Causes and Types of Tissue Infarction
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Causes and Types of Tissue Infarction
- 2. Common clinical examples ofCommon clinical examples of infarction:infarction: • Myocardial infarction • Cerebral infarction • Pulmonary infarction • Gangrene of limbs
- 7. Atrial fibrillationAtrial fibrillation with mural thrombiwith mural thrombi
- 10. INFARCTIONINFARCTION Def: An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue
- 11. Basis of infarction:Basis of infarction: Vascular compromise • Obstruction to arterial supply • Impeded venous drainage
- 12. Common causes:Common causes: Arterial occlusion:Arterial occlusion: • 99% result from arterial occlusion (thrombotic or embolic events) • Other causes: local vasospasm expansion of an atheroma (hemorrhage within a plaque) extrinsic compression of a vessel (e.g., by tumor) twisting of the vessels (e.g., in testicular torsion or bowel volvulus) compression of the blood supply by edema or by entrapment in a hernia sac traumatic rupture of the blood supply Venous occlusion:Venous occlusion: (organs with single veinous out flow) • Thrombosis
- 13. ClassificationClassification Based on the colour & presence or absence of infection
- 14. MorphologyMorphology Red (hemorrhagic) infarctsRed (hemorrhagic) infarcts occur (1) with venous occlusions (such as in ovarian torsion); (2) in loose tissues (such as lung), which allow blood to collect in the infarcted zone; (3) in tissues with dual circulations (e.g., lung and small intestine), permitting flow of blood from the unobstructed vessel into the necrotic zone (obviously such perfusion is not sufficient to rescue the ischemic tissues); (4) in tissues that were previously congested because of sluggish venous outflow; and (5) when flow is re-established to a site of previous arterial occlusion and necrosis (e.g., following fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion)
- 15. MorphologyMorphology White (anemic) infarctsWhite (anemic) infarcts occur with arterial occlusions in solid organs with end-arterial circulation (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds
- 16. Most of the infarcts are wedgeMost of the infarcts are wedge shapedshaped • with the occluded vessel at the apex and the periphery of the organ forming the base • when the base is a serosal surface, there is often an overlying fibrinous exudate. • The lateral margins may be irregular, reflecting the pattern of vascular supply from adjacent vessels.
- 17. Margins become hyperemicMargins become hyperemic • Initially:Initially: all infarcts are poorly defined and slightly hemorrhagic • Later:Later: margins tend to become better defined by a narrow rim of hyperemia attributable to inflammation at the edge of the lesion.
- 18. Examples of infarcts: A, Hemorrhagic, roughly wedge-shaped pulmonary infarct. B, Sharply demarcated white infarct in the spleen.
- 23. Histology of infarctionHistology of infarction Changes depends on time Ischemic coagulative necrosis Inflammation Liquifactive necrosis Abscess formation Scar tissue
- 24. Remote kidney infarct, now replaced by a large fibrotic cortical scar.
- 25. Factors That InfluenceFactors That Influence Development of an InfarctDevelopment of an Infarct The major determinants include: (1) the nature of the vascular supply; (2) the rate of development of the occlusion; (3) the vulnerability of a given tissue to hypoxia; and (4) the blood oxygen content.
- 26. Factors That InfluenceFactors That Influence Development of an InfarctDevelopment of an Infarct The major determinants: (1) Nature of the vascular supply (double or single blood supply) The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage. Lungs, for example, have a dual pulmonary and bronchial artery blood supply; thus, obstruction of a small pulmonary arteriole does not cause infarction in an otherwise healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, and the hand and forearm, with their dual radial and ulnar arterial supply, are all relatively insensitive to infarction. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction.
- 27. Factors That InfluenceFactors That Influence Development of an InfarctDevelopment of an Infarct The major determinants: (2) Rate of development of occlusion. Slowly developing occlusions are less likely to cause infarction because they provide time for the development of alternative perfusion pathways. For example, small interarteriolar anastomoses —normally with minimal functional flow—interconnect the three major coronary arteries in the heart. If one of the coronaries is only slowly occluded (i.e., by an encroaching atherosclerotic plaque), flow within this collateral circulation may increase sufficiently to prevent infarction, even though the major coronary artery is eventually occluded.
- 28. Factors That InfluenceFactors That Influence Development of an InfarctDevelopment of an Infarct The major determinants: (3) Vulnerability to hypoxia. The susceptibility of a tissue to hypoxia influences the likelihood of infarction. Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. Myocardial cells, although hardier than neurons, are also quite sensitive and die after only 20 to 30 minutes of ischemia. In contrast, fibroblasts within myocardium remain viable even after many hours of ischemia
- 29. Factors That InfluenceFactors That Influence Development of an InfarctDevelopment of an Infarct The major determinants: (4) Oxygen content of blood. The partial pressure of oxygen in blood also determines the outcome of vascular occlusion. Partial flow obstruction of a small vessel in an anemic or cyanotic patient might lead to tissue infarction, whereas it would be without effect under conditions of normal oxygen tension. In this way, congestive heart failure, with compromised flow and ventilation, could cause infarction in the setting of an otherwise inconsequential blockage.
- 30. Factors That InfluenceFactors That Influence Development of an InfarctDevelopment of an Infarct The major determinants: (4) Oxygen content of blood. What is the critical value for HGB ?
- 33. Inguinal hernia
- 34. Inguinal hernia
- 36. Umbilical hernia
- 37. Umbilical Hernia
- 38. Umbilical hernia
- 39. Volvulus
- 40. Volvulus
- 42. Torsion - ovary
- 43. Torsion - ovary
- 44. Torsion - ovary
- 45. Torsion – Fallopian tube
- 46. Torsion testis – torsion of hydatid
- 47. Torsion - testis
- 50. Gangrene ofGangrene of the fingersthe fingers
- 54. E N DE N D
Hinweis der Redaktion
- Nearly 99% of all infarcts result from thrombotic or embolic events, and almost all result from arterial occlusion. Occasionally, infarction may also be caused by other mechanisms, such as local vasospasm, expansion of an atheroma owing to hemorrhage within a plaque, or extrinsic compression of a vessel (e.g., by tumor). Other uncommon causes include twisting of the vessels (e.g., in testicular torsion or bowel volvulus), compression of the blood supply by edema or by entrapment in a hernia sac, or traumatic rupture of the blood supply. -------------------------------- Although venous thrombosis may cause infarction, it more often merely induces venous obstruction and congestion. Usually, bypass channels rapidly open after the thrombosis, providing some outflow from the area, which, in turn, improves the arterial inflow. Infarcts caused by venous thrombosis are more likely in organs with a single venous outflow channel, such as the testis and ovary. -------------------------
- Infarcts are classified on the basis of their color and the presence or absence of microbial infection. Therefore, infarcts may be either red (hemorrhagic) or white (anemic) and may be either septic or bland.   •   Red (hemorrhagic) infarcts occur (1) with venous occlusions (such as in ovarian torsion); (2) in loose tissues (such as lung), which allow blood to collect in the infarcted zone; (3) in tissues with dual circulations (e.g., lung and small intestine), permitting flow of blood from the unobstructed vessel into the necrotic zone (obviously such perfusion is not sufficient to rescue the ischemic tissues); (4) in tissues that were previously congested because of sluggish venous outflow; and (5) when flow is re-established to a site of previous arterial occlusion and necrosis (e.g., following fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion) •   White (anemic) infarcts occur with arterial occlusions in solid organs with end-arterial circulation (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds.
- Morphology. Infarcts are classified on the basis of their color (reflecting the amount of hemorrhage) and the presence or absence of microbial infection. Therefore, infarcts may be either red (hemorrhagic) or white (anemic) and may be either septic or bland.   •   Red (hemorrhagic) infarcts occur (1) with venous occlusions (such as in ovarian torsion); (2) in loose tissues (such as lung), which allow blood to collect in the infarcted zone; (3) in tissues with dual circulations (e.g., lung and small intestine), permitting flow of blood from the unobstructed vessel into the necrotic zone (obviously such perfusion is not sufficient to rescue the ischemic tissues); (4) in tissues that were previously congested because of sluggish venous outflow; and (5) when flow is re-established to a site of previous arterial occlusion and necrosis (e.g., following fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion) ( Fig. 4-19A ).  •   White (anemic) infarcts occur with arterial occlusions in solid organs with end-arterial circulation (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds ( Fig. 4-19B ).
- Morphology. Infarcts are classified on the basis of their color (reflecting the amount of hemorrhage) and the presence or absence of microbial infection. Therefore, infarcts may be either red (hemorrhagic) or white (anemic) and may be either septic or bland.   •   Red (hemorrhagic) infarcts occur (1) with venous occlusions (such as in ovarian torsion); (2) in loose tissues (such as lung), which allow blood to collect in the infarcted zone; (3) in tissues with dual circulations (e.g., lung and small intestine), permitting flow of blood from the unobstructed vessel into the necrotic zone (obviously such perfusion is not sufficient to rescue the ischemic tissues); (4) in tissues that were previously congested because of sluggish venous outflow; and (5) when flow is re-established to a site of previous arterial occlusion and necrosis (e.g., following fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion) ( Fig. 4-19A ).  •   White (anemic) infarcts occur with arterial occlusions in solid organs with end-arterial circulation (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds ( Fig. 4-19B ).
- At the outset, all infarcts are poorly defined and slightly hemorrhagic. With time margins tend to become better defined by a narrow rim of hyperemia attributable to inflammation at the edge of the lesion.
- Figure 4-19Â Examples of infarcts. A, Hemorrhagic, roughly wedge-shaped pulmonary infarct. B, Sharply demarcated white infarct in the spleen.
- The dominant histologic characteristic of infarction is ischemic coagulative necrosis ( Chapter 1 ). It is important to recall that if the vascular occlusion has occurred shortly (minutes to hours) before the death of the patient, no demonstrable histologic changes may be evident; if the patient survives even 12 to 18 hours, the only change present may be hemorrhage. An inflammatory response begins to develop along the margins of infarcts within a few hours and is usually well defined within 1 or 2 days. Inflammation at these sites is incited by the necrotic material; given sufficient time, there is gradual degradation of the dead tissue with phagocytosis of the cellular debris by neutrophils and macrophages. Eventually the inflammatory response is followed by a reparative response beginning in the preserved margins ( Chapter 2 ). In stable or labile tissues, some parenchymal regeneration may occur at the periphery where the underlying stromal architecture has been spared. However, most infarcts are ultimately replaced by scar tissue ( Fig. 4-20 ). The brain is an exception to these generalizations; as with all other causes of cell death, ischemic injury in the central nervous system results in liquefactive necrosis. Septic infarctions may develop when embolization occurs by fragmentation of a bacterial vegetation from a heart valve or when microbes seed an area of necrotic tissue. In these cases, the infarct is converted into an abscess, with a correspondingly greater inflammatory response ( Chapter 2 ). The eventual sequence of organization, however, follows the pattern already described.
- Figure 4-20Â Remote kidney infarct, now replaced by a large fibrotic cortical scar.
- Nature of the vascular supply. The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage. Lungs, for example, have a dual pulmonary and bronchial artery blood supply; thus, obstruction of a small pulmonary arteriole does not cause infarction in an otherwise healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, and the hand and forearm, with their dual radial and ulnar arterial supply, are all relatively insensitive to infarction. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction.
- Nature of the vascular supply. The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage. Lungs, for example, have a dual pulmonary and bronchial artery blood supply; thus, obstruction of a small pulmonary arteriole does not cause infarction in an otherwise healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, and the hand and forearm, with their dual radial and ulnar arterial supply, are all relatively insensitive to infarction. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction.
- Nature of the vascular supply. The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage. Lungs, for example, have a dual pulmonary and bronchial artery blood supply; thus, obstruction of a small pulmonary arteriole does not cause infarction in an otherwise healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, and the hand and forearm, with their dual radial and ulnar arterial supply, are all relatively insensitive to infarction. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction.
- Nature of the vascular supply. The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage. Lungs, for example, have a dual pulmonary and bronchial artery blood supply; thus, obstruction of a small pulmonary arteriole does not cause infarction in an otherwise healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, and the hand and forearm, with their dual radial and ulnar arterial supply, are all relatively insensitive to infarction. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction.