Leukocytosis becomes pathological in conditions of acute inflammation where the neutrophiles (A) show the greatest relative increase. The degree of leukocytosis depends on two different factors: the intensity or the virulence of the infection, and the vitality or resisting power of the individual. These vary within such wide limits that it is hard to predicate anything definite in a given case. In general the increase is supposed to be proportionate to the severity of the infection, though the greater the reactionary ability of the patient the larger the number of white cells. Where vitality is very low leukocytosis is less pronounced. It is possible to have toxemia to such a degree that the activity of the leukocytes seems to be destroyed. The following summary from Cabot puts things in very distinct form.

Infection mild, vital reaction good—small leukocytosis.

Infection less mild, vital reaction less good—moderate leukocytosis.

Infection severe, vital reaction good—very marked leukocytosis.

Infection severe, vital reaction poor—no leukocytosis.

From this it will appear that the absence of leukocytosis in cases where it naturally would be expected is a serious indication and justifies an unfavorable prognosis; or else it may be interpreted in evidently favorable cases as indicating infection of very mild grade.

There are but few diseases in which leukocytosis by itself (or for that matter any other indication which the ordinary examination or blood count may give) is wholly sufficient for diagnostic purposes. But a blood count and estimate of the amount of hemoglobin present will often be of such advantage to the surgeon that he may well afford to wait in order to secure them. This is rarely necessary in acute cases, but in chronic cases, and especially the anemias, he may gain great benefit by such investigation. In trichinosis, for example, eosinophilia is most pronounced, B forming even as high as 70 per cent. of the leukocytes present.

The anemias which are of particular interest to the surgeon may be classified as follows:

1. A. Anemias due to hemorrhage may assume one of two forms, that resulting from sudden and extensive loss of blood or that resulting from constant oozing. Example of the former is seen in hemorrhages of the stomach or intestines after perforating ulcer, etc. Examples of the latter are met with in hemophilia and in uterine hemorrhages, or in excessive menstruation where the loss of blood extends over a considerable length of time. It is known, moreover, that certain entozoa in the intestines will produce a chronic anemia. Thus the red corpuscles may be reduced to even less than 1,000,000 per cubic millimeter. Immediately after acute hemorrhage the hemoglobin percentage is still normal, but after a short time it becomes reduced. If such cases do not speedily end fatally, nucleated red corpuscles appear in the blood and the observer will recognize both normoblasts and megaloblasts. At the same time the bone-marrow, which is normally yellow, becomes red, vascular, and richly cellular, and seems to furnish these cells just mentioned. Certain drugs, like potassium chlorate and glycerin, affect also the number of red corpuscles, but such poisons as these cause not only disintegration of the red cells, but produce also jaundice and hemoglobinuria. Pernicious anemia sometimes interferes with or fatally complicates surgical treatment. It is characterized by the extreme changes already mentioned, with which it marches steadily to a fatal termination. Quincke has reported an instance in which their number was reduced to 43,000 per cubic millimeter, while the hemoglobin was reduced to 20 or 25 per cent. of the normal amount.