INFLAMMATION I

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Skin and soft tissues of foot: Phlegmon (cellulitis)

This specimen is from a 72-year-old woman with vascular insufficiency of a lower extremity. She had a long-standing ulcer which ultimately gave rise to a spreading infection.

• Under scanning power, note the diffuse cellular infiltrate deep in the section, largely in adipose tissue.

• This is a great slide with which to become familiar with the appearance of polymorphonuclear neutrophils (PMNs, “polys”). Practically every inflammatory cell in the infiltrate is a PMN. Some of them are readily recognized by their nuclear morphology, while others have distorted degenerating nuclei. In yet other areas, there has been karyorrhexis leaving basophilic bits of nuclear debris.

• Study the neutrophil infiltrate at the lower powers of your scope. With a little practice, you’ll be able to tell a PMN infiltrate from a horde of lymphocytes or plasma cells or macrophages even with the scanning or low power objective.

• What distinguishes phlegmon or cellulitis from other PMN-containing inflammatory reactions?

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Appendix: Acute Appendicitis

This slide shows the appendix of a 16-year-old lad. The slide contains one more-or-less longitudinal section and two cross-sections of the appendix. How do you recognize the tissue as appendix? One of the cross-sections is nearly normal and serves as a good “control” for the others.

• In the diseased areas note that the mucosa is either missing or necrotic. In what way does some of this mucosa qualify as gangrenous?

• Note the presence of a dense inflammatory infiltrate spreading transmurally to the serosal surface. The predominant cell type is the PMN. In some areas the infiltrate might be characterized as simply purulent, while in other areas there is liquefactive destruction of underlying tissue qualifying the process as suppurative. On some of the serosal surface, the PMNs are mixed with fibrin (hence, a fibrinopurulent serositis).

• How might a person with this condition present clinically? What is the correct treatment?

• What complication might be produced by the suppuration? What other consequences might follow appendicitis, especially if treatment is delayed?

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Lung: Acute Purulent Bronchopneumonia

This specimen comes from a patient who was hospitalized for several days in a comatose state before death.

• Under “scanning” power, how does this lung differ from normal? Some of the alveolar spaces, under higher power, are seen to contain a pink, acellular material. What is this and where did it come from? Many other alveoli are filled with polymorphonuclear neutrophils. How did they arrive there?

• The features shown in this slide are those of a purulent pneumonia (or pneumonitis). How would the appearance differ if the process were suppurative?

• What sort of etiologic agents might be responsible for the pneumonia? How does this patient’s history relate to the pneumonia? Can you relate the histopathologic findings in this case to the likely appearance of the chest x-ray?

• See if you can trace the course of histologic events that might have taken place had this patient’s pneumonia been successfully treated.

• What are the possible complications when pneumonia does not resolve?

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Lung: Fungal Pneumonia and Pleuritis

This slide comes from an immunocompromised patient who died with signs and symptoms of systemic infection. (The slide is inserted here just to give you a quick look at a fungus in tissue.)

• Clumps of fungus can be seen at low magnification, projecting out from the pleural surface. Study these clumps under higher magnification, and then try to find fungal invasion of lung itself.

• Immunocompromised patients often fall victim to invasive infections with organisms in the environment that are harmless to immunocompetent persons.

• What are some clinical situations resulting in immunocompromise?

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Colon: Pseudomembranous Colitis

This specimen is from a 38-year-old woman who developed diarrhea in the course of treatment for bronchopneumonia.

• What features of the tissue allow you to identify it as colon? Identify the various layers of the wall.

• The abnormalities in the specimen are largely mucosal, with some lesser abnormalities of the submucosa. Under scanning power, note the areas of more intact mucosa. Emanating from each area of destruction is a “cloud” of fibrin and PMNs (fibrinopurulent exudate) along with karyorrhectic debris from necrotic epithelium and leukocytes, and patches of mucus. These patches of exudate adherent to damaged mucosa constitute pseudomembranes. Can you account for the route of arrival of each of the elements (i.e. PMNs fibrin, mucus)? What would the gross appearance be?

• The submucosa is also abnormal, but to a lesser degree. It appears edematous and has a sparse infiltrate of inflammatory cells.

• How does this colitis relate to the patient’s pneumonia? What would be appropriate treatment? Can you visualize the histologic sequence of events in the resolution of this process?

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Bone: Joint, and Soft Tissue, Gout

This specimen represents a digit from a 68-year-old man.

• Identify skin, bone and cartilage. How would the preparation of this section have differed from that of the other slides you’ve seen today?

• Under the scanning power, you will note irregular nodular deposits within bone and extending into soft tissue. Some of these deposits are amorphous, some seem to contain empty spaces, and some contain crystalline material.

• While the deposits are partly rimmed by fibrous connective tissue, most are surrounded by a peculiar inflammatory infiltrate. What types of cells compose this infiltrate? Can you account for their origin? When have you seen similar reactions? What is the general significance of granulomatous inflammation?

• The deposits here are urates, characteristic of gout. What would the gross appearance be? What might be the effects of urate deposits?