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Histopath Lab 5:
Circulatory Derangements I

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Robbins and Cotran Pathologic Basis of Disease 9th Ed.

Suggested Reading:
Pages 113-116 – Edema and Congestion
Pages 122-129 – Thrombosis and Embolism
Pages 129-131 – Infarction
Pages 526-531 – Heart Failure
Pages 540-550 – Ischemic Heart Disease
Pages 697-699 – Pulmonary Embolism/Infarction
Pages 779-780 – Ischemic Bowel Disease
Pages 864-865 – Hepatic Circulatory Disorders


CIRCULATORY DERANGEMENTS I


Slide 41 [WebScope][ImageScope]

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

  • Under the lowest power of your microscope, you can readily identify sectors of fairly normal lung parenchyma. 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).
  • A rather diffuse change associated with the edema is vascular engorgement, i.e., congestion, manifested by an excessive number of erythrocytes in alveolar septa.  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.
  • What is your diagnosis?
  • In many of the alveolar spaces, there are air bubbles in the edema fluid. How did they come to be there? How would this manifest on clinical exam?
  • Under what clinical circumstances would you encounter this histopathology?
  • What would you expect to see grossly in this lung?  What would you expect to see on chest X-ray?
  • An added feature in this case is the presence of circumscribed foci of inflammation. Scan under low power and identify the 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).  Suppurative lesions usually reflect infection. How can microbial agents reach the lung?

 

Slide 42 [WebScope][ImageScope]

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

  • 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 Slide 41 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 sectioned in the right plane) 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.
  • What does the finding of hemosiderin-laden macrophages indicate?
  • In the lung that remains congested over a period of time, the continuing hemorrhage by diapedesis leads to accumulation of hemosiderin. The pigment-containing macrophages which can also be seen in expectorated sputum, have been called “heart failure cells.” Therefore, what is your diagnosis for this case?
  • If sufficiently prolonged (i.e., late chronic passive congestion), what would you expect to see in the lung?
  • Can you list some cardiac conditions that might lead to a lung of this sort?

 

Slide 43 [WebScope][ImageScope]

Liver: This liver specimen was obtained at autopsy of a 44-year-old woman who died after many months of cardiac dysfunction.

  • Under the lowest power of your microscope, you’ll note that this liver has a peculiar pattern of lighter areas alternating with darker areas. (The normal liver would have a fairly homogeneous appearance at this power, i.e., uniformly the darker staining.)
  • With higher magnification it can be seen that the lighter areas are characterized by smaller, atrophic hepatocytes than in the darker areas. The sinusoids are correspondingly widened.
    (The blood has partly drained during specimen dissection yielding an “empty” appearance.)
  • Are the lighter areas with the atrophic hepatocytes centered around the portal triads or central veins? What is the pathophysiology behind this?
  • What is your diagnosis? What can cause this?
  • 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, called “central hemorrhagic necrosis,” is seen only focally in your slide, but can be seen more or less globally in some cases.
  • What would be the appearance of this liver grossly?
  • What clinical evidence might there be of the findings in your slide, in a living patient? If left untreated, what is a possible outcome?

 

Slide 46 [WebScope][ImageScope]

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

  • Within a background of skeletal muscle are large veins, distended with blood. Their distended state immediately suggests that something is wrong. Generally vessels appear 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.
  • The slide is indicative of a thrombus in deep leg vein. Did the patient suddenly die because of this thrombus? If this had been only fluid blood at the time of the patient’s demise, how would it appear in the sections?
  • 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. This is consistent with an ante-mortem thrombus. How would the appearance of this appear from that of a post-mortem clot?
  • Note, also, 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. What does this organization tell you about the age of the thrombus?
  • Had the patient survived, how would the histologic picture in these vessels evolve?
  • What factors might have led to the formation of these thrombi?
  • Can you relate these thrombi to the patient’s demise?

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