Introduction

Hemograms consist of both quantitative data (total cell counts, differential cell counts, hematocrit, hemoglobin, red cell indices, etc.) and qualitative data (blood film evaluation). Proper interpretation depends upon the integration of the two.

Proper interpretation also depends upon a systematic approach. For all cell compartments, interpretation can be guided by asking and answering a series of key questions.

Key Leukogram Questions

Key Leukogram questions include the following:

1.  Is there evidence of inflammation?

2.  Is there evidence of stress (high circulating glucocorticoids)?

3.  Is there evidence of tissue necrosis?

4.  Is there evidence of systemic hypersensitivity?

5.  If there is evidence of inflammation, can the inflammation be classified as acute, chronic, or overwhelming?

6.  Is there Evidence of Systemic Toxemia?

The following paragraphs will provide guidelines for answering each of these questions in turns.

Is There Evidence of Inflammation?

The presence of a neutrophilic left shift (increased numbers of circulating immature neutrophils, monocytosis, and persistent eosinophilia, either alone or in combination, are suggestive of inflammation. Absolute neutrophilias of greater than 25,000/μl also suggest inflammation. Total white cell counts merely reflect the balance between marrow production and tissue utilization. In inflammatory disorders, total white cell counts can be low, normal, or high.

Is There Evidence of Stress?

Stress (high circulating levels of glucocorticoids) typically causes mild to moderate lymphopenia (lymphocyte counts between 750/μl and 1500/μl). Eosinopenia, mild mature neutrophilia, and mild monocytosis can also be present but are less consistent and specific than the lymphopenia.

Is There Evidence of Tissue Necrosis?

Monocytosis is an indicator of demand for phagocytosis and/or tissue necrosis. Monocytosis ha soften been considered to be an indicator of chronicity, but it can occur in as little as 8-12 hours.

Is There Evidence of Systemic Hypersensitivity?

Persistent eosinophilia is an indicator of systemic hypersensitivity. It is important to remember that systemic hypersensitivity reactions represent a special form of inflammatory reaction. Causes include: parasitic diseases with a systemic phase (flea bite dermatitis, heartworm disease), feline asthma, allergic tracheobronchitis in dogs, systemic mastocytosis, allergic gastroenteritis, and disseminated eosinophilic granuloma complex in cats. It is important to recognize that parasitic disease confined to the gastrointestinal tract (e.g., whipworms) does not cause systemic persistent eosinophilia.

If There is Inflammation, Can it be Classified as Acute, Chronic or Overwhelming?

In many cases, inflammatory leukograms cannot be further classified. In other instances, the differential cell count (in absolute numbers) is typical of acute, chronic or overwhelming inflammation. Leukogram patterns are determined by leukocyte kinetics, or the balance between bone marrow production and release on the one hand and tissue utilization on the other. Leukocyte kinetics in turn are regulated through the actions of chemotactic factors and cytokines.

The typical acute inflammatory leukogram is characterized by neutrophilia with a left shift, lymphopenia and variable monocytosis. The neutrophilia reflects the relatively large bone marrow storage pool in the dog and cat, and the movement of more neutrophils from marrow into blood than from blood into tissue. The left shift indicates depletion of the marrow storage pool of mature neutrophils and recruitment of younger cells into circulation. The lymphopenia is reflective of stress. The presence or absence of monocytosis depends on the presence or absence of tissue necrosis.

There are two patterns indicative of chronic inflammation. The first is characterized by extremely high white cell counts (150 to 200,000/μl or more) with marked neutrophilia and a left shift. Monocytosis and neutrophil toxicity are also usually present. In this circumstance neutrophil production in the marrow is greatly expanded and the number of neutrophils entering the blood is far greater than the number leaving the blood for the site of inflammation. Because the inflammation is chronic, the anemia of inflammatory disease and increased total protein as a result of hyperglobulinemia are also often present. This pattern of chronic inflammation is commonly seen with severe focal suppurative lesions such as abscesses.

The second form of chronic inflammation is characterized by a normal to slightly elevated white cell count characterized by high normal or slightly elevated mature neutrophils, no left shift, normal lymphocyte counts, and monocytosis. The normal to slightly elevated neutrophil count and absence of a left shift reflect a new balance between marrow production and tissue demand. The normal lymphocyte count represents the counterbalancing effect of stress and antigenic stimulation on lymphocyte numbers. Monocytosis reflects demand for phagocytosis and tissue necrosis. This kind of chronic inflammatory response is generally seen with chronic low grade more diffuse inflammatory processes.

Overwhelming inflammation is a circumstance where tissue demand outstrips marrow production. Overwhelming inflammatory processes are therefore characterized by normal or decreased neutrophil counts with a left shift. Lymphopenia reflects stress. Monocytosis again indicates demand for phagocytosis and/or tissue necrosis.

Is there Evidence of Systemic Toxemia?

The presence of toxic neutrophils on the blood film indicates systemic toxemia. Toxic changes in neutrophils include foamy basophilia of the cytoplasm, the presence of Döhle bodies in the cytoplasm (basophilic precipitates of cytoplasmic RNA), grantism, and the presence of bizarre nuclear morphology. These changes occur as a result of abnormal maturation of neutrophil precursors in the marrow. Toxicity is the result either of the direct action of circulating toxins on neutrophil precursors or shortened maturation time of neutrophils in response to increased tissue demand. Systemic toxemia is most commonly associated with bacterial infections. However, other causes, such as extensive tissue necrosis, must also be considered.

General patterns of leukocyte responses in disease are summarized in Table 1.

Table 1. General patterns of leukocyte responses.

Reprinted with permission from Teton New Media; A Guide to Hematology in Dogs and Cats, A.H. Rebar, P.S. MacWilliams, B.F. Feldman, F.L. Metzger, R.V.H. Pollock, J. Roche; Jackson WY; 2002