Platelets Bloodmed.com  
   
     
The global source for hematology education, practice and research

Login

Forgotten password?
Not registered?

Trainees and CME
Myeloid malignancy section
Lymphoid malignancy section
Pediatrics section
Bone marrow transplantation section
Red cells section
Platelets and hemostasis section
Transfusion science section
Transfusion practice section
Featured Profile
Elizabeta Nemeth
Elizabeta Nemeth
Featured Profile
Finbarr Cotter
Finbarr Cotter
British Society of Haematology
Wiley-Blackwell
Disclaimer
Privacy statement

ISSN: 1478-1247

E-books

 

A beginner's guide to blood cells

Barbara J. Bain


CHAPTER 3
Assessing White Cells and Platelets

White cells and platelets may be increased or decreased in number. They may also show morphological abnormalities, either inherited or acquired.

Assessing whether the numbers of individual types of white cell are increased or decreased requires a differential count.

However, the differential count is of little importance in itself and should only be used to calculate the absolute numbers of each cell type. The absolute counts are then compared with those expected in healthy people of the same age, sex and ethnic group. The terms used in describing numerical abnormalities in white cells and platelets are defined in Table 3.1.

Top of page Assessing white cell and platelet numbers  Next section

White blood cell counts can be assessed by examining a blood film, preferably by low power, but an instrumental WBC is much more precise. Figure 3.1 illustrates leucocytosis. In comparison, if the WBC were normal, no more than one or two cells would be expected in a microscopic field of this size and if there were leucopenia many such fields would contain no white cells.

Platelet numbers can also be assessed on a film, by relating their number to the number of red cells present. An instrument platelet count is generally much more precise than an estimate from a film but is prone to errors because of poor specimen collection techniques or characteristics of the sample.

If a platelet count is unexpectedly low it is important to check that this is not because the specimen is partially clotted. Some automated instruments have a mechanism for checking for clots but otherwise this has to be done manually by the laboratory worker. It is important that all low platelet counts are confirmed on a blood film. Figures 3.1, 3.2, 3.3 contrast normal, high and low platelet counts.

It is also important to examine a blood film in all cases with apparent thrombocytopenia to exclude platelet aggregation or satellitism (see Figs 1.21 and 1.23) as a cause of a falsely low count.

Top of page Assessing neutrophil morphology  Previous section Next section

Neutrophils may show increased (Fig. 3.4) or decreased (see Fig. 1.13) granulation. Increased granulation is usually a reaction to infection or inflammation and is therefore referred to as toxic granulation. However, it does also occur as a normal phenomenon, during pregnancy.

Cytoplasmic inclusions may be present as an inherited or acquired abnormality. The commonest such abnormality is a small, pale, blue–grey inclusion that occurs both during pregnancy and in infection and inflammation and is known as a Döhle body (Fig. 3.5).

Another common cytoplasmic abnormality, which is strongly suggestive of infection, is cytoplasmic vacuolation (Fig. 3.4).

Neutrophils may have congenital or acquired abnormalities of nuclear lobulation. An increase in band forms and less lobulated neutrophils in relation to more mature, well-lobulated neutrophils is known as a left shift (Fig. 3.4). This term is also used when neutrophil precursors are present in the blood.

Neutrophils may also be hypolobulated, but with very round lobes and with some nuclei being shaped like a pair of spectacles or a peanut. This occurs as a congenital abnormality known as the Pelger–Huët anomaly (Fig. 3.6).

There will be some neutrophils with completely round nuclei. This congenital anomaly is of no clinical significance but it is important not to confuse it with left shift. A similar abnormality can develop as an acquired condition known as the pseudo- or acquired Pelger–Huët anomaly.

The acquired Pelger–Huët anomaly is clinically very significant because it is a feature of a neoplastic condition, called a myelodysplastic syndrome, which may lead on to acute leukaemia.

The nuclei have similar abnormal shapes in the congenital and acquired Pelger–Huët anomalies but in the latter there are often associated abnormalities (e.g. neutropenia or hypogranular neutrophils). Neutrophils may also show increased lobulation (Fig. 3.7). This is known as right shift.

Neutrophils with six or more lobes are said to be hypersegmented. Neutrophil hypersegmentation is an important clue to the presence of deficiency of vitamin B12 or folic acid.

Macropolycytes (Fig. 3.8) should not be confused with hypersegmented neutrophils: they are twice the size of normal neutrophils and the nucleus is twice as big. This is because one cell division has been missed during neutrophil production.

Macropolycytes are likely to have 92 rather than 46 chromosomes, i.e. they are likely to be tetraploid rather than diploid. Although their nuclei may have six or more lobes, macropolycytes do not have the same significance as hypersegmented neutrophils and should be distinguished from them.

Granulocyte precursors and nucleated red cells may be present simultaneously in the peripheral blood. This can occur as a normal phenomenon in pregnancy but otherwise it is mainly seen in severely ill patients, who are usually anaemic.

The anaemia is referred to as a leucoerythroblastic anaemia. Leucoerythroblastic anaemia is indicative of either a bone marrow disease (e.g. idiopathic myelofibrosis), bone marrow infiltration (e.g. by carcinoma cells) or a severe systemic illness (e.g. severe infection or haemorrhagic shock).

Top of page Assessing lymphocyte morphology  Previous section Next section

Congenital abnormalities of lymphocytes are rare. Most abnormalities of lymphocyte morphology are caused by viral infections.

Less often, increased numbers of lymphocytes showing a variable degree of morphological abnormality are indicative of a neoplastic process, either a lymphoid leukaemia or a lymphoma (see Chapter 4).

The most striking reactive changes in lymphocyte morphology are seen in infectious mononucleosis, an illness caused by an acute infection by the Epstein–Barr (EB) virus.

There is lymphocytosis and lymphocytes are morphologically very abnormal (Fig. 3.9). Some are very large, some have primitive nuclei with a diffuse chromatin pattern and nucleoli, some nuclei are lobulated, some cells have voluminous basophilic cytoplasm. The cells are pleomorphic, i.e. they vary greatly in size and shape.

The lymphocytes are so abnormal that initially their true nature was not known and they were referred to as atypical mononuclear cells. Now they are more often referred to as atypical lymphocytes.

Large numbers of atypical lymphocytes, similar to those seen in infectious mononucleosis, can also occur in infection by cytomegalovirus, hepatitis A virus, and adenovirus and during the parasitic infection toxoplasmosis.

Smaller numbers of atypical lymphocytes are seen in many other viral infections (including acute infection by the human immunodeficiency virus—HIV) and in some bacterial, rickettsial and protozoan infections.

Other reactive changes, in addition to those typical of infectious mononucleosis, occur in lymphocytes both during infection and during exposure to other antigenic stimuli. B lymphocytes may differentiate into plasma cells (Fig. 3.10) with an increased amount of basophilic cytoplasm, a pale-staining area near the nucleus (the Golgi zone) and an eccentric nucleus with clumped chromatin. There may also be plasmacytoid lymphocytes with characteristics intermediate between those of lymphocytes and plasma cells.

An increase of large granular lymphocytes can also occur as a reactive change, e.g. during chronic viral infection. These cells may be indistinguishable from normal large granular lymphocytes but sometimes they show features of activation such as a larger size and more voluminous basophilic cytoplasm.

Characteristic morphological changes occur in lymphocytes in different types of leukaemia and lymphoma (see Chapter 4).

Top of page Assessing morphology of monocytes, eosinophils and basophils  Previous section Next section

Numerical changes in monocytes, eosinophils and basophils are often useful in diagnosis but this is less often the case with morphological changes.

Monocytes can show increased size and cytoplasmic vacuolation during infection. Immature monocytes with increased granulation and cytoplasmic basophilia can occur both in infections and in leukaemia and related conditions.

Eosinophils can show a variety of morphological abnormalities (Fig. 3.11) including hyper- and hypolobulation, reduced granulation and cytoplasmic vacuolation. However, these changes occur in reactive eosinophilia (e.g. in parasitic infection) and also in eosinophilic leukaemia so they are not useful in differential diagnosis.

Basophils sometimes show reduced granulation but since this can occur as a laboratory artefact as well as during allergic reactions and in leukaemia and related disorders its detection is not very helpful in diagnosis.

Top of page Assessing platelet morphology  Previous section

Platelets may be smaller than normal (Fig. 3.2) or, more often, larger than normal (Fig. 3.3). Very large platelets are sometimes referred to as giant platelets. An increased variability in platelet size is referred to as platelet anisocytosis (Fig. 3.3).

Platelet size is of diagnostic significance, particularly if considered in relation to the platelet count. Small or normal-sized platelets in association with thrombocytopenia suggest that the cause is a failure of bone marrow production, whereas thrombocytopenia with large platelets is more likely to be caused by peripheral destruction or consumption of platelets with the bone marrow responding by increasing platelet production.

Platelet size is also useful in assessing the likely cause of thrombocytosis. In reactive thrombocytosis (e.g. caused by severe infection or inflammation) the platelets are usually of normal size whereas when thrombocytosis is a feature of a myeloproliferative disorder (chronic myeloid leukaemia, essential thrombocythaemia or polycythaemia vera) platelet size is generally increased and some giant platelets are present.

Platelets may show defective or absent granulation. Often this is an artefactual change, because the blood specimen has partly clotted or because platelets have aggregated and have discharged some or all of their granules (see Fig. 1.21). If an artefact is excluded then the detection of defectively granulated platelets is of diagnostic significance. It occurs as a rare congenital anomaly (the grey platelet syndrome), but usually it is consequent on a bone marrow disease such as one of the myeloproliferative or myelodysplastic disorders.

Table 3.1  Terminology used for abnormalities of white cell and platelet numbers.

Leucocytosis Increased white cell count
Neutrophilia (or neutrophil leucocytosis) Increased neutrophil count
Lymphocytosis Increased lymphocyte count
Monocytosis Increased monocyte count
Eosinophilia Increased eosinophil count
Basophilia* Increased basophil count
Thrombocytosis Increased platelet count
Leucopenia Decreased white cell count
Neutropenia Decreased neutrophil count
Lymphopenia (or lymphocytopenia) Decreased lymphocyte count
Monocytopenia Decreased monocyte count
Eosinopenia Decreased eosinophil count
Basopenia Decreased basophil count
Thrombocytopenia Decreased platelet count
*Note: the same word is used to mean increased uptake of basic dyes giving a deep blue colour to cytoplasm.

Copyright © Blackwell Publishing 2003

Blood
The blood film
  Red cells
  White cells
   Neutrophils
   Eosinophils
   Basophils
   Lymphocytes
   Monocytes
  Platelets
  Haemopoietic cells
   Myeloblasts
   Promyelocytes
   Myelocytes
   Metamyelocytes
   Band cells
   Nucleated red blood cells
The blood count
  Haemoglobin concentration
  Haematocrit or packed cell volume
  Cell counts
  Red cell indices
Normal ranges
How to examine a blood film
  Learning to look at blood films
  Recognizing problems with the blood sample
  Interpreting blood films
Assessing red cell number and distribution (anaemia, polycythaemia, rouleaux formation, red cell agglutination)
Assessing red cell size (microcytosis, macrocytosis, anisocytosis)
Assessing red cell shape (poikilocytosis)
Assessing red cell colour (hypochromia, hyperchromia, anisochromasia, polychromasia)
Detecting red cell inclusions (Pappenheimer bodies, basophilic stippling, Howell–Jolly bodies)
The full blood count in red cell assessment
Assessing white cell and platelet numbers
Assessing neutrophil morphology
Assessing lymphocyte morphology
Assessing morphology of monocytes, eosinophils and basophils
Assessing platelet morphology
The blood film and count in healthy individuals
   Gender
   Neonates, infants, and children
   Pregnancy
   Ethnic variation
Abnormalities of red cells
  Polycythaemia
   Polycythaemia vera
  Anaemia and other disorders of red cell production
   Megaloblastic anaemia
   Iron deficiency anaemia
   Anaemia of chronic disease
   Beta thalassaemia trait
   Alpha thalassaemia trait
   Haemoglobin H disease
   Hyposplenism
   Hereditary spherocytosis
   Hereditary elliptocytosis
   Glucose-6-phosphate dehydrogenase deficiency
   Autoimmune haemolytic anaemia
   Beta thalassaemia major
   Sickle cell anaemia
   Sickle cell trait
   Sickle cell/haemoglobin C disease
   Haemoglobin C disease
Abnormalities of white cells
  Neutrophil leucocytosis (neutrophilia)
   Bacterial infection
   Chronic myeloid leukaemia
  Lymphocytosis and morphologically abnormal lymphoid cells
   Chronic lymphocytic leukaemia
   Prolymphocytic leukaemia
   Follicular lymphoma
   Hairy cell leukaemia
   Multiple myeloma
  The acute leukaemias and related conditions
   Acute lymphoblastic leukaemia
   Acute myeloid leukaemia
   The myelodysplastic syndromes
  Idiopathic myelofibrosis
Free trial