Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Leukocytosis
Leukocytosis is an elevation in the total leukocyte or white blood cell (WBC) count that is 2 SD above the mean for age (see Chapter 748 ). It is most often caused by elevated numbers of neutrophils (i.e., neutrophilia), although marked increases in monocytes, eosinophils, basophils, and lymphocytes can be seen. Before extensive evaluation, it is important to assess for spurious elevations in the WBC count caused by platelet clumping (secondary to insufficient sample anticoagulation or the presence of EDTA-dependent agglutinins), high numbers of circulating nucleated red blood cells (RBCs), and the presence of cryoglobulins by review of the peripheral smear.
Malignancy, namely leukemia and lymphoma, is a primary concern for patients with leukocytosis. For discussion of WBC elevation caused by immature leukocytes in acute and chronic leukemias, see Chapter 522 . Nonmalignant WBC counts exceeding 50,000/µL have historically been termed a leukemoid reaction. Unlike leukemia, leukemoid reactions show relatively small proportions of immature myeloid cells, consisting largely of band forms, occasional metamyelocytes, and progressively rarer myelocytes, promyelocytes, and blasts. Leukemoid reactions are most often neutrophilic and are frequently associated with severe bacterial infections, including shigellosis, salmonellosis, and meningococcemia; physiologic stressors; and certain medications.
The presence of a left shift , defined as having >5% immature neutrophils in the peripheral blood, is consistent with marrow stress. Higher degrees of left shift with more immature neutrophil precursors are indicative of serious bacterial infections and may be a dire sign of depletion of the bone marrow reserve pool of neutrophils. Marked left shift may occasionally be encountered with trauma, burns, surgery, acute hemolysis, or hemorrhage.
Neutrophilia
Neutrophilia is an increase in the total number of blood neutrophils that is 2 SD above the mean count for age (see Chapter 748 ). Elevated absolute neutrophil counts represent disturbances of the normal equilibrium involving bone marrow neutrophil production, migration out of the marrow compartments into the circulation, and neutrophil destruction. Neutrophilia may arise either alone or in combination with enhanced mobilization into the circulating pool from either the bone marrow storage compartment or the peripheral blood marginating pool , by impaired neutrophil egress into tissues, or by expansion of the circulating neutrophil pool secondary to increased granulocytopoiesis. Myelocytes are not released to the blood except under extreme circumstances.
Acute Acquired Neutrophilia
Neutrophilia is usually an acquired, secondary finding associated with inflammation, infection, injury, or an acute physical or emotional stressor ( Table 158.1 ). Bacterial infections, trauma (especially with hemorrhage), and surgery are among the most common causes encountered in clinical practice. Neutrophilia may also be associated with heat stroke, burns, diabetic ketoacidosis, pregnancy, or cigarette use.
Table 158.1
Causes of Neutrophilia
| TYPE | CAUSE | EXAMPLE |
|---|---|---|
| Acute acquired | Bacterial infections | |
| Surgery | ||
| Acute stress | Burns, diabetic ketoacidosis, heat stroke, postneutropenia rebound, exercise | |
| Drugs | Corticosteroids, epinephrine, hematopoietic growth factors, lithium | |
| Chronic acquired | Chronic inflammation | Inflammatory bowel disease, rheumatoid arthritis, vasculitis, cigarette exposure |
| Persistent infection | Tuberculosis | |
| Persistent stress | Chronic blood loss, hypoxia, sickle cell and other chronic hemolytic anemias | |
| Drugs | Corticosteroids, lithium; rarely ranitidine, quinidine | |
| Other | Postsplenectomy, tumors, Hodgkin disease, pregnancy, Sweet syndrome | |
| Lifelong | Congenital asplenia | |
| Hereditary disorders | Familial cold urticaria, hereditary neutrophilia, leukocyte adhesion deficiencies, periodic fever syndromes |
Drugs commonly associated with neutrophilia include epinephrine, corticosteroids, and recombinant growth factors such as recombinant human granulocyte colony-stimulating factor (G-CSF) and recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF). Epinephrine causes release into the circulation of a sequestered pool of neutrophils that normally marginate along the vascular endothelium. Corticosteroids accelerate the release of neutrophils and bands from a large storage pool within the bone marrow and impair the migration of neutrophils from the circulation into tissues. G-CSF and GM-CSF cause acute and chronic neutrophilia by mobilizing cells from the marrow reserves and stimulating neutrophil production.
Acute neutrophilia in response to inflammation and infections occurs because of release of neutrophils from the marrow storage pool. The postmitotic marrow neutrophil pools are approximately 10 times the size of the blood neutrophil pool, and about half of these cells are bands and segmented neutrophils. Exposure of blood to foreign substances such as hemodialysis membrane activates the complement system and causes transient neutropenia, followed by neutrophilia secondary to release of bone marrow neutrophils. Reactive neutrophils often have toxic granulation and Döhle bodies present.
Chronic Acquired Neutrophilia
Chronic acquired neutrophilia is usually associated with continued stimulation of neutrophil production resulting from persistent inflammatory reactions or chronic infections (e.g., tuberculosis), vasculitis, postsplenectomy states, Hodgkin disease, chronic myelogenous leukemia, chronic blood loss, sickle cell disease, some chronic hemolytic anemias, and prolonged administration of corticosteroids (see Table 158.1 ). Chronic neutrophilia can arise after expansion of cell production secondary to stimulation of cell divisions within the mitotic precursor pool, which consists of promyelocytes and myelocytes. Subsequently, the size of the postmitotic pool increases. These changes lead to an increase in the marrow reserve pool, which can be readily mobilized for release of neutrophils into the circulation. The neutrophil production rate can increase greatly in response to exogenously administered hematopoietic growth factors, such as G-CSF, with a maximum response taking at least 1 wk to develop.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here
