait

Anaemia of chronic disorders

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9
Q

Iron deficiency anaemia - management

A

• Dietary advice
• Supplement with oral iron
Sytron (sodium iron edetate) or Nifirex (polysaccharide iron) Until Hb is normal and then 3 months to replenish stores

If non responsive, investigate for other causes (e.g. coeliac)

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10
Q

Iron deficiency anaemia - dietary advice

A
  • High in iron: Red meat, liver, kidney, Oily fish
  • Average iron: Pulses, beans, Fortified cereals, Dark green vegetables – broccoli, spinach, Dried fruits, nuts seeds
  • Foods to avoid in excess: Cow’s milk, Tea, High fibre foods
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11
Q

Diagnostic clues for haemolytic anaemias

A
  • Anaemia, hepatosplenomegaly
  • Raised reticulocyte count (polychromasia on blood film)
  • Unconjugated bilirubinaemia and increased urobilinogen
  • Abnormal red cells on blood film
  • Increased red cell precursors in bone marrow
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12
Q

Intrinsic abnormalities of the red cells

A
  • Red cell membrane – hereditary spherocytosis
  • Red cell enzyme disorders - G6PD
  • Haemoglobinopathies – sickle cell, thalassemias
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13
Q

Clinical features of Hereditary spherocytosis

A
  • Jaundice: Intermittent in childhood or Severe haemolytic jaundice in neonatal period
  • Anaemia
  • Splenomegaly
  • Aplastic crisis
  • Gallstones
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14
Q

Manage of Hereditary spherocytosis

A
  • Oral folic acid

* Splenectomy in select patients after 7 years

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15
Q

Clinical features of Glucose –6-phosphate dehydrogenase (G6PD) deficiency

A
  • Neonatal jaundice: May need exchange transfusion
  • Acute haemolysis: Triggered by infections, fava beans, drugs, naphthalene balls
  • Fever, malaise and passing dark urine (haemoglobin and urobilinogen)
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16
Q

Diagnosis of of Glucose –6-phosphate dehydrogenase (G6PD) deficiency

A
  • Between episodes normal blood picture
  • G6PD activity in red cells
  • Management – advice
17
Q

Pathophysiology of sickle cell disease

A

• Commonest genetic disorder in Uk; Autosomal recessive
• HbS – point mutation in codon 6 of B-globin gene leading to
change in amino acid encoded from glutamine to valine
• HbS polymerises in RBCs deforming red cells into a sickle shape
• Reduced red cell lifespan
• RBC trapped in microcirculation leading to vaso-occlusion and organ ischaemia

18
Q

three main forms of of sickle cell disease

A
  • Sickle cell anaemia (HbSS) • HbSC disease (HbSC)

* Sickle β-thalassemia

19
Q

Clinical manifestations of sickle cell

A

Infections: encapsulated organisms, Osteomyelitis due to salmonella, Due to hyposplenism and microinfarction of spleen

Painful crises

Haemolytic or sequestration crisis

Priapism

Long-term issues: pubertal delay, stroke, gall stones, HF

20
Q

Sickle cell triggers

A

Precipitated by cold, dehydration, stress, hypoxia, infections

21
Q

Management of sickle cell

A
  • Prophylaxis against encapsulated organisms: Fully immunised including pneumococcal infections. Daily oral penicillin
  • Folic acid daily oral: increased demand by chronic haemolytic anaemia
  • Crises minimised: Avoidance of triggers, Practical measures; dress warmly, Extra drinks before exercise, Keep children warm after swimming or playing outside
22
Q

Management of sickle cell crisis

A
  • Oral or intravenous analgesia
  • Good hydration – oral or intravenous
  • Prompt treatment of infections with antibiotics
  • Oxygen if saturations reduced
  • Exchange transfusion
23
Q

Prognosis of sickle cell

A
  • Prognosis
  • Premature death
  • 50% of severe patients die before 40 years
  • 3% mortality in childhood
  • Prenatal diagnosis and screening
  • Part of neonatal screening test • Early penicillin prophylaxis
24
Q

Clinical features of Beta-thalassemia

A
  • Severe anaemia – transfusion dependant from 3-6 months of age • Failure to thrive
  • Extramedullary haemopoiesis
  • Prevented by regular transfusions
25
Q

management of Beta-thalassemia

A
  • Management regular transfusions to keep Hb>10g/dL
  • Chronic iron overload: Cardiac failure, liver cirrhosis, diabetes, infertility, growth failure
  • Iron chelation from 2-3 years of age
26
Q

Clinical features of haemophilia

A
  • Recurrent and spontaneous bleeding in joints, muscles leading to crippling arthritis
  • 40% present in neonatal period with Intracranial haemorrhage or Bleeding post circumcision
  • Non accidental injury may be suspected
27
Q

lab findings in haemophilia

A

Normal PT, Prolonged APTT, Low Factor VIII levels

28
Q

Management of haemophilia

A

• Recombinant Factor VIII/IX concentrate iv during bleeding episodes or
for surgery
• Minor bleeds – raise levels to 30% normal
• Life threatening bleeds – raise to 100%
• Avoid all intramuscular injections, aspirin and NSAIDs
• Home treatment
• Prophylactic FVIII from 2-3 years
• Desmopressin for mild haemophilia A

29
Q

Clinical features of Von Willebrand disease/ vWF deficiency

A

Bruising, prolonged bleeding, mucosal bleeding

30
Q

Management of Bruising, prolonged bleeding, mucosal bleeding

A

• Mild disease – Desmopressin (causes secretion of both Factor VIII and
vWF)
• Severe – plasma-derived Factor VIII concentrate

31
Q

What is Immune Thrombocytopenic Purpura?

A

Destruction of platelets by antiplatelet IgG autoantibodies

32
Q

Clinical features of Immune Thrombocytopenic Purpura?

A
  • 2-10 years of age
  • 1-2 weeks post viral illness
  • Petechiae, purpura and/or superficial bruising
  • Epistaxis and mucosal bleeding but profuse bleeding is rare
  • Intracranial bleeding serious but rare
33
Q

How is Immune Thrombocytopenic Purpura diagnosed

A

• Clinical history, examination, blood film to exclude sinister diagnosis,
other lab findings
• Atypical features – bone marrow examination to exclude leukaemia

34
Q

Management of Immune Thrombocytopenic Purpura

A
  • Mostly self limiting (80%) within 6-8 weeks
  • Treatment is controversial
  • If major (GI or intracranial) or persistent minor bleeding
  • Oral steroids
  • Immunoglobulins
  • Platelet transfusions only for life threatening haemorrhage (effect lasts only few hours)

MK SR INDEX CASES CHILD HEALTH (24 decks)

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