[Haematology] Atlas of Erythrocyte and Thrombocyte Abnormalities

1. Iron Deficiency Anemia Fig. 1a. 

1. Iron Deficiency Anemia

Fig. 1a. 

Fig. 1b.

a and b Erythrocyte morphology in iron deficiency anemia: ring-shaped erythrocytes (1), microcytes (2) faintly visible target cells (3), and a lymphocyte (4) for size comparison. Normal-sized erythrocytes (5) after transfusion.

Fig. 1c. Bone marrow cytology in iron deficiency anemia shows only
increased hematopoiesis and left shift to basophilic erythroblasts (1).

Fig. 1d. Absence of iron deposits after iron staining
(Prussian blue reaction). Megakaryocyte (1).

2. Hypochromic Infectious or Toxic Anemia (Secondary Anemia)

Fig. 2a.

Fig. 2b.

a and b Erythrocyte morphology in secondary hypochromic anemia: the erythrocytes vary greatly in size (anisocytosis) and shape (1) (poikilocytosis), and show basophilic stippling (2). Burr cell (3), which has no specific diagnostic significance. Occasionally, the erythrocytes stain a soft gray–blue (4) (polychromasia).

Fig. 2c. Bone marrow cell overview in secondary anemia. Cell counts in the white cell series are elevated (promyelocytes = 1), eosinophils (2), and plasma cells (3); erythropoiesis is reduced (4).

3. Thalassemias

Fig. 3a. Thalassemia minor: often no target cells, but an increase in the number of small erythrocytes (shown here in comparison with a lymphocyte), so that sometimes there is no anemia.

Fig. 3b. More advanced thalassemia minor: strong anisocytosis and poikilocytosis (1), basophilic stippling (2), and sporadic target cells (3).

Fig. 3c. Thalassemia major: erythroblasts (1), target cell (2), polychromatic erythrocytes (3), and Howell–Jolly bodies (4) (in a case of functional asplenia). Lymphocyte (5) and granulocyte (6).

4. Normochromic Hemolytic Anemias

Fig. 4a.

Fig. 4b.

a and b Newly formed erythrocytes appear as large, polychromatic erythrocytes (1) after Pappenheim staining (a); supravital staining (b) reveals spot-like precipitates (reticulocyte = 2). Thrombocyte (3).

Fig. 4c. Bone marrow cells in hemolytic anemia at low magnification: increased hematopoiesis with cell clusters. Orthochromatic erythroblasts predominate. A basophilic erythroblast shows loosened nuclear structure (arrow), a sign of secondary folic acid deficiency.

5. Autoagglutination and fragmentocytes

Fig. 5a. Clumps of erythrocytes. If this is the picture in all regions of the smear, an artifact is unlikely and serogenic (auto) agglutination should be suspected (in this case due to cryoagglutinins in mycoplasmic pneumonia). Thrombocytes are found between the agglutinated erythrocytes.

Fig. 5b.

Fig. 5c.

b and c Conspicuous half-moon and egg-shell-shaped erythrocytes: fragmentocytosis in microangiopathic hemolytic anemia. Fragmentocytes (1), target cell (2), 
and echinocytes (3) (this last has no diagnostic relevance).

6. Cytomorphological Anemias with Erythrocyte Anomalies

Fig. 6a. Microspherocytes and sickle cells. All erythrocytes are strikingly small in comparison with lymphocytes (1) and lack a lighter center: these are microspherocytes (diameter 6 µm). Polychromatic erythrocyte (2).

Fig. 6b. Erythrocytes with an elongated rather than round lighter center: these are stomatocytes, which are rarely the cause of anemia.

Fig. 6c. Native sickle cells (1) are found only in homozygous sickle cell anemia, otherwise only target cells (2) are present.

Fig. 6d. Sickle cell test under reduced oxygen tension: almost all erythrocytes appear as sickle cells in the homozygous case presented here.

7. Bone Marrow Aplasia

Fig. 7a. Bone marrow cytology in erythroblastopenia: only activated cells of the granulopoietic series are present. The megakaryopoiesis (not shown here) show no abnormalities.

Fig. 7b. Bone marrow aplasia: hematopoiesis is completely absent: only
adipocytes and stroma cells are seen.

Fig. 7c. Giant erythroblast (arrow) in the bone marrow in acute parvovirus B19 infection.

Fig. 7d. Conspicuous binuclear erythroblasts in the bone marrow of a patient with congenital dyserythropoietic anemia (type II CDA).

8. Bone marrow carcinosis

Fig. 8a.

Fig. 8b.

a and b Bone marrow smear at low magnification showing islands of infiltration by a homogeneous cell type (a), or, alternatively, by apparently different cell types which do, however, all display identical chromatin structure and cytoplasm: bone marrow carcinosis in breast carcinoma (a) or bronchial non-small-cell carcinoma (b).

Fig. 8c. Island of dedifferentiated cells in the bone marrow which cannot be assigned to any of the hematopoietic lineages: bone marrow carcinosis (here in a case of embryonal testicular cancer).

9. Hyperchromic Anemias

Fig. 9a. Marked anisocytosis. In addition to normal- sized erythrocytes (1), macrocytes (2) and large ovoid megalocytes are seen (3). Hypersegmented granulocyte (4).

Fig. 9b. In hyperchromic anemia, red cell precursors may be released into
the peripheral blood: here, a polychromatic erythroblast.

Fig. 9c.

Fig. 9d.

c and d Bone marrow in megaloblastic anemia: slight (1) or marked (2) loosening up of the nuclear structure, in some cases with binuclearity (3). Giant forms of band granulocytes and metamyelocytes (4) are often present.

10. Myelodysplastic syndrome (MDS)

Fig.10a. Strongly basophilic stippling in the cytoplasm of a macrocyte (in myelodysplasia).

Fig. 10b. Myeloblast with hyperchromic erythrocyte as an example of a myelodysplastic blood sample in the differential diagnosis versus hyper- chromic anemia.

Fig. 10c. A high proportion of reticulocytes speaks against megaloblastic anemia and for hemolysis (in this case with an absence of pyruvate kinase activity).

Fig. 10d. Bone marrow in myelodysplasia (type RAEB), with clinical hyperchromic anemia.

11. Erythrocyte inclusions.

Fig. 11a. Polychromatic erythrocyte with fine, dense ba- sophilic stippling.

Fig. 11b Erythrocyte with Howell–Jolly bodies (arrow) in addition to a lymphocyte (after splenectomy).

Fig. 11c. Erythrocyte with two Howell–Jolly bodies (arrow) alongside an orthochromatic erythroblast with basophilic stippling (thalassemia, in this case with functional asplenia).

Fig. 11d. Erythrocyte with a delicate Cabot ring (arrow) (here in a case of osteomyelosclerosis).

Fig. 11e. Thrombocyte layered onto an erythrocyte (arrow).

Fig. 11f.

Fig. 11g.

f and g Fixation and staining artifacts.

12. Blood analysis in malaria.

Fig. 12a. Trophozoites in Plasmodium falciparum (falciparum or malignant tertian malaria) infection. Simple signet-ring form (1), double-invaded erythrocyte with basophilic stippling (2). Erythrocyte with basophilic stippling without plasmodium (3) and segmented neutrophilic granulocyte with toxic granulation (4).

Fig. 12b.

Fig. 12c.

b and c Plasmodium falciparum: single invasion with delicate trophozoites (1), multiple invasion (2). 

Fig. 12d.

Fig. 12e.

d and e In the gametocyte stage of falciform malaria, the pathogens appear to reside outside the erythrocyte, but remnants of the erythrocyte membrane may be seen (arrow, e). For a systematic overview of malarial inclusions.

13. Polycythemia vera and secondary erythrocytosis.

Fig. 13a. In reactive secondary erythrocytosis there is usually only an increase in erythropoiesis.

Fig. 13b. In polycythemia vera megakaryopoiesis (and often granulopoiesis) are also increased.

Fig. 13c. Bone marrow smear at low magnification in polycythemia vera, with a hyperlobulated megakaryocyte (arrow).

Fig. 13d. Bone marrow smear at low magnification in polycythemia vera, showing increased cell density and proliferation of megakaryocytes

Fig. 13e. In polycythemia vera, iron staining shows no iron storage particles.

14. Forms of thrombocytopenia

Fig. 14a. This blood smear shows normal size and density of thrombocytes.

Fig. 14b. In this blood smear thrombocyte density is lower and
size has increased, a feature typical of immunothrombocytopenia.

Fig. 14c. Pseudothrombocytopenia. The thrombocytes are not lying  free and scattered around, but agglutinated together, leading to a reading of thrombocytopenia from the automated blood analyzer.

Fig. 14d. Giant thrombocyte (as large as an erythrocyte) in thrombocytopenia. Döhle-type bluish inclusion (arrow) in the normally granulated segmented neutrophilic granulocyte: May-Hegglin anomaly.

Fig. 14e. Large thrombocyte (1) in thrombocytopenia. Thrombocyte-like fragments from destroyed granulocytes (cytoplasmic fragments) (2), which have the same structure and staining characteristics as the cytoplasm of band granulocytes (3). Clinical status of sepsis with disseminated intravascular coagulation. In automated counters cytoplasmic fragments are included in the thrombocyte fraction.

15. Morphology of thrombocytes and megakaryocytes

Fig. 15a. Bone marrow in thrombocytopenia due to increased turnover (e.g., immunothrombocytopenia). Mononuclear “young” megakaryocytes clearly
 budding a thrombocyte (irregular, cloudy cytoplasm structure).

Fig. 15b. In thrombocytopenia against a background of myelodysplasia, the bone marrow shows various megakaryocyte anomalies: here, too small a nucleus surrounded by too wide cytoplasm.

Fig. 15c.

Fig. 15d.

Fig. 15e.

Fig. 15f.

c–f In myelodysplasia (c and d) and acute myeloid leukemia (e and f), bizarre anomalous thrombocyte shapes (arrows) may occasionally be found.

16. Essential thrombocythemia.

Fig. 16a. Increased thrombocyte density and marked anisocytosis in essential thrombocythemia.

Fig. 16b. Large thrombocytes (1) and a micro(mega)karyocyte nucleus (2) in essential thrombocythemia. Micro(mega)karyocytes are characterized by a small, very dense and often lobed nucleus with narrow, uneven cytoplasm, the processes of which correspond to thrombocytes (arrow).

Fig. 16c.

Fig. 16d.

This is only a part of the book : Color Atlas of Hematology: Practical Microscopic and Clinical Diagnosis (Clinical Sciences) 2nd of authors: Harald Theml, M.D; Heinz Diem, M.D and Torsten Haferlach, M.D. If you want to view the full content of the book and support author. Please buy it here: https://goo.gl/sxasqM