Case No.: N-003

Diagnosis: Multiple small necrosis secondary to sepsis and disseminated intravascular coagulation.

Organ: Cerebral Cortex and White Matter

Last Updated: 12/31/2009

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Hematoxylin & eosin	Area 1: These necrotic areas are characterized by a pale core (1), a spongiotic band (2), and surrounding white matter (3). The details are illustrated in the panels below.
Hematoxylin & eosin	Area 1: This image is taken from the core of the necrosis. Note that there are very few nuclei that are well stained by hematoxylin. The tissue is disintegrating and the morphologic details are not preserved. Some swollen axons are also present.
Hematoxylin & eosin	Area 1: This image is taken from the spongiotic band around the necrotic core. Numerous small, round vacuoles are present and there is also evidence of tissue disintegration. Compare with the previous panel, more cells are well stained by hematoxylin.
Hematoxylin & eosin	Area 1: This image is taken from white matter immediately adjacent to the previous panel. Note the preservation of morphologic details and nuclei are well stained by hematoxylin. A small number of vacuoles indicating edema is also present.
Hematoxylin & eosin	White matter: This image is taken from the white matter remote from the necrotic area. Note the markedly reduced number of vacuoles. Morphological details are well preserved.
Hematoxylin & eosin	Cortex: The cortex does not show significant abnormal histopathologic changes. The neurons do not show evidence of hypoxic and/or ischemic changes. No spongiotic changes are present.

History: The patient was a 66 year-old man who developed respiratory failure secondary to pneumonia. In the later course of his disease, he also developed sepsis and disseminated intravascular coagulation. In the cerebellum, the patient developed multiple infarcts that measures up to 1.5 cm in greatest dimension (see Case 1a).

Gross Pathology: In the cerebral hemispheres, there are many small (arrows) to large(L), irregular, geographic pale gray lesion that predominantly involves the white matter. No hemorrhage or golden discoloration indicative of previous hemorrhage are noted. The cut surface of these lesions are very similar to the surrounding white matter in consistency and with no gross evidence of tissue disintegration.

Histologic Highlights of this Case:

Multiple geographic areas of necrosis are present through out the cerebral hemispheres. These lesions (L) are characterized by a pale staining core rimmed by a band of even more pale spongiotic band (Area 1). One of the salient feature of necrosis is that most if not all of the nuclei lost hematoxylin staining and there is evidence of tissue disintegration as illustrated here. The unaffected white matter and gray matter (cortex) appear to be in viable condition.
Pathophysiology: One of the most likely pathologic mechanisms of these necrosis is obstruction of small blood vessels supplying these areas due to the disseminated intravascular coagulations. For this reason, the distribution of these necrotic areas are also disseminated.
Timing: Judging from the fact that there is no histiocytic (macrophage) infiltration, the insult leading to these necrosis is most likely to have happened about 24-72 hours ago. Infarction that is less than 24 hours old typically show only reduce staining. Those that are between 24-72 hours show reduced staining and tissue disintegration. Those that are older than 72 hours typically show histiocytic infiltration.

Original slide is contributed by Dr. Kar-Ming Fung, University of Oklahoma Health Sciences Center, Oklahoma, U.S.A.

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