Haemolytic Anaemia

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Slide1

Haemolytic Anaemia

Elliot Catchpole

PCMD

Slide2

Recap

Mean Cell Volume = The size of each RBC

Microcytic<76

Normocytic76-96

MACROCYTIC>96

-IRON deficiency

Thalassaemias

Sideroblastic

Chronic Disease

Haemolysis

B12

and Folate

-Alcohol-Liver Disease-MYLODYSPLASIA

Megaloblastic

Non-

Megaloblastic

-G6PD Deficiency

-Hereditary

spherocytosis

-Paroxysmal Nocturnal Haemoglobinurea

-Autoimmune Haemolysis

-Sickle Cell

Slide3

What is haemolysis?

Slide4

Haemoglobin Cycle

Haem

Iron

Bilirubin

Blood

ALBUMIN

Bilirubin

Haem

SPLEEN

LIVER

‘

Unconjugated

/indirect’

(destruction)

Bilirubin

‘Conjugated/direct’

CONJUGATION!!!

Water solubility

K

Bilirubin

GI

Urobilinogen

Slide5

Haemolysis

Haemolysis

MCV

= Normal/raised

Generally ACUTE

Indirect Bilirubin

Haptoglobin

(Intravascular)

LDH

Reticulocyte

?Dark urine?

?Jaundice?

Gallstone risk

Slide6

Sickle Cell

CAUSES: SCD = homozygote, Trait = heterozygote*PRESENTATION* - Trait = only haematuria in normal circumstancesSCD = PAIN Parvovirus B19 = HCT drops precipitouslyINVESTIGATIONS – Blood smear – best initialShows Sickled cells for SCD, nothing for trait - Hb electrophoresisTREATMENT – Pain = Supportive (O2, fluids, pain meds) Fever/infection = above + antibiotics Parvovirus = Transfusion/Ig for virus CNS = give exchange transfusion Prophylaxis = Folate + HydroxyureaCOMPLICATIONS - GallstonesOcclusion problems = leg ulcers, osteomyelitis, CNS complications (stroke, visual disturbance)

Intravascular

Slide7

Autoimmune Haemolysis

CAUSES: Autoimmune – PHx of autoimmune conditions, medications (penicillin, quinidine)*PRESENTATION*Warm = chronic haemolysis (extravascular)Cold = in the cold (<4*) (intravascular)INVESTIGATIONS – COOMBS TEST based on the 2 risks (autoimmune Hx and medications)TREATMENT – Steroids  stop  Recurs? More steroids  stop  Constant recurrence?  SPLENECTOMY

Either

Slide8

Hereditary Spherocytosis

CAUSES: Autosomal dominant RBC membrane defect.*PRESENTATION* - Young – extravascular – splenomegaly, jaundiceINVESTIGATIONS – Osmotic fragility test – cells will burstTREATMENT – Splenectomy

Extravascular

Slide9

PNH (Paroxysmal Nocturnal Haemoglobinurea)

CAUSE: Genetic defect in creating DAF/CD55 *PRESENTATION* - Dark urine IN MORNING (haemolysis at night)INVESTIGATIONS – Test for DAF/CD55TREATMENT + Steroids + Anticoagulation (prevent thrombosis) + SCT (stem cell transplant, curative)COMPLICATIONS – Large vessel thrombosis (so give anticoagulants) - Associated with Leukaemia and Aplastic Anaemia

Intra.

Slide10

G6PD deficiency

CAUSES: X-linked recessive – defective G6PD enzyme*PRESENTATION* - Oxidising crisis (jaundice + anaemia) on oxidising stressors (e.g. Henna, infection)INVESTIGATIONS – G6PD levels >8weeks ‘Heinz Body’ smear Exclude other causesTREATMENT – Avoid stressors

Intravascular

Slide11

Questions

A patient comes to the ED with sudden onset of fatigue and SOB. The HCT is 20 and the MCV is slightly elevated. The

reticulocyte

count, LDH, and indirect

bilirubin

are all elevated, with a low

haptoglobin

.

1) History SLE and Lymphoma

2) Recurrent episodes with a large spleen, with a European family history

3) Sudden onset of haemolysis in a male with acute infection. A similar reaction occurs when certain medications are used.

Slide12

Questions

An African American man comes into the ED with back, chest and thigh pain. He has a history of sickle-cell disease. He has a temperature of 38.5C. CXR and urinalysis are normal. Oxygen, fluids and analgesics are started. His HCT is 28.

1) What is the most urgent step at this time?

2) How would you confirm a Parvovirus infection?

3) How would you treat this?

Slide13

Slide14

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