Integration: Unifying Concept
The expressions morphologic of septic vasculitis vary markedly, for example, from petechiae, vesiculopustules on a broad erythematous base, and hemorrhagic bullae of chronic gonococcemia and chronic meningococcemia to diffuse purpura in the Waterhouse-Friderichsen syndrome, from hemorrhagic pustules of staphylococcal septicemia to large hemorrhagic bullae that ulcerate in the septicemia caused by pseudomonas (ecthyma gangrenosum).
Irrespective of the presentation morphologic of lesions of septic vasculitis and irrespective of the cause of it, there are certain denominators in common, both clinical and histopathologic. Clinically, there always is purpura, i.e., a purple hue as a result of extravasation of erythrocytes into at least the upper part of the dermis. Macules, papules, vesicles, bullae, and even pustules are purpuric. Histopathologically, there always are thrombi within the lumen of some venules within the dermis and sometimes in the subcutaneous fat, too. As a result of thrombosis, infarction ensues. It may take the form of simple necrosis of the epidermis, which sloughs to leave behind an erosion or superficial ulcer, or it may be expressed as ballooning intraepidermal vesiculation in conjunction with epidermal necrosis, changes that also soon lead to erosion or ulceration. When thrombi are numerous and infarction extensive, as in the case of ecthyma gangrenosum, hemorrhagic bullae appear, and they are succeeded by deep ulcers.
In sum, septic vasculitis can be caused by many types of gram-positive and gram-negative bacteria, and the morphologic manifestations of that infection result from an interplay between the type of organism on one hand and the capability of the host to respond to it on the other. Irrespective of those considerations, septic vasculitis is characterized by typical clinical and histopathologic findings that permit diagnosis to be made with specificity.
When the process of septic vasculitis is “acute,” bacteria can be demonstrated in sections of tissue stained specially for them. When, in contrast, the process is “chronic,” as in that particular presentation of gonococcemia and meningococcemia, bacteria can neither be demonstrated in tissue sections nor cultured from lesions, the reason being that they have been ingested by inflammatory cells and have been destroyed.