Haematology Data Interpretation

Microcytic (MCV 68 fL), hypochromic (MCH 21 pg) anaemia. The iron studies confirm iron deficiency: low ferritin (most sensitive marker of iron stores), low serum iron, raised TIBC (the body upregulates transferrin to maximise iron capture), and low transferrin saturation. The reactive thrombocytosis is a common finding in IDA and usually resolves with treatment.

• Heavy menstrual loss (menorrhagia) — the most common cause of IDA in premenopausal women. Quantify blood loss with menstrual history; refer to gynaecology if significant.
• Dietary deficiency — vegetarian diet; haem iron from meat is far more bioavailable than non-haem iron. Review diet; consider dietitian referral.

Also consider GI blood loss (even in young women) — ask about GI symptoms; consider coeliac screen (anti-tTG IgA) as this can impair iron absorption. Urine dipstick for haematuria.

Oral ferrous sulfate 200 mg TDS (or ferrous fumarate/gluconate if intolerant). Take on an empty stomach or with vitamin C to maximise absorption; avoid calcium, tea and antacids around dosing. Treat the underlying cause. Recheck FBC after 4 weeks — expect Hb to rise by ~10–20 g/L/month. Continue iron for 3 months after Hb normalises to replenish stores. IV iron (e.g. ferric carboxymaltose) if oral iron is not tolerated or absorbed.

The combination of a markedly raised WBC with a full spectrum of granulocytes on the film (left shift), prominent basophilia (a hallmark of CML), thrombocytosis, splenomegaly and constitutional symptoms in a middle-aged man is classic for CML. The raised LDH and uric acid reflect high cell turnover.

The Philadelphia chromosome — a reciprocal translocation between chromosomes 9 and 22, t(9;22)(q34;q11). This creates the BCR-ABL1 fusion gene, which encodes a constitutively active tyrosine kinase driving uncontrolled myeloid proliferation. Detected by:

• FISH (fluorescence in situ hybridisation) on bone marrow or blood
• RT-PCR for BCR-ABL1 transcript (also used to monitor response to treatment)
• Conventional cytogenetics (bone marrow)

Imatinib (Gleevec/Glivec) — a BCR-ABL1 tyrosine kinase inhibitor (TKI), taken orally. It was a landmark treatment; CML went from a disease requiring bone marrow transplant to one managed with a daily tablet. Second-generation TKIs (dasatinib, nilotinib) are now often first-line in younger patients or high-risk disease. Treatment is typically lifelong unless deep molecular remission is sustained. Regular BCR-ABL1 PCR monitoring guides treatment decisions.

DIC is a consumptive coagulopathy. The underlying trigger (here: placental abruption releasing tissue factor into the maternal circulation) activates the coagulation cascade systemically. This simultaneously causes:

• Widespread microvascular thrombosis — fibrin clots consume platelets and coagulation factors, causing organ ischaemia
• Consumptive coagulopathy — depleted platelets, fibrinogen and factors II, V and VIII → prolonged PT and APTT
• Secondary fibrinolysis — fibrin is broken down, releasing D-dimers (markedly elevated)
• Microangiopathic haemolytic anaemia (MAHA) — red cells are sheared by fibrin strands → schistocytes on film, raised LDH and bilirubin

1. Thrombocytopenia (platelets consumed in clots)
2. Prolonged PT and APTT (clotting factors consumed)
3. Very low fibrinogen (consumed and not replaced fast enough)
4. Markedly elevated D-dimer (fibrin degradation products from secondary fibrinolysis)

Schistocytes on film confirm MAHA, supporting the diagnosis.

Treat the underlying cause — control haemorrhage (surgical if needed), deliver placenta if retained. Simultaneously:

• Blood products: FFP (replaces all coagulation factors) · Cryoprecipitate (concentrated fibrinogen — target fibrinogen >1.5 g/L) · Platelet transfusion (target >50 × 10⁹/L if actively bleeding) · Packed red cells (target Hb >80 g/L)
• Tranexamic acid — antifibrinolytic; evidence in post-partum haemorrhage (WOMAN trial) if given within 3 hours
• Activate major haemorrhage protocol; involve haematology, obstetrics, anaesthetics and ITU
• Monitor with repeated coagulation studies, VHA (TEG/ROTEM) if available

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive enzyme deficiency causing impaired protection against oxidative stress. In normal red cells, G6PD generates NADPH which maintains glutathione in its reduced form, neutralising reactive oxygen species. Without adequate G6PD, oxidative stress (triggered here by primaquine) causes:

• Oxidation of haemoglobin → denatured Heinz bodies form and attach to the cell membrane
• Splenic macrophages "bite" out Heinz bodies → bite cells (degmacytes)
• Intra- and extravascular haemolysis → haemoglobinaemia, haemoglobinuria (dark urine), unconjugated hyperbilirubinaemia (jaundice)

The negative Coombs test distinguishes this from autoimmune haemolytic anaemia. Schistocytes are absent (no TMA).

• Drugs: primaquine, dapsone, rasburicase, nitrofurantoin, some sulfonamides
• Infection: most common trigger overall — oxidative stress from illness
• Foods: fava beans (broad beans) — "favism"
• Other: napthalene (mothballs), methylene blue, high-dose aspirin, metabolic acidosis

Diagnosis: G6PD enzyme assay (quantitative spectrophotometric assay). Important caveat — a falsely normal result can occur during an acute crisis because reticulocytes have higher G6PD activity; retest when the patient has recovered. Genetic testing for known variants (>200 described).

Acute management:

• Stop the offending drug (primaquine) immediately
• Supportive care: IV fluids (prevent acute kidney injury from haemoglobin precipitation in tubules)
• Transfuse packed red cells if Hb is critically low or patient is symptomatic (Hb 74 g/L here — likely requires transfusion)
• Monitor renal function, urine output, and repeat FBC
• Most crises are self-limiting once the trigger is removed
• Patient education: provide a list of drugs and foods to avoid lifelong