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Slide 30 [WebScope] [ImageScope]

Organ: Lung
Pathology: Acute passive congestion and edema

Clinical History: This lung came from a 37-year-old man who died with signs and symptoms of sepsis.

Histopathological Features: In much of this slide, however, the usually “empty” air spaces are filled with a pale pink, homogenous to slightly granular material which is edema fluid. Most of this fluid has fairly low protein content (and is therefore pale-staining), but in very limited foci there are deposits of fibrin which stain more deeply. An added feature in this case is the presence of circumscribed foci of inflammation. The slide shows clusters of alveoli filled with polymorphonuclear neutrophils, and other areas where actual suppuration has taken place, i.e., where the parenchyma has undergone liquefactive necrosis leaving a puddle of pus. (Localized suppuration = abscess) The rim of fibroblastic proliferation around these lesions indicate that the process is at least several days to a week old. Suppurative lesions usually reflect infection.

A rather diffuse change associated with the edema is vascular engorgement, i.e., congestion, manifested by an excessive number of erythrocytes in alveolar septa. This is a difficult determination to make microscopically but grossly the congestion is not subtle. The lung would have had a dusky, purplish hue. Some of the “excess” erythrocytes have been extruded into alveolar spaces reflecting the increased hydrostatic pressure within the lungs, and the delicate structure of the alveolar septa. This so-called “hemorrhage by diapedesis” is often sufficient to produce a gross blood-tinging of the edema fluid.

Slide 31 [WebScope] [ImageScope]

Organ: Lung
Pathology: Early chronic passive congestion

Clinical History: This specimen of lung was obtained from a 66-year-old patient who had been in congestive cardiac failure for some weeks.

Histopathological Features: Alveolar septa everywhere in the section are engorged with red cells, reflecting passive congestion. Hemorrhage by diapedesis is prominent. A feature which distinguishes this slide from the previous one is the presence of numerous intra-alveolar clumps of brown pigment –- evident even on low power. On higher powers, the clumps are seen to be aggregates of pigment granules, which seem to be intracellular as judged from their smooth circumscription. If you search a bit, you’ll find a nucleus in some of these cells (if cut just right) allowing you to conclude that the cells are macrophages. The pigment granules are quite large, have a sort of “waxy” appearance, and a warm brown color. These features are typical of hemosiderin granules.

In the lung, you can also encounter macrophages containing variable dirty brown-black granules representing inhaled then phagocytosed crud. This must be distinguished from hemosiderin. The most common source of hemosiderin, as in this case, is blood breakdown. Therefore, you can expect to encounter hemosiderin in areas of hemorrhage that are being mopped up, or in thrombi that are undergoing resolution or organization.

In the lung that remains congested over a period of time (“chronic passive congestion”), the continuing hemorrhage by diapedesis and microhemorrhage leads to accumulation of hemosiderin. The pigment-containing macrophages, which can also be seen in expectorated sputum, have been called “heart failure cells.” If sufficiently prolonged, the congestion can lead to an increase in interstitial connective tissue. Then, the lung grossly is brown and firm----leading to the old term “brown induration” to describe the chronically congested lung.

Slide P13 [WebScope] [ImageScope]

Organ: Liver
Pathology: Chronic passive congestion

Clinical History: This liver specimen was obtained at autopsy of a 74-year-old man who died after many months of cardiac dysfunction.

Histopathological Features: Under the lowest power of a microscope, one may notice that this liver has a peculiar pattern of redder areas alternating with purple/blue areas. (The normal liver would have a fairly homogeneous appearance at this power.)

With higher magnification, it can be seen that the redder areas are characterized by smaller hepatocytes and the sinusoids are widened and filled with red blood cells. Using the portal tracts (with their bile duct/arterial branch/portal vein branch) for orientation, one can discern that the redder areas are around central veins, i.e., centrilobular, with preservation of normal structure more peripherally. This pattern of centrilobular sinusoidal congestion and hepatocyte atrophy can be produced by chronic impairment of outflow of blood through central-veins, hepatic veins, and vena cava, and has been classically called chronic passive congestion.

This chronic passive congestion pattern is frequently found in the livers of patients with “right-sided” heart failure (usually secondary to “left-sided” failure with changes of passive congestion in the lungs). Other non-cardiac circumstances that might produce a similar pattern in the liver include vena caval obstruction or even hepatic vein obstruction, which could lead to “outflow” problems in liver with congestive changes.

Although there are examples of primary right-sided heart failure, most often both sides are involved. Therefore, there is frequently an aspect of failure of “forward” flow due to decreased left ventricular output. When this is severe, particularly with hypotension as the cardiac patient is decompensating, arterial perfusion drops, and centrilobular areas in the liver, farthest from the blood supply, begin to undergo ischemic necrosis.

In many of the central zones in your slide, close inspection will reveal pyknosis and karyolysis in some hepatocytes, occasionally with a few leukocytes clustered about -- reflecting very early ischemic necrosis. Sometimes the combination of poor perfusion and passive congestion results in necrotic centrilobular areas stuffed with blood. This pattern is called “central hemorrhagic necrosis.”

Slide 35 [WebScope] [ImageScope]

Organ: Soft tissues of leg
Pathology: Organizing venous thrombi

Clinical History: These fragments of soft tissue were obtained at autopsy from the left leg of a 73-year-old woman who had died suddenly.

Histopathological Features: Within a background of skeletal muscle are large veins, distended with blood. Their distended state immediately suggests that something is wrong. Generally vessels are more collapsed, as seen in routine sections, unless fixed by perfusion under pressure, or unless something is holding the vessel open. In this case, it is blood that appears to be holding the vessels open. If this had been only fluid blood at the time of the patient’s demise, how would it appear in the sections? A post-mortem clot would not have the complex structure of a thrombus.

Note that in several of the veins, the blood is not simply a mixture of red cells and leukocytes, but is traversed by bands of fibrin and platelets, trapping the various formed elements. In a post-mortem clot (as opposed to an ante-mortem thrombus) how would the appearance of any fibrin or platelets differ? Layering but no organization. Also note that in some of the thrombi there is very early ingrowth of capillaries and fibroblasts from the vessel wall, i.e. organization. This, of course, would not happen in a postmortem clot. This organization indicates that the thrombus is at least several days old. Had the patient survived, the histologic picture in these vessels would evolve: resolution, organization and ultimately re-endothelialization. The patient’s sudden death is the result of pulmonary embolus, originating in DVT.

Slide 36 [WebScope] [ImageScope]

Organ: Lung
Pathology: Pulmonary arterial emboli and infarct

Clinical History: This lung came from a 77-year-old woman who was incapacitated by advanced Alzheimer’s disease and confined to bed.

Histopathological Features: Under the lowest power of a microscope, one notices that the alveoli in part of the section appear to contain air or variable amounts of edema, while in other parts of the section, the alveoli are filled by something more substantial. Under higher magnification, the material that is obliterating alveoli appears to be blood in varying stages of disintegration. Compare the alveolar septa in the “filled” area with those in the more normal area. What is it that allows you to conclude that the pulmonary parenchyma is actually necrotic in this area of density? Coagulation necrosis of septal cells.

In and around this infarcted zone, there is irregular leukocyte infiltration in response to the necrosis, and in one set of sections (trade sections-looking for the one with a more triangular outline) there is a zone of organization at the margin of the infarct. Within a number of pulmonary arterial branches, you’ll note dense blood clots. In most instances, there is ingrowth of capillaries and fibroblasts at the periphery of the clots. What does this tell you about the duration of the process? It has been going on for a while.

Can you tell from the histopathologic features whether these clots are thrombi or emboli? What gross features would be helpful? What do the clinical circumstances suggest? Can you relate the patient’s history to what you see on the slides? Histopathologic features do not distinguish thrombi from emboli. Context and gross findings (i.e., coiling up of the embolus) are helpful. Patients who are bedridden are susceptible.

Slide 97 [WebScope] [ImageScope]

Organ: Esophagus
Pathology: Varices

Clinical History: This specimen was obtained from a 56-year-old man who died of a massive upper gastrointestinal hemorrhage.

Histopathological Features: The most striking feature of this slide is the presence of numerous, markedly dilated veins at all levels of the wall, but particularly in the submucosa. These vessels are engorged with blood, and are associated with extensive hemorrhage into the adjacent tissues. Dilated and tortuous veins are called “varicose veins” or varices (singular: varix).

Some of these varices contain thrombi particularly evident as masses of fibrin with entrapped blood elements. Some of the thrombi have been around long enough to be organizing, as shown by the ingrowth (from the vessel lining) of fibroblasts and capillaries. In most of your sections, the largest varix, partly thrombosed, is just under the squamous epithelium with an area of erosion. This vessel, or one like it, was probably the source of the massive GI hemorrhage.

Varices generally result from prolonged engorgement of veins. How can you account for such a condition in esophageal veins. Where else are varices commonly encountered? In esophagus, varices are related to portal hypertension, most often secondary to cirrhosis. Varices can be seen in various areas: varicose veins in the legs, hemorrhoids in the anus, etc.


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