Pulmonary changes: Brown induration
During venous congestion, erythrocytes escape vessels (diapedesis) and break down. The pigment hemosiderin is formed, which is engulfed by macrophages. These cells, called hemosiderophages, can be found in the patient's sputum — clinically referred to as "heart failure cells".
Macroscopically, the lungs become dense and acquire a brown tint (induratio fusca pulmonum). Perl's stain is used for precise identification of iron in the pigment.
Chronic congestion triggers diffuse connective tissue proliferation in the interalveolar septa and around bronchovascular bundles. Two factors contribute to the progression of sclerosis:
- Lymphatic system insufficiency (goes through resorption and mechanical stages when capillaries become clogged with siderophages).
- Action of SH-ferritin (a component of hemosiderin). It has a sclerogenic effect and paralyzes vessels, further increasing hyperemia.
Liver changes: Nutmeg liver
Venous blood pools in the central regions of the hepatic lobules. High pressure in the hepatic artery system prevents it from moving toward the periphery. Because of this, the organ enlarges, becomes dense, and its edges become rounded.
On cross-section, the liver acquires a mottled appearance resembling a nutmeg:
- Lobule center: dark red due to pronounced hyperemia, hemorrhages, and hepatocyte necrosis.
- Lobule periphery: yellowish-brown due to the development of cellular fatty change.
Chronic hypoxia leads to connective tissue proliferation along the sinusoids — their capillarization occurs. This forms a capillary-parenchymal block. At the final stage of the process, nutmeg fibrosis or cardiac micronodular cirrhosis of the liver develops.
Renal changes: Cyanotic induration
Kidneys in congestion enlarge, become dense and cyanotic. The pathological process is due to a combination of venous congestion and lymphostasis. Maximum changes are localized in the medulla, which is associated with blood shunting through the juxtamedullary shunt.
In chronic heart failure, the damage mechanism looks like this:
- Cardiac output decreases, renal blood flow drops.
- Tissue hypoxia increases, which stimulates the renin-angiotensin-aldosterone system (RAAS).
- RAAS activation causes spasm of intrarenal arteries.
- Result: epithelial dystrophy of the renal tubules increases and stromal sclerosis is activated.
Splenic changes: Cyanotic induration
Congestive splenomegaly develops — the organ significantly increases in size and becomes dense. Specific macroscopic sign: on cross-section, the pulp yields absolutely no scrapings.
Microscopic examination shows that lymphoid follicles are atrophied, and the red pulp is markedly hyperemic and sclerosed. Clinically, such morphological changes are most pronounced in portal hypertension syndrome.
Briefly: answers to topical questions
What hemoglobinogenic pigments are formed during erythrocyte destruction in hemorrhage sites besides hemosiderin?
Besides hemosiderin, hematoidin is formed during erythrocyte destruction in hemorrhage sites.
- Hematoidin is a non-iron-containing hemoglobinogenic pigment. It forms under conditions of oxygen deficiency in the center of old hemorrhages and gives the tissue a characteristic yellowish tint. Unlike hemosiderin, which is deposited by macrophages at the periphery of the hematoma, hematoidin is localized in the central zone.
To remember organ colors during congestion: Lungs — "rusty" (brown from iron). Liver — "mottled" (nutmeg: red and yellow). Kidneys and spleen — "blue" (cyanotic from venous blood).
Class and exam questions
What are "heart failure cells"?
These are macrophages (hemosiderophages) laden with hemosiderin pigment. They are detected in the sputum of patients with brown induration of the lungs.
Why is precisely the center of the lobule affected in nutmeg liver?
Venous blood pools in the central part of the sinusoids, causing hypoxia and necrosis there. Higher pressure in the hepatic artery system prevents it from moving to the periphery.
Which biochemical factor enhances sclerosis in the lungs during congestion?
This is SH-ferritin, a part of hemosiderin. It stimulates fibrosis and dilates vessels, exacerbating venous congestion.
Why does the medulla suffer during renal congestion?
Due to the redistribution of blood flow and blood shunting through the juxtamedullary shunt, which leads to pronounced venous congestion specifically in this zone.
What else to study on this topic
- Mechanisms of formation and metabolism of hemosiderin in tissues
- Stages of lymphatic insufficiency in chronic congestion
- Pathogenesis of the capillary-parenchymal block in the liver
- The role of the juxtamedullary shunt in renal hemodynamics
- Impact of RAAS activation on the progression of nephrosclerosis
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Morphology of chronic venous congestion" and 4,414 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in the section "Disorders of Blood and Lymph Circulation"
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.