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Approach to Diagnosi s of Haemolytic Anaemias
History Taking
Family History – Hereditary conditions
Ethnic Origin – G6PD common in Mediterranean & Chinese populations
Past History – NNJ indicative of Congenital conditions (eg. HS, G6PD Def.)
(NNJ – NeoNatal Jaundice)(HS – Hereditary Spherocytosis)
Triggering Events – History of Drugs, Infections
Clinical
Pallor of mucous membranes
Mild fluctuating Jaundice
Splenomegaly in Chronic Haemolysis
Dark Urine
Pigment Gall Stones
Ulcers around ankle
Aplastic Crisis – complicate viral infections
Growth Retardation
Hypertrophic skeletal changes
Lymphadenopathy/ Hepatosplenomegaly – lymphoproliferative disorder,
malignancy
Aplastic Crisis
Acute Arrest of Erythropoiesis
Following Parvovirus Infection
Chronic Haemolytic Disorders (common )
Growth Retardation & Delayed Puberty
Severe Congenital Haemolytic Disorders (Homozygous β Thalassaemia) Site of Defect
Hypertrophic Skeletal Changes Skeletal Changes Intrinsic (Intracorpus cular) Extrinsic (Extracorpuscular)
Expansion of Erythropoietic Marrow β Thalassaemia Structural, Functional Defect within Abnormality in Red Cell
Congenital Haemolytic Disorders Only the Red Cell Environment
Prominent Inherited/ Acquired
Frontal Bone Inherited (Hereditary) Acquired
Maxillary Bone Caused by Intrinsic Defect Caused by Extrinsic Defect
Membrane Defects Immune
(eg. Hereditary Spherocytosis) (Autoimmune – AIHA)
(Alloimmune – HDA, HTR, Drugs)
Metabolic Defect Red cell Fragmentation Syndromes
(eg. G6PD Deficiency) March Haemoglobinuria
Haemoglobin Defects Infections
(Qualitative – Sickle Cell) Chemical, Physical Agents
(Quantitative – Thalassaemia) PNH
Exception Exception
Severe Hereditary G6PD Deficiency Paroxysmal Nocturnal
(Presence of E xtrinsic Trigger – Haemoglobinuria (PNH)
AntiMalarial Drug for Intrinsic (Acquired Intrinsic Defect)
Defect to manifest)
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Laboratory Findings
↑ Red Cell Breakdown ↑ Red Cell Production Damaged Red Cell
↑ Serum Bilirubin (Unconjugated) Reticulocytosis Morphology
↑ Urine Urobilinogen BM Erythroid Hyperplasia Microspherocytes, Elliptocytes, Fragments
↑ Faecal Stercobilinogen Special Tests
↑ LDH In absence of concomitant BM Disease, a brisk Osmotic Fragility, Autohaemolysis
Serum Haptoglobin Absent reticulocytosis should be observed within 3-5 days Red Cell Survival Shortened
after a decline in Hb 51Cr Labelling with study of sites of destruction
Polychromatic cell
(Red cell with Blue staining) Haemolytic Anaemia
Reticulocyte (appears in the usual stain) Fragmented cells, Bitten Cells
Signs of Damaged cells occurring in Haemolysis
Cold AIHA
Red cell clumping (agglutination)