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Haemoglobinopathies

Key points


Normal adult Hb (HbA) has 2 copies of α & β globin genes - chains

HbA2 - small amounts has 2 copies of α & δ globin genes - chains

Foetal Hb (HbF) has 2 copies of α & γ globin genes - chains

Gamma γ

Delta δ


Sickle cell disease


Sickle cell: 2 substitutions in β globin gene (chromosome 11) = HbS

Autosomal recessive

Heterozygous mutation - 'Sickle cell trait'

Homozygous mutation - moderate to severe phenotype with crises


10-15,000 in UK

1:365 black population

1: 16,000 hispanic population


Chronic haemolytic anaemia


Sickle crisis:

Abdominal manifestations

Mesenteric ischaemia

Cholelithiasis

Splenic infarct - wedge shaped infiltrate - conservative management

Splenic sequestration - Acute LUQ pain, splenomegaly, drop of >20 Hb


Other complications:

Stroke

Lung infarct

Obstructive sleep apnoea due to adenotonsillar hypertrophy - from compensatory asplenia and chronic infection

Priapism

Avascular necrosis of hip + shoulder, bone pain

Renal papillary necrosis

Renal medullary carcinoma

Rhabdomyolysis


Management

Sickle cell trait: Adequate hydration, avoid extremes of temperature and hypoxia

With abdominal pain, give IV fluids and oxygen 97% of crises should resolve in 48 hours. If it does not, consider surgical pathology

Pre-operative simple transfusion is as effective as exchange transfusions

Hydroxyurea - increases HbF, prevents sickling through multiple mechanisms


Splenic infarct - wedge shaped infiltrate - conservative management

Splenic sequestration - conservative, transfuse, or splenectomy - unclear which is optimal

Splenic abscess - percutaneous aspiration. Splenectomy if not possible


Hereditary Spherocytosis


Defect in red blood cell membrane proteins

In Europeans - combined Spectrin and Ankyrin deficiency

75% autosomal dominant

25% recessive forms and de novo mutations


Isolated beta-spectrin defects 15-30% - mild or moderate - autosomal dominant and do not require transfusion

Isolated alpha-spectrin defects 5% - usually severe, autosomal recessive


30% mild disease

70% moderate to severe

Neonates may drop Hb in first few weeks of life

Jaundice, haemolytic anaemia, splenomegaly


British Society for Haematology guidelines:

Grading Mild, Moderate, Severe

Based on Hb, Reticulocytes, Spectrin count, Bilirubin

Direct antiglobulin test to differentiate from autoimmune causes

Blood film - spherocytes


Management

Folate supplementation

Mild - Do not perform splenectomy in childhood

Moderate - Consider splenectomy based on symptoms

Severe - Perform splenectomy in childhood

Splenectomy around age 7, if either symptomatic, or before spleen too large - Splenectomy usually curative of anaemia and hyperbilirubinaemia

Cholecystectomy if symptomatic gallstones

Unclear evidence for benefit of cholecystectomy in asymptomatic gallstones, however cholecystectomy in childhood is risk of colonic cancer in later life

If doing partial splenectomy - can take 70-90% to preserve immune function

Can be complicated by parvovirus infection


 

Page edited by Mrs Charnjit Seehra BSc November 2024

 

References


Holcomb and Ashcraft’s Pediatric Surgery, 7th edition, 2020, Chapter 5


https://patient.info/doctor/sickle-cell-disease-and-sickle-cell-anaemia-pro


https://patient.info/doctor/thalassaemia-pro


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Please note that all information on this site is for professional educational purposes only, it does not constitute medical advice

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