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Cover
Title Page
Preface
Abbreviations
CHAPTER 1: The Blood Film and Count
1. Blood
2. The blood film
3. The blood count
4. Normal ranges
5. How to examine a blood film
CHAPTER 2: Assessing Red Cells
1. Assessing red cell number and distribution (anaemia, polycythaemia, rouleaux formation, red cell agglutination)
2. Assessing red cell size (microcytosis, macrocytosis, anisocytosis)
3. Assessing red cell shape (poikilocytosis)
4. Assessing red cell colour (hypochromia, hyperchromia, anisochromasia, polychromasia)
5. Detecting red cell inclusions (Pappenheimer bodies, basophilic stippling, Howell–Jolly bodies)
6. The full blood count in red cell assessment
CHAPTER 3: Assessing White Cells and Platelets
1. Assessing white cell and platelet numbers
2. Assessing neutrophil morphology
3. Assessing lymphocyte morphology
4. Assessing morphology of monocytes, eosinophils and basophils
5. Assessing platelet morphology
CHAPTER 4: Haematological Findings in Health and Disease
1. The blood film and count in healthy individuals
2. Abnormalities of red cells
3. Abnormalities of white cells
CHAPTER 5: Emergency Morphology: The Relevance of the Full Blood Count and Blood Film in Acute Illness
1. Thrombocytopenia
2. Thrombotic microangiopathy and microangiopathic haemolytic anaemia
3. Other acute anaemia
4. Kidney injury and disease
5. Acute hepatic damage and liver failure
6. Acute leukaemia
7. Bacterial infection and other causes of leucocytosis
8. Eosinophilia
9. Lymphocytosis
10. Malaria
11. Neutropenia
12. Pancytopenia and leucoerythroblastic blood films
13. Neonatal emergencies
CHAPTER 6: Self‐assessment
Index
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List of Tables

Chapter 01
1. Table 1.1 The functions of leucocytes.
2. Table 1.2 Normal ranges for healthy Caucasian adults.
3. Table 1.3 Normal ranges for Afro‐Caribbean and Africans for those haematological variables where the ranges differ from those of Caucasians.
4. Table 1.4 Approximate 95% ranges for red cell variables and for automated total and differential* white cell counts for Caucasian infants and children.
Chapter 02
1. Table 2.1 Definitions of cells by shape.
Chapter 03
1. Table 3.1 Terminology used for abnormalities of white cell and platelet numbers.
Chapter 04
1. Table 4.1 Some important causes of polycythaemia, classified according to mechanism.
2. Table 4.2 Some important causes of anaemia, classified according to mechanism.
3. Table 4.3 Some causes of anaemia with microcytic, normocytic or macrocytic red cells.
4. Table 4.4 Some important causes of neutrophil leucocytosis.
5. Table 4.5 Some important causes of lymphocytosis.
6. Table 4.6 Simplified French–American–British (FAB) classification of acute myeloid leukaemia.

List of Illustrations

Chapter 01
1. Fig. 1.1 Diagram of a tube of anticoagulated blood that has been allowed to sediment, showing the separation of blood into red cells, a buffy coat (white cells and platelets) and plasma.
2. Fig. 1.2 A diagram of a red cell viewed from above and in cross‐section.
3. Fig. 1.3 Normal red cells (erythrocytes) showing little variation in size and shape, an approximately round outline and a small area of central pallor in some of the cells. The small structures containing lilac‐staining granules between the red cells are platelets.
4. Fig. 1.4 A diagram showing how white cells are classified.
5. Fig. 1.5 A normal neutrophil with a bilobed nucleus and cytoplasm containing delicate lilac‐staining granules. The other nucleated cell is a small lymphocyte.
6. Fig. 1.6 A normal neutrophil from a female showing a nucleus with four lobes and a ‘drumstick’.
7. Fig. 1.7 A normal bilobed eosinophil. The granules are reddish‐orange and pack the cytoplasm.
8. Fig. 1.8 A normal basophil. The nucleus has three lobes. The cytoplasm is packed with large purple granules. The other nucleated cell is a large lymphocyte.
9. Fig. 1.9 A large lymphocyte with a less densely staining nucleus than occurs in a small lymphocyte and more plentiful pale blue cytoplasm. A nucleolus is apparent, top left in the nucleus.
10. Fig. 1.10 A large granular lymphocyte showing a moderate number of prominent azurophilic granules in clear cytoplasm.
11. Fig. 1.11 A monocyte, showing a lobulated nucleus and voluminous, opaque cytoplasm containing very fine azurophilic granules. Several platelets are also visible. (Monocytes should not be confused with large granular lymphocytes. Lymphocytes have clear, pale blue cytoplasm and discrete, sometimes prominent granules whereas monocytes usually have more opaque, grey‐blue cytoplasm with very fine granules.)
12. Fig. 1.12 A diagram showing the relationship of haemopoietic precursors to each other and to the end cells into which they differentiate. Proliferation of cells occurs simultaneously with maturation or differentiation so that one myeloblast is likely to give rise to 16 mature granulocytes and one proerythroblast to 16 red cells. Myeloblasts, promyelocytes and myelocytes are all cells capable of cell division, or mitosis. Metamyelocytes and all later cells are non‐dividing cells. All red cell precursors, with the exception of late erythroblasts, are dividing cells. Myeloblasts differentiate not only into neutrophils, as shown in the diagram, but also into eosinophils and basophils.
13. Fig. 1.13 A blood film of a patient with a myelodysplastic syndrome showing a myeloblast and a neutrophil. The myeloblast has a high nucleocytoplasmic ratio, a diffuse chromatin pattern and a single nucleolus. The neutrophil is hypogranular.
14. Fig. 1.14 A promyelocyte showing a lower nucleocytoplasmic ratio than that of a myeloblast, an eccentric nucleus, azurophilic granules and a Golgi zone to the left of the nucleus.
15. Fig. 1.15 A neutrophil myelocyte showing a smaller cell than a promyelocyte with some condensation of nuclear chromatin and no visible nucleolus. On microscopic examination myelocytes can be recognized as precursors of neutrophils, eosinophils or basophils on the basis of the staining characteristics of the granules they contain.
16. Fig. 1.16 A neutrophil metamyelocyte between two segmented neutrophils. The nucleus is indented.
17. Fig. 1.17 A neutrophil band form (left) compared with a segmented neutrophil (right).
18. Fig. 1.18 A nucleated red blood cell (NRBC) in a patient with haemolytic anaemia showing a small round nucleus with condensed chromatin and cytoplasm that is bluish‐pink because of the presence of both ribosomes, responsible for the blue tinge, and haemoglobin, responsible for the pink tinge.
19. Fig. 1.19 Smoothed histograms showing (a) the normal distribution of haemoglobin concentration (Hb) and (b) the log normal distribution of the white cell count (WBC).
20. Fig. 1.20 Storage artefact. The red cells are crenated and one neutrophil (top left) has a nucleus that has become round, dense and homogeneous. A second neutrophil has retained its form but a third leucocyte (right) has a fuzzy outline and has disintegrated to the extent that its lineage cannot be recognized with certainty. (Compare the degenerating neutrophil, top left, with the nucleated red cell shown in Fig. 1.18.)
21. Fig. 1.21 A platelet aggregate containing a mixture of intact and degranulated platelets.
22. Fig. 1.22 Fibrin strands passing between and over red cells.
23. Fig. 1.23 Platelet satellitism.
Chapter 02
1. Fig. 2.1 Anaemia (caused by iron deficiency).
2. Fig. 2.2 Normal distribution of red cells in a healthy subject with normal Hb.
3. Fig. 2.3 Polycythaemia. Red cells appear ‘packed’ together.
4. Fig. 2.4 Rouleaux.
5. Fig. 2.5 Red cell agglutinates.
6. Fig. 2.6 Severe anisocytosis; the MCV was 133 fl but the macrocytosis is not uniform.
7. Fig. 2.7 Microcytic red cells (MCV 62 fl).
8. Fig. 2.8 Normocytic red cells.
9. Fig. 2.9 Macrocytic red cells (MCV 105 fl).
10. Fig. 2.10 Severe poikilocytosis; cells vary considerably in shape but no single shape dominates. (This was a case of transient severe poikilocytosis in the neonatal period in a baby with hereditary elliptocytosis.)
11. Fig. 2.11 Diagrammatic representation of different types of poikilocyte.
12. Fig. 2.12 Moderate numbers of spherocytes (in hereditary spherocytosis).
13. Fig. 2.13 Several irregularly contracted cells (in haemoglobin C disease). The majority of the other cells are target cells.
14. Fig. 2.14 Numerous elliptocytes and ovalocytes (in hereditary elliptocytosis).
15. Fig. 2.15 Several dacrocytes (tear‐drop poikilocytes) (in primary myelofibrosis).
16. Fig. 2.16 Numerous stomatocytes (in hereditary stomatocytosis).
17. Fig. 2.17 Several keratocytes (in microangiopathic haemolytic anaemia); keratocytes are sometimes called ‘bite cells’ because they look as if a bite has been taken from them.
18. Fig. 2.18 Several schistocytes (red cell fragments) including a microspherocyte (in haemolytic uraemic syndrome).
19. Fig. 2.19 Echinocytes (crenated cells) (in chronic renal failure).
20. Fig. 2.20 Acanthocytes (in abetalipoproteinaemia).
21. Fig. 2.21 One sickle cell and several boat‐shaped cells (in sickle cell anaemia).
22. Fig. 2.22 SC poikilocytes (in sickle cell/haemoglobin C disease).
23. Fig. 2.23 A population of severely hypochromic cells with only a thin rim of haemoglobinized cytoplasm (in refractory anaemia with ring sideroblasts); there are other cells that stain normally and the film is therefore described as dimorphic. In addition one cell, just left of centre, has small basophilic inclusions, known as Pappenheimer bodies, towards the periphery of the cell.
24. Fig. 2.24 Normochromic cells (in a healthy subject).
25. Fig. 2.25 Hyperchromic cells (which in this case are microspherocytes in a severely burned patient; spherocytes and irregularly contracted cells are also hyperchromic).
26. Fig. 2.26 A polychromatic macrocyte.
27. Fig. 2.27 Numerous cells showing basophilic stippling (in lead poisoning). Punctate basophilia is an alternative term used to describe this abnormality.
28. Fig. 2.28 A cell containing a Howell–Jolly body in a patient who has had a splenectomy. There are also several target cells.
Chapter 03
1. Fig. 3.1 Leucocytosis.
2. Fig. 3.2 Thrombocytopenia (in Wiskott–Aldrich syndrome). There are only two platelets in the film. The platelets are also abnormally small, although their staining characteristics are normal.
3. Fig. 3.3 Thrombocytosis (in chronic myeloid leukaemia). The platelets also show increased variation in size and some are agranular.
4. Fig. 3.4 Toxic granulation, vacuolation and left shift (the two white cells are band forms).
5. Fig. 3.5 A neutrophil containing a Döhle body, a small blue‐grey cytoplasmic inclusion, which can be seen just below the nucleus.
6. Fig. 3.6 A neutrophil with two very round lobes in a patient with the congenital Pelger–Huët anomaly.
7. Fig. 3.7 A hypersegmented neutrophil in a patient with megaloblastic anaemia. The neutrophil nucleus has seven lobes.
8. Fig. 3.8 A macropolycyte compared with a normal neutrophil. The macropolycyte is twice as large as the normal neutrophil and has a nucleus with seven or eight lobes, which is also twice as large as a normal neutrophil nucleus.
9. Fig. 3.9 Atypical lymphocytes (in infectious mononucleosis).
10. Fig. 3.10 A plasma cell (occurring as a reactive change in a patient with infection). The chromatin is clumped and a Golgi zone is apparent below the nucleus.
11. Fig. 3.11 Eosinophil leucocytosis with one of the three eosinophils being markedly hypogranular.
Chapter 04
1. Fig. 4.1 Megaloblastic anaemia showing macrocytosis and a circulating megaloblast.
2. Fig. 4.2 Iron deficiency anaemia showing anisocytosis, anisochromasia and the presence of poikilocytes including elliptocytes (pencil cells).
3. Fig. 4.3 Anaemia of chronic disease showing microcytosis, hypochromia and anisochromasia.
4. Fig. 4.4 Beta thalassaemia trait showing microcytosis, hypochromia and poikilocytosis. The poikilocytes include target cells and several irregularly contracted cells.
5. Fig. 4.5 Haemoglobin H disease showing moderate hypochromia and marked microcytosis, anisocytosis and poikilocytosis.
6. Fig. 4.6 Spherocytes, spheroacanthocytes and red cells containing Pappenheimer bodies following splenectomy for hereditary spherocytosis.
7. Fig. 4.7 Blood film during an acute haemolytic episode in glucose‐6‐phosphate dehydrogenase (G6PD) deficiency showing anaemia, irregularly contracted cells (some with protrusions) and a hemighost.
8. Fig. 4.8 Warm autoimmune haemolytic anaemia showing anaemia, spherocytosis and several polychromatic macrocytes.
9. Fig. 4.9 Dimorphic blood film in a patient with beta thalassaemia major who was being transfused. The transfused red cells appear normal whereas the patient’s red cells show hypochromia, anisocytosis, poikilocytosis and Pappenheimer bodies. One hypochromic cell (bottom right) contains an alpha chain precipitate. There are three NRBCs, which show cytoplasmic defects consequent on the failure of haemoglobin synthesis.
10. Fig. 4.10 Blood film in acute bacterial infection showing neutrophil leucocytosis, toxic granulation and vacuolation.
11. Fig. 4.11 Chronic myeloid leukaemia showing three basophils, an eosinophil myelocyte and mature and immature cells of neutrophil lineage.
12. Fig. 4.12 Chronic lymphocytic leukaemia, showing lymphocytosis with an increase of mature small lymphocytes. There are two smear cells.
13. Fig. 4.13 Prolymphocytic leukaemia (B‐lineage) showing three prolymphocytes. These cells are larger than the cells of chronic lymphocytic leukaemia and have large, prominent nucleoli.
14. Fig. 4.14 Cleft lymphocyte in follicular lymphoma.
15. Fig. 4.15 Two hairy cells in hairy cell leukaemia.
16. Fig. 4.16 Acute lymphoblastic leukaemia. There is one NRBC; all the other cells are lymphoblasts.
17. Fig. 4.17 Acute lymphoblastic leukaemia with less typical cytology.
18. Fig. 4.18 Acute myeloid leukaemia of M1 subtype showing six myeloblasts and a lymphocyte. The blast cell adjacent to the lymphocyte contains an Auer rod.
19. Fig. 4.19 Acute myeloid leukaemia of M2 subtype showing two promyelocytes.
20. Fig. 4.20 Acute myeloid leukaemia of M4 subtype showing a myeloblast (left) and two promonocytes (right).
21. Fig. 4.21 Acute myeloid leukaemia of M3 subtype showing hypergranular promyelocytes, one of which contains a giant granule.
22. Fig. 4.22 Acute myeloid leukaemia of M3 variant subtype showing the characteristic bilobed hypogranular promyelocytes.
Chapter 05
1. Fig. 5.1 Blood film showing satellitism. In this case the neutrophils are bound together by the adherent platelets.
2. Fig. 5.2 Blood film of a patient with HELLP syndrome showing keratocytes and small angular schistocytes.
3. Fig. 5.3 Autoimmune haemolytic anaemia, showing spherocytes, polychromatic macrocytes and one Howell–Jolly body.
4. Fig. 5.4 Hereditary spherocytosis complicated by megaloblastic anaemia. Note that in addition to spherocytes there are oval macrocytes and a circulating megaloblast.
5. Fig. 5.5 Hereditary spherocytosis complicated by pigment gallstones (formed as a result of the chronic haemolysis) leading to acute cholecystitis. As a result of the acute inflammation, there are now not only spherocytes but also a population of hypochromic microcytes; because of the short red cell life‐span these have rapidly become a significant proportion of red cells.
6. Fig. 5.6 Paroxysmal cold haemoglobinuria showing spherocytes, red cell agglutination and phagocytosis of an erythrocyte by a neutrophil. There is a second phagocytic vacuole representing an ingested erythrocyte that has already been destroyed.
7. Fig. 5.7 Acute copper‐induced haemolytic anaemia in Wilson’s disease with liver failure. There are polychromatic macrocytes, crenated cells and irregularly contracted cells, some of which have protruding Heinz bodies; there are also several spherocytes.
8. Fig. 5.8 Megaloblastic anaemia due to vitamin B₁₂ deficiency showing macrocytes, oval macrocytes, marked anisocytosis and poikilocytosis, and a hypersegmented neutrophil (six lobes).
9. Fig. 5.9 Increased rouleaux formation in multiple myeloma.
10. Fig. 5.10 Increased rouleaux formation and circulating myeloma cells in plasma cell leukaemia. Their lineage is recognized by the cytoplasmic basophilia and the paler Golgi zone adjacent to the nucleus.
11. Fig 5.11 Adult T‐cell leukaemia/lymphoma showing a circulating lymphoma cell with a flower‐shaped nucleus.
12. Fig. 5.12 Burkitt lymphoma cells showing strongly basophilic cytoplasm containing round vacuoles.
13. Fig. 5.13 Renal failure due to hepatitis C infection. The subtle abnormality shown is apparent as gaps in red cells, which are the effect of a non‐staining cryoglobulin deposit overlying the red cells. The nature of the deposit can be confirmed by chilling a serum sample and observing the precipitate that forms.
14. Fig. 5.14 Zieve’s syndrome showing irregularly contracted cells and polychromatic macrocytes.
15. Fig. 5.15 ‘Spur cell haemolytic anaemia’ in terminal liver failure, showing numerous acanthocytes.
16. Fig. 5.16 Microgranular variant of acute promyelocytic leukaemia: (a) bilobed cells; (b) two bilobed cells, one with fine granules and one containing three Auer rods, and a cell with more numerous fine granules. With thanks to Dr Mili Shah.
17. Fig. 5.17 Microgranular variant of acute promyelocytic leukaemia showing two typical bilobed cells and another lobated cell with numerous fine granules and plentiful Auer rods (a cell of this type is virtually diagnostic of acute promyelocytic leukaemia). With thanks to Dr Wenchee Siow.
18. Fig. 5.18 Meningococcal septicaemia showing meningococci within a neutrophil.
19. Fig. 5.19 Escherichia coli within a neutrophil of a hyposplenic patient.
20. Fig. 5.20 Campylobacter canimorsus within a neutrophil of a hyposplenic patient.
21. Fig. 5.21 Hyperleucocytosis in Ph‐positive BCR‐ABL1‐positive chronic myeloid leukaemia. Note the full spectrum of cells of neutrophil lineage, several basophils and an eosinophil and an eosinophil myelocyte.
22. Fig. 5.22 Microfilariae of Loa loa.
23. Fig. 5.23 An eosinophilic leukaemoid reaction to B‐lineage acute lymphoblastic leukaemia. There is a single leukaemic lymphoblast surrounded by six eosinophils.
24. Fig. 5.24 Chronic eosinophilic leukaemia showing two eosinophils and a myeloblast.
25. Fig. 5.25 Reactive eosinophilia in cutaneous T‐cell lymphoma showing an eosinophil and a lymphocyte with a cerebriform nucleus.
26. Fig. 5.26 Circulating neoplastic mast cell in a patient who also had eosinophilia and degranulation of eosinophils.
27. Fig. 5.27 Thin film in Plasmodium falciparum malaria showing numerous ring forms and an early gametocyte. Note the non‐enlarged red cells, the delicacy of the rings, some double chromatin dots and a cell containing two parasites.
28. Fig. 5.28 Thin film in Plasmodium vivax malaria showing a medium‐sized ring trophozoite and a large amoeboid trophozoite; the parasitized cells are enlarged and decolourized.
29. Fig. 5.29 Thin film in Plasmodium ovale malaria showing a large trophozoite in an enlarged, oval and decolourized red cell.
30. Fig. 5.30 Thin film in Plasmodium malariae malaria showing a band‐shaped trophozoite in a red cell that is not enlarged or decolourized.
31. Fig. 5.31 Thin film in Plasmodium knowlesi malaria showing band‐shaped trophozoites in red cells that are neither enlarged nor decolourized. The presence also of delicate rings and the usually heavy parasitaemia helps to make the distinction from P. malariae. P knowlesi is rarely seen outside the endemic area in Southeast Asia but can cause a serious illness. With thanks to Dr Janet Cox‐Singh.
32. Fig. 5.32 Acquired or pseudo‐Pelger–Huët anomaly; one neutrophil has a peanut‐shaped nucleus and the other is bilobed and also hypogranular. The anisocytosis and poikilocytosis are indicative of the dyserythropoiesis that was also present.
33. Fig. 5.33 Blast cells and a hypogranular neutrophil in a patient with a myelodysplastic syndrome.
34. Fig. 5.34 Primary myelofibrosis showing a neutrophil myelocyte, a nucleated red blood cell and tear‐drop poikilocytes.
35. Fig. 5.35 A circulating megakaryocyte in primary myelofibrosis.
Chapter 06
1. Fig. 6.1 Peripheral blood film (Exercise 5, Q1).
2. Fig. 6.2 Peripheral blood film (Exercise 5, Q2).
3. Fig. 6.3 Peripheral blood film (Exercise 5, Q3).
4. Fig. 6.4 Peripheral blood film (Exercise 5, Q6).
5. Fig. 6.5 Peripheral blood film (Exercise 5, Q8).