When an infarct develops as a consequence of ischemia following complete or partial occlusion of an artery, secondary bleeding will occur from the surrounding veins (which anastomose between the areas supplied by other arteries).
When the infarct is a solid coagulation necrosis (e.g. as is seen in heart and kidney) this hemorrhage will stay at the edge of the infarct and it will appear pale (anemic) with a hemorrhagic border zone.
When the infarct is without a solid structure (e.g. lung, liver and brain) this secondary bleeding will flood the tissue and the infarct will appear red (hemorrhagic).
The morphologically different infarct types thus have a common pathogenesis.
Hemorrhagic infarcts occur in the bowel and the bowel is a pretty solid organ. The hemorrhage occurs when there are blood vessels in the affected area which are still supplied with blood, and is only the case when the organ or the specific area (eg watershed areas in the colon) has two arterial supplies.
The question should rather be: What is the patophysiological mechanism underlying red and pale infarcts, respectively?
Is it possible to generalize on this point: This mechanism leads to red infarcts and that mechanism leads to pale infarcts? Or should one rather take into account that the mechanism leading red/pale infarcts is unique in the specific organ and case where infarction occurs?
I think that red/versus white infarct issue depends on the dual blood supply and the presence of “terminal arteries” providing the blood supply to a defined area without anastomoses. But it is also a “didactic simplification” and in real life many initially pale infarcts become at least “partially red” (e.g. myocardial or cerebral infarcts).This simplification is however clinically important in some cases, such as lung and intestine, because it results in bleeding (hemoptysis and hematochezia).I hope I did not confuse the entire class!
I was of the impression that the red marginal areas occuring in myocardial infarctions after af few days were caused by formation of granulation tissue. Am I wrong?
Ben, I hate to tell a colleage that your are wrong , but maybe it is good for the students to see that the professors do not agree among themselves.
I think that the “mottled appearance” of myocradial infarctions is quite common in the period between 3 and 7 days, well before the granulation tissue develops. My explanation is that the ischemia causes ischemic necrosis of capillaries in the infarcted area and and when the anastomoses (which form in most hearts, thus transforming the ‘terminal arteries” into “non-terminal arteries”) provide the blood it end is disrupted capillaries and hence the bleeding. Actually some of the best microscopic pictures I have taken are from hearts of persons who have died 5-7 days after the onset of infarction, because is their hearts you can see almost all the changes from early ischemia to complete necrosis, neutrophils and complete lysis of neutrophils( corresponding to pus formation). At the edges one may also see contraction band necrosis.
As an aside, I have been asked for legal purposes to “date infarcts” histologically. If you start reading the literature on that topic, most of it is more than 40 years old, and try to apply it to present day situation, you will discover for yourself how unreliable that “scientific approach” is.Infarcts often do not READ THE PATHOLOGY BOOKS, at least that is what I hve concluded at age 70!
My message for the students starting their studies of pathology: let’s keep it simple and talk about an idealized myocardial infarct which is classsifies as PALE infarct , and the type of necrosis is COAGULATIVE.
My main question is, what is the difference between lung stasis and pulmonary arterial hypertension? Why does the stasis give microbleeds in the surrounding tissue, when the pulm. hypertension gives edema in the alveoli? I am especially confused because both pathologic conditions cause stasis of blood in the pulm. Arteries.
So, what are the differences and similarities between stasis and pulmonary hypertension? And are they both caused by left heart insufficiency?
Pulmonary hypertension = High blood pressure in the pulmonary blood circuit (According to current thinking, pulmonary endothelial cell and/or vascular smooth muscle cell dysfunction is the probable cause of pulmonary hypertension). The hypertension leads to the extravasation of fluid thus causing edema.
Lung stasis = Severely reduced blood flow in the pulmonary blood circuit. Leading to the accumulation of blood cells and mechanical stress of the vessel walls and red blood cells, causing these to break thus leading to bleeding.
I think that part of the problems in your understanding the concepts of pulmonary hypertension and stasis pertains to the fact that both terms describe pathophysiologic , i.e. dynamic events and we as pathologists see the consequences.Also these two processes are interrelated one to another.
PULMONARY HYPERTENSION= increased blood pressure in the pulmonary circulation.It is expressed as > 30 mmHg systolic and 12 mmHg diastolic pressure. Most common cause left heart failure .
PULMONARY STASIS= stoppage or diminution of outflow of blood from the lungs.Again the most common cause is left heart failure.It can be seen in histology slides as blood vessels full of blood.
NOTE:Both pulmonary hypertension and stasis can be acute (e.g. myocardial infarction) or chronic ( in chronic left heart failure).
PATHOLOGY: Pathologists can recognize changes of chronic pulmonary hypertension because hypertension damages the blood vessels in the lungs.Later you will learn that similar changes can occur in a disease called primary pulmonary hypertension, a deadly disease of uknown etiology.
Chronic stasis due to heart failure is also known as chronic passive congestion of lungs and it causes fibrosis, bleeding into the alveoli etc, i.e. changes that pathologists sometimes call chronic brown induration of the lungs (“brown” from old hemorrhage and accumulation of RBC derived iron rich pigment hemosiderin!)
There seems to be some confusion amongst the different books and teachers regarding the definitions of a thrombus and a blood clot (Danish: Koagel).
Can someone please define:
1) What is a clot, what is it made of and when does it form?
2) What is a thrombus, what is it made of and when does it form?
3) Do thrombi only form under pathological circumstances?
1) A clot is coagulated blood regardless of where it is found. It is composed of the cells and fibrin of the blood.
2) A thrombus is formed in vivo in a vessel and adheres to the vessel wall. It is composed of the cells and fibrin of the blood.
3) Yes.
– Also, see chapter four (p.94 – ) in Robbins basic pathology.
Deep venous thrombosis is caused by stasis and reduced blood flow – however, what is the initial event triggering venous thrombosis – is it thrombocytes adhering to endothelial irregularities or may several factors be involved?
The initial event in thrombosis (often referred to as primary hemostasis) traditionally is described as the adherence of platelets to the injured vessel wall (damaged endothelium of subendothelial tissue leading to the formation of a plug of platelets). When you observe individual patients however, it is often hard to judge whether stasis, endothelial injury or hypercoagulability (e.g. thrombofilia) is the primary cause and many cases of clinical thrombosis are “spontaneous” without any clear-cut explanation.
However, we do know that the above mentioned three factors of Virchow’s triade can trigger and increases rik of thrombosis.
Our ‘virtual microscopy’ describes lines of Zahn as appearing in veins and small arteries (characterized by slow blood flow). However, Robbins states that they appear in settings of flowing blood and therefore NOT in veins and small arteries.
Which is it?
Lines of Zahn can be seen in veins with low flow – one example is given in Lars B Nielsen’s lecture. The crucial question is probably how low the flow can be before you have complete occlusion rather than progressive growth of the trombus?
Hi Yohannes – what do you mean by ‘make me use the website’?
This is our official welcome:
Welcome to the blog for the pathology courses on the faculty of health science in Copenhagen. The intention of this blog is to provide a forum for discussion of issues and controversial topics of general pathological nature. Students, teachers and visitors of the site are welcome to post comments or ask questions on any topic within the field of general pathology.
Indeed, biology is seldom completely correctly described as dichotomic. There is some overlap between white and red infarcts: liver infarction is one example.
Liver infarctions are rare because of the liver’s dual blood supply and the hepatic sinusoid structure.
Acute occlusion of the hepatic artery is unusual but may occur as a result of embolism, polyarteritis nodosa, or accidental surgical ligation. In these settings irregular, pale areas – often surrounded be a hyperemic zone – reflect the causative ischemic necrosis.
I am having some trouble distinguishing between etiology and pathogenesis.
E.g. during atherosclerosis:
– Etiology = e.g. cholesterol, hypertension, smoking, obesity, diabetes etc.
– Pathogenesis = intimal inflammation (possibly caused by the deposition of cholesterol).
Is it “simply” a question of cause and effect/process?
Etiology states the cause of the disease, whereas pathogenesis states the disease mechanisms.
For atherosclerosis the distinction is perhaps a little difficult, since we have not demonstrated a single (or few) causes leading the the changes, but rather a combination of several issues. Another example might better illustrate the difference: For a simple acute cystitis (Danish: blærebetændelse), the etiology is most often bacterial infection with E. coli, whereas the pathogenesis includes the effects on the epithelial lining of the bacteria and the initiation and progression of an acute inflammatory response. It is the latter inflammation that causes the symptoms and the signs.
The books state that a hyperemic or hemorrhagic border zone surrounding the infarction often arises – do these conditions coexist or is it one or the other, or are they the same? If they are the same, which is more correct to state (i.e. is it hyperemia or hemorrhage)?
Dear Nikolaj,
Hyperemic and haemorrhagic is not the same, although the clinical presention might be identical. Hyperemia is a passive change with increased blood flow in a localized area caused by dilatation of capillaries. That is, in hyperemia the blood components do not leave the vessels. Haemorrhage is bleeding into the tissue. The redness in this case is thus caused by the leaving of red blood cells from the blood vessels to the surrounding tissue. When this is said, hyperemia and haemorrhage can occur simultaneously, depending of the cause of the disorder.
The nomenclature differs slightly between the recommended textbooks. It is correct that “progression” means enlargement of the thrombus with additional accretion of platelets and fibrin. The risk of occlusion and embolization increases with the enlargement.
In Robbins Basic Pathology, the different fates of a thrombus are called (8th ed. p. 97, 9th ed. p. 89):
1) propagation (=progression)
2) embolization
3) dissolution (=thrombolysis)
4) organization and recanalization
I have a question concerning lung infarct (as many others apparently):
The Danish book states that an embolus in general only results in lung infarct in patients with an already defective lung circulation, according to left sided heart failure, lung fibrosis i.e. Chronic heart failure results in lung stasis and destruction of the lung capillaries and thereby creates physiological end arteries.
My question is: will we expect to see an anaemic or haemorhagic lung infarct in this case?
My guess would be an anaemic, but I am unsure if you see this sort of infarct in organs supplied by two sets of arteries.
Thank you!
About anemic and hemorhagic infarcts in the brain:
It is considered a general rule that anemic infarcts develop following thrombosis whereas hemorhagic infarcts develop following embolic occlusions of the arteries. Is there however any systematic research supporting these presumptions?
– In the brain both anemic and hemorhagic infarcts are known to occur.
What is the difference between red (hemorrhagic) and white (anemic) infarcts?
When an infarct develops as a consequence of ischemia following complete or partial occlusion of an artery, secondary bleeding will occur from the surrounding veins (which anastomose between the areas supplied by other arteries).
When the infarct is a solid coagulation necrosis (e.g. as is seen in heart and kidney) this hemorrhage will stay at the edge of the infarct and it will appear pale (anemic) with a hemorrhagic border zone.
When the infarct is without a solid structure (e.g. lung, liver and brain) this secondary bleeding will flood the tissue and the infarct will appear red (hemorrhagic).
The morphologically different infarct types thus have a common pathogenesis.
I have to disagree.
Hemorrhagic infarcts occur in the bowel and the bowel is a pretty solid organ. The hemorrhage occurs when there are blood vessels in the affected area which are still supplied with blood, and is only the case when the organ or the specific area (eg watershed areas in the colon) has two arterial supplies.
The question should rather be: What is the patophysiological mechanism underlying red and pale infarcts, respectively?
Is it possible to generalize on this point: This mechanism leads to red infarcts and that mechanism leads to pale infarcts? Or should one rather take into account that the mechanism leading red/pale infarcts is unique in the specific organ and case where infarction occurs?
Can someone please comment on this?
I think that red/versus white infarct issue depends on the dual blood supply and the presence of “terminal arteries” providing the blood supply to a defined area without anastomoses. But it is also a “didactic simplification” and in real life many initially pale infarcts become at least “partially red” (e.g. myocardial or cerebral infarcts).This simplification is however clinically important in some cases, such as lung and intestine, because it results in bleeding (hemoptysis and hematochezia).I hope I did not confuse the entire class!
I was of the impression that the red marginal areas occuring in myocardial infarctions after af few days were caused by formation of granulation tissue. Am I wrong?
Ben, I hate to tell a colleage that your are wrong , but maybe it is good for the students to see that the professors do not agree among themselves.
I think that the “mottled appearance” of myocradial infarctions is quite common in the period between 3 and 7 days, well before the granulation tissue develops. My explanation is that the ischemia causes ischemic necrosis of capillaries in the infarcted area and and when the anastomoses (which form in most hearts, thus transforming the ‘terminal arteries” into “non-terminal arteries”) provide the blood it end is disrupted capillaries and hence the bleeding. Actually some of the best microscopic pictures I have taken are from hearts of persons who have died 5-7 days after the onset of infarction, because is their hearts you can see almost all the changes from early ischemia to complete necrosis, neutrophils and complete lysis of neutrophils( corresponding to pus formation). At the edges one may also see contraction band necrosis.
As an aside, I have been asked for legal purposes to “date infarcts” histologically. If you start reading the literature on that topic, most of it is more than 40 years old, and try to apply it to present day situation, you will discover for yourself how unreliable that “scientific approach” is.Infarcts often do not READ THE PATHOLOGY BOOKS, at least that is what I hve concluded at age 70!
My message for the students starting their studies of pathology: let’s keep it simple and talk about an idealized myocardial infarct which is classsifies as PALE infarct , and the type of necrosis is COAGULATIVE.
How do inflammatory cells invade necrotic tissue in case of an infarct when the definition of infarction is necrosis caused by ischemia?
Inflammatory cells can enter infarcted tissue by chemotaxis through the surrounding non-ischemic tissue.
My main question is, what is the difference between lung stasis and pulmonary arterial hypertension? Why does the stasis give microbleeds in the surrounding tissue, when the pulm. hypertension gives edema in the alveoli? I am especially confused because both pathologic conditions cause stasis of blood in the pulm. Arteries.
So, what are the differences and similarities between stasis and pulmonary hypertension? And are they both caused by left heart insufficiency?
They both derive from the same cause. High pressure in the pulmonary system due to most commonly congestive heart failure.
Is it possible to predict which one will appear in a patient?
Pulmonary hypertension = High blood pressure in the pulmonary blood circuit (According to current thinking, pulmonary endothelial cell and/or vascular smooth muscle cell dysfunction is the probable cause of pulmonary hypertension). The hypertension leads to the extravasation of fluid thus causing edema.
Lung stasis = Severely reduced blood flow in the pulmonary blood circuit. Leading to the accumulation of blood cells and mechanical stress of the vessel walls and red blood cells, causing these to break thus leading to bleeding.
AL:
I think that part of the problems in your understanding the concepts of pulmonary hypertension and stasis pertains to the fact that both terms describe pathophysiologic , i.e. dynamic events and we as pathologists see the consequences.Also these two processes are interrelated one to another.
PULMONARY HYPERTENSION= increased blood pressure in the pulmonary circulation.It is expressed as > 30 mmHg systolic and 12 mmHg diastolic pressure. Most common cause left heart failure .
PULMONARY STASIS= stoppage or diminution of outflow of blood from the lungs.Again the most common cause is left heart failure.It can be seen in histology slides as blood vessels full of blood.
NOTE:Both pulmonary hypertension and stasis can be acute (e.g. myocardial infarction) or chronic ( in chronic left heart failure).
PATHOLOGY: Pathologists can recognize changes of chronic pulmonary hypertension because hypertension damages the blood vessels in the lungs.Later you will learn that similar changes can occur in a disease called primary pulmonary hypertension, a deadly disease of uknown etiology.
Chronic stasis due to heart failure is also known as chronic passive congestion of lungs and it causes fibrosis, bleeding into the alveoli etc, i.e. changes that pathologists sometimes call chronic brown induration of the lungs (“brown” from old hemorrhage and accumulation of RBC derived iron rich pigment hemosiderin!)
What leads to lung infarction following embolized deep venous thrombosis?
Poor perfusion of the lung, typically manifested when the patient displays chronic lung stasis.
There seems to be some confusion amongst the different books and teachers regarding the definitions of a thrombus and a blood clot (Danish: Koagel).
Can someone please define:
1) What is a clot, what is it made of and when does it form?
2) What is a thrombus, what is it made of and when does it form?
3) Do thrombi only form under pathological circumstances?
1) A clot is coagulated blood regardless of where it is found. It is composed of the cells and fibrin of the blood.
2) A thrombus is formed in vivo in a vessel and adheres to the vessel wall. It is composed of the cells and fibrin of the blood.
3) Yes.
– Also, see chapter four (p.94 – ) in Robbins basic pathology.
Deep venous thrombosis is caused by stasis and reduced blood flow – however, what is the initial event triggering venous thrombosis – is it thrombocytes adhering to endothelial irregularities or may several factors be involved?
The initial event in thrombosis (often referred to as primary hemostasis) traditionally is described as the adherence of platelets to the injured vessel wall (damaged endothelium of subendothelial tissue leading to the formation of a plug of platelets). When you observe individual patients however, it is often hard to judge whether stasis, endothelial injury or hypercoagulability (e.g. thrombofilia) is the primary cause and many cases of clinical thrombosis are “spontaneous” without any clear-cut explanation.
However, we do know that the above mentioned three factors of Virchow’s triade can trigger and increases rik of thrombosis.
Our ‘virtual microscopy’ describes lines of Zahn as appearing in veins and small arteries (characterized by slow blood flow). However, Robbins states that they appear in settings of flowing blood and therefore NOT in veins and small arteries.
Which is it?
I agree with Robbins – Lines of Zahn appear in the setting of flowing blood.
Lines of Zahn can be seen in veins with low flow – one example is given in Lars B Nielsen’s lecture. The crucial question is probably how low the flow can be before you have complete occlusion rather than progressive growth of the trombus?
make me use the website.I am a medical student
Hi Yohannes – what do you mean by ‘make me use the website’?
This is our official welcome:
Welcome to the blog for the pathology courses on the faculty of health science in Copenhagen. The intention of this blog is to provide a forum for discussion of issues and controversial topics of general pathological nature. Students, teachers and visitors of the site are welcome to post comments or ask questions on any topic within the field of general pathology.
For a quick overview of the blog structure – use our sitemap:
http://pathology.edublogs.org/files/2012/03/Site-map-voypeo.jpg
Read the guide on posting comments and questions:
http://pathology.edublogs.org/how-to-post-comments-and-questions/
Best regards,
Flemming Fryd Johansen & Ida Søndergaard Rasmussen
With regards to liver infarctions: Are they red or white or both?
Ivan’s lecture mentioned liver infarctions as an example of hemorrhagic infarcts, however, this is controversial if you look into various text books.
Indeed, biology is seldom completely correctly described as dichotomic. There is some overlap between white and red infarcts: liver infarction is one example.
Liver infarctions are rare because of the liver’s dual blood supply and the hepatic sinusoid structure.
Acute occlusion of the hepatic artery is unusual but may occur as a result of embolism, polyarteritis nodosa, or accidental surgical ligation. In these settings irregular, pale areas – often surrounded be a hyperemic zone – reflect the causative ischemic necrosis.
Dear teachers (and students) of pathology,
I am having some trouble distinguishing between etiology and pathogenesis.
E.g. during atherosclerosis:
– Etiology = e.g. cholesterol, hypertension, smoking, obesity, diabetes etc.
– Pathogenesis = intimal inflammation (possibly caused by the deposition of cholesterol).
Is it “simply” a question of cause and effect/process?
Dear Sara,
Etiology states the cause of the disease, whereas pathogenesis states the disease mechanisms.
For atherosclerosis the distinction is perhaps a little difficult, since we have not demonstrated a single (or few) causes leading the the changes, but rather a combination of several issues. Another example might better illustrate the difference: For a simple acute cystitis (Danish: blærebetændelse), the etiology is most often bacterial infection with E. coli, whereas the pathogenesis includes the effects on the epithelial lining of the bacteria and the initiation and progression of an acute inflammatory response. It is the latter inflammation that causes the symptoms and the signs.
Regarding infarction:
The books state that a hyperemic or hemorrhagic border zone surrounding the infarction often arises – do these conditions coexist or is it one or the other, or are they the same? If they are the same, which is more correct to state (i.e. is it hyperemia or hemorrhage)?
Dear Nikolaj,
Hyperemic and haemorrhagic is not the same, although the clinical presention might be identical. Hyperemia is a passive change with increased blood flow in a localized area caused by dilatation of capillaries. That is, in hyperemia the blood components do not leave the vessels. Haemorrhage is bleeding into the tissue. The redness in this case is thus caused by the leaving of red blood cells from the blood vessels to the surrounding tissue. When this is said, hyperemia and haemorrhage can occur simultaneously, depending of the cause of the disorder.
There are 4 turn outs for thrombosis:
Thrombolysis
Emboly
Organisation
Progression
What is progression?
Thank you
Am a student myself but as I understand it,
progression means that the thrombus grows in size – is this correct?
The nomenclature differs slightly between the recommended textbooks. It is correct that “progression” means enlargement of the thrombus with additional accretion of platelets and fibrin. The risk of occlusion and embolization increases with the enlargement.
In Robbins Basic Pathology, the different fates of a thrombus are called (8th ed. p. 97, 9th ed. p. 89):
1) propagation (=progression)
2) embolization
3) dissolution (=thrombolysis)
4) organization and recanalization
One of the teachers talked about a new article regarding septic shock. I’d very much like to read it, but I can’t figure out where to find it.
Hi Carolina,
Do you remember the teacher’s name?
I have a question concerning lung infarct (as many others apparently):
The Danish book states that an embolus in general only results in lung infarct in patients with an already defective lung circulation, according to left sided heart failure, lung fibrosis i.e. Chronic heart failure results in lung stasis and destruction of the lung capillaries and thereby creates physiological end arteries.
My question is: will we expect to see an anaemic or haemorhagic lung infarct in this case?
My guess would be an anaemic, but I am unsure if you see this sort of infarct in organs supplied by two sets of arteries.
Thank you!
Kind regards,
Marie
About anemic and hemorhagic infarcts in the brain:
It is considered a general rule that anemic infarcts develop following thrombosis whereas hemorhagic infarcts develop following embolic occlusions of the arteries. Is there however any systematic research supporting these presumptions?
– In the brain both anemic and hemorhagic infarcts are known to occur.