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Infarction
- 1. GOOD MORNING DR V.VASUNDHARA DEPARTMENT OF CONSERVATIVEDENISTRY AND ENDODONTICS.
- 2.
- 3. CONTENTS Definition Etiology Types Pathogenesis Pathologic changes Infarcts ofdifferent organs References
- 4. DEFINITION Localized area ofischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage………………….ROBBINS
- 5. ETIOLOGY •Most Commonly,Infarcts arecaused by Interruption in arterial blood supply, called ischemic necrosis •Less commonly,Venous obstruction can produce infarcts termed stagnant hypoxia
- 6. •Generally,Sudden, complete andcontinuous occlusion by thrombosis or embolism •Torsion of a vessel, e.g. in testicular torsion •Traumatic rupture or vascular compromise by edema, e.g. anterior compartment syndrome. • Nonocclusive circulatory insufficiency.
- 7. TYPES COLOUR Red or hemorrhagicPaleor anemic
- 8. • Depending onAge a.Recent or fresh. b.Old or healed. •Presence or absence of infection. a.Bland – when free of bacterial contamination b.Septic – when infected.
- 9. PATHOGENESIS Localized hyperemia Edema andhemorrhage Cellular changes Progressive proteolysis of necrotic tissue and lysis of red cells An acute inflammatory reaction and hyperaemia Blood pigments liberated by hemolysis Progressive ingrowth of granulation tissue
- 10. PATHOLOGIC CHANGES •Grossly, infarctsof solid organs -wedge-shaped • apex -pointing towards occluded artery wide base - on the surface of the organ. •Infarcts due to arterial occlusion -pale venous obstruction - hemorrhagic. •Most infarcts become pale later as the red cell are lysed but pulmonary infarcts never become pale due to extensive amount of blood.
- 11. •Cerebral infarcts :poorly defined with central softening (encephalomalacia). •Recent infarcts : slightly elevated over the surface • Old infarcts : shrunken , depressed under the surface of the organ.
- 12. Microscopically •The pathognomic cytologicchange in all infarcts is coagulative (ischaemic) necrosis of the affected area of tissue or organ. •In cerebral infarcts- characteristic liquefactive necrosis.
- 13. At periphery ofan infarct, inflammatory reaction is noted. Initially neutrophils predominate ,later macrophages and fibroblasts appear. Eventually, necrotic area is replaced by fibrous scar tissue, may show dystrophic calcification. In cerebral infarcts, the liquefactive necrosis is followed by gliosis i.e. replacement by microglial cells distended by fatty material (gitter cells).
- 14. INFARCTS OF DIFFERENTORGANS Location Gross appearance Outcome 1 Myocardial infraction Pale Frequently lethal 2 Pulmonary infraction Hemorrhagic Less commonly fatal 3 Cerebral infraction Hemorrhagic & Pale Fatal if massive 4 Intestinal infraction Hemorrhagic Frequently lethal 5 Renal infraction Pale Not lethal unless massive & bilateral 6 Infract spleen Pale Not lethal 7 Infract liver Pale Not lethal 8 Infracts of lower extremity Pale Not lethal
- 15. LUNG INFARCTION •Embolism ofthe pulmonary arteries • May occur in patients who have inadequate circulation : Chronic lung diseases • Congestive heart failure.
- 17. GROSS: pulmonary infarcts :wedge-shaped Base on the pleura, hemorrhagic, variable in size lower lobes. Cut surface : dark purple Shows blocked vessel near the apex of the infarcted area. Old organized and healed pulmonary infarcts appear as retracted fibrous scars.
- 18. Microscopically • Characteristic histologicfeature : coagulative necrosis of the alveolar walls. •Initially: infiltration by neutrophils and intense alveolar capillary congestion hemosiderin, phagocytes and granulation tissue.
- 19. KIDNEY INFARCTION Renal infarctsare Common caused by Thromboemboli most commonly originating from heart such as mural thrombi in the left atrium ,MI,Vegetative endocarditis Less commonly renal artery atherosclerosis, arteritis sickle cell anemia.
- 20. Grossly:multiple and bilateral Characteristically:wedgeshape Base - under capsule Apex-pointing towards medulla Narrow rim of preserved renal tissue is spared Cut surface in first 2 to 3 days : red and congested 4th day: centre turns pale yellow. 1 week: typically anemic , depressed below the surface
- 21. Microscopically Characteristic: affected area showscoagulative necrosis of renal parenchyma i.e. ghosts of renal tubules and glomeruli without intact nuclei and cytoplasmic content. The margin of the infarct shows inflammatory reaction – initially acute but later macrophages and fibrous tissue predominate.
- 22. INFARCT SPLEEN •Common sitefor infarcts •It results from Occlusion of one of the splenic arteries or its branches. Most common cause : thromboemboli arising in heart (eg.mural thrombi in the left atrium vegetative endocarditis myocarditis myocardial infarction)
- 23. •Less frequently byobstruction of microcirculation (e.g. in myeloproliferative diseases, sickle cell anemia, arteritis, Hodgkin's disease, bacterial infections). •Grossly, splenic infarcts are often multiple. •Characteristically pale or anemic, wedge-shaped • base - at the periphery • apex -pointing towards hilum.
- 24. •Features are similarto those found in anemic infarcts in kidney. •Coagulative necrosis and inflammatory reaction are seen. •Later, the necrotic tissues is replaced by shrunken fibrous scar. MICROSCOPICALLY
- 25. INFARCT LIVER • Uncommon •Dual blood supply •Obstruction of the portal vein is usually secondary to other diseases : Hepatic cirrhosis, IV invasion of primary CA of liver, CA of pancreas • Generally does not produce ischemic infarction but instead reduced blood supply to hepatic parenchyma causes non-ischemic infarct called infarct of Zahn.
- 26. •Obstruction of thehepatic artery or its branches: arteritis, arterio-sclerosis, bland or septic emboli. •Grossly, anemic but sometimes hemorrhagic due to stuffing of the site by blood from the portal vein. •Infarcts of Zahn (non-ischemic infarcts) produce sharply defined red-blue area in liver parenchyma.
- 27. Microscopically Infarcts of Zahnoccurring due to reduced portal blood flow result in atrophy of hepatocytes and dilatation of sinusoids .
- 28. CEREBRAL INFARCTION •Local vascularocclusion •Occasionally, non-occlusive cause compression of the cerebral arteries from outside and from hypoxic encephalopathy.
- 29. •Clinically, the signsand symptoms depend upon the region infarcted. •In general, the focal neurologic deficit termed stroke, is present. •However, significant atherosclerotic cerebrovascular disease may produce transient ischemic attacks (TIA).
- 30. ARTERIAL OCCLUSION •Occlusion ofthe cerebral arteries by thrombi- common •Embolic arterial occlusion is commonly derived from the heart mural thrombosis complicating MI arterial fibrillation and endocarditis.
- 31. VENOUS OCCLUSION • Infrequentphenomenon due to good communications of the cerebral venous drainage. •However in cancer, due to increased predisposition to thrombosis, superior sagittal thrombosis may occur leading to bilateral, parasagittal, multiple hemorrhagic infarcts.
- 32. NON-OCCLUSIVE CAUSES Compression ofthe cerebral arteries from outside occurs during herniation
- 33. PATHOLOGIC CHANGES • Anemicor hemorrhagic • Affected area : soft and swollen blurring of junction between grey and white matter.
- 34. •Within 2-3days, theinfarct undergoes softening and degeneration. • Central liquefaction with peripheral firm glial reaction • thickened leptomeninges, forming a cystic infarct. • Hemorrhagic infarct : red and superficially resembles a hematoma
- 37. MYOCARDIAL INFARCTION MostImportant consequence of coronary artery disease Patient may die within first few hours of the onset while remainder suffer from effects of cardiac function INCIDENCE:Occurs at all age but more common in elderly.
- 38. PREDISPOSING FACTORS FOR CORONARYARTHEROSCLEROSIS Hyperlipidaemia Hypertension DM Cigarette smoking etc DOCUMENTED WELL BY AUTOPSY STUDIES AND CORONARY ANGIOGRAPHIC STUDIES.
- 39. ETIOPATHOGENESIS 1.Mechanism of myocardialischemia 2.Role of platelets 3.Complicated plaques 4.Non – atherosclerotic causes 5.Transmural versus subendocardial infarcts
- 40. MECHANISM OF MYOCARDIAL ISCHEMIA DIMINISHEDCORONARY BLOOD FLOW Coronary artery disease,shock •MYOCARDIAL OXYGEN DEMAND •Exercise,emotion HYPERTROPHY OF HEART W/O SIMULTANEOUS INCREASE IN CORONARY BLOOD FLOW Hypertension,Valvular heart disease
- 41. ROLE OF PLATELETS •Ruptureof atherosclerotic plaque exposes : sub endothelial collagen to platelets which undergo aggregation, activation & release reaction. •These events contribute to the build up of the platelet mass that gives rise to emboli or initiate thrombosis.
- 42. COMPLICATED PLAQUES Two complicationsoccur Superimposed coronary thrombosis – seen in about half of the cases of acute MI. Infusion of fibrinolysins in the first few hours of development of acute MI in such cases restores blood flow in the blocked vessel in majority of cases. Intramural hemorrhage – is found in about one third of cases of acute MI. Hemorrhage and thrombosis may occur together in some cases.
- 43. NON-ATHEROSCLEROTIC CAUSES Coronary vasospasm Coronary ostialstenosis, Embolism, Thrombotic diseases, Trauma and outside compression.
- 44. 1 Feature Transmural infractSubendoc ardial infarct 1 Definition Full-thickness, solid Inner third to half, patchy 2 Frequency Most frequent (95%) Less frequent 3 Distribution Specific area of coronary supply Circumferent ial 4 Pathogenesis > 75% coronary stenosis Hypoperfusio n of myocardium 5 Coronary thrombosis Common Rare 6 Epicarditis Common None
- 45. LOCATION OF INFARCTS •LV •RV is less susceptible , due to its thin wall, having less metabolic requirements and is thus adequately nourished •Atrial infarcts, whenever usually accompany infarct of LV •LA is relatively protected because it is supplied by oxygenated blood in the left atrial chamber.
- 46. REGION OF INFARCTION Areaof obstructed blood supply by one or more of three coronary arterial trunks in descending order: 1.Left anterior descending coronary artery :40 to 50% 2.Right coronary artery :30 to 40% 3.Left circumflex coronary artery:15 to 20%
- 47. 3 Regionsof myocardial infraction. Stenosis of the left anterior descending coronary artery is the most common (40- 50%). Region of infarction in the anterior part of the left ventricle including the apex and the anterior two-thirds of the interventricular septum.
- 48. Stenosis of theright coronary artery is the next most frequent (30-40%) . It involves the posterior part of the left ventricle and the posterior one- third of the interventricular septum.
- 49. Stenosis of theleft circumflex coronary artery is seen least frequently (15-20%). Its area of involvement is the lateral wall of the left ventricle.
- 50. 50 Microscopically The changes aresimilar in both transmural and subendocardial infracts. There is ischemic coagulative necrosis of the myocardium which eventually heals by fibrosis. However, sequential microscopic changes are observed.
- 51. REFERENCES 1.Robbins and Cotran- Pathologic basis of diseases. 8th edition. 2. Harsh Mohan – Text book of pathology. 3rd edition. 3.Mc Gee, Isaacson and Wright – Oxford text book of Pathology. Principles of Pathology volume 1. 4.Anderson’s Pathology – 10th edition
- 52. God gave us healinghands ..……. To heal the wounds of the world
Editor's Notes
- #5 is the process of tissue necrosis resulting from some form of circulatory insufficiency; the localized area of necrosis so developed is called an infarct.
- #7 A compartment space is anatomically determined by an unyielding fascial (and osseous) enclosure of the muscles. The anterior compartment syndrome of the lower leg (often referred to simply as anterior compartment syndrome), can affect any and all four muscles of that compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius..incomplete arthersclerotic narrowing of coronary arteries produces mi. This term is often mistakenly used to describe various related/proximal conditions, including Anterior Shin Splints. It is important to distinguish between the two, as shin splints rarely causes serious health problems, while Anterior Compartment Syndrome can lead to irreversible damage. The true compartment syndrome arises due to increased pressure within the unyielding anterior compartment of the leg. The pressure obstructs venous outflow, which causes further swelling and increased pressure. The resultant ischemia leads to necrosis (death of tissue) of the muscles and nerves. The process can begin with swelling of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and/or the peroneus tertius muscles in response to strong eccentric contractions sufficient to produce postexercise soreness. Symptoms Diffuse tightness and tenderness over the entire belly of the tibialis anterior that does not respond to elevation or pain medication can be early warning signs and suggestive of Anterior Compartment Syndrome. Other common symptoms include excessive swelling that causes the skin to become hot, stretched and glossy. Pain, paresthesias, and tenderness in both the ischemic muscles and the region supplied by the deep common fibular nerve are exhibited by patients suffering from this condition. Sensitivity to passive stretch and active contraction are common, and tend to increase the symptoms. Diagnosis If these symptoms are observed/experienced it is important to contact a physician specializing in sports medicine (MD/DO), a doctor of podiatric medicine (DPM), or other qualified health care professional immediately so as to get the appropriate advice/treatment before serious damage occurs. The 5 Ps of Anterior Compartment Syndrome: Pain Pallor Paresthesia Pulselessness Paralysis (If not treated)
- #8 arterial occlusion,compact organs.Kidney,heart ,spleen. –venous occlusion seen in soft loose tissues and are caused either by pulmonary arterial obstruction, e.g. in the lungs ,intestine or by arterial or venous occlusion, e.g. in the intestines. Pale infarcts r due to arterial obstruction in solid organs n red due to venous n loose tissues
- #10 Local anoxaemia occurs immediately after obstruction of the blood supply. Within few hours the affected part becomes swollen due to oedema and haemorrhage, amount is veriable, being more marked in the lungs and spleen, and less extensive in the kidneys and heart. Cellular changes such as cloudy swelling and degeneration appears early, while death of the cells or necrosis occurs in 12-48hours. There is progressive autolysis of the necrotic tissue and haemolysis of the red cells. Inflammatory reaction and hyperaemia appear at the same time in the surrounding tissues in response to products of autolysis. Blood pigments, hematoidin and haemosiderin, liberated by haemolysis are deposited in the infract. At this stage most infracts becomes pale due to loss of red cells. Following this, there is progressive ingrowth of granulation tissue from the margin of the infract so that eventually the infract is replaced by a fibrous scar. Dystrophic calcification may occur sometimes. However, in the case of infract brain, there is liquefactive necrosis which heals by gliosis. DIAGRAM REPRESENTS GRANULATION TISSUE
- #12 Diagram- cerebral infarct
- #13 however, there is giagram represents – liquefactive necrosis
- #16 arteries may produce pulmonary infarction, though not always. This is because the lungs receive blood supply from bronchial arteries as well, and thus occlusion of pulmonary artery ordinarily does not produce infarcts.
- #18 Arrow represents wedge shaped
- #19 Later place is taken by
- #20 Found in 5%of autopsies. originating from the heart such as in
- #21 Because it draws its blood supply from under the capsule.
- #24 Pointing towards
- #26 Just as in lungs, infracts in the liver are uncommon due to dual blood supply – from portal vein and from hepatic artery. Occlusion of portal vein or its branches
- #27 Infracts of Zahn (non-ischemic infracts) produce sharply defined red-blue area in liver parenchyma.
- #29 Arterial or venous. Occasionally, it may be the result of non-occlusive cause such as compression of the cerebral arteries from outside and from hypoxic encephalopathy.
- #31 Thrombotic occlusion of the cerebral arteries is most frequently the result of atherosclerosis, and rarely, from arteries of the cranial arteries.
- #32 Thrombotic occlusion of the cerebral arteries is most frequently the result of atherosclerosis, and rarely, from arteries of the cranial arteries.
- #34 Grossly, an anemic infract becomes evident 6-12hrs after its occurrence.
- #35 Hemorrhagic infract : red and superficially resembles a hematom, it is usually a result of fragmentation of occlusive arterial emboli or venous thrombosis.lt of fragmentation of occlusive arterial emboli or venous thrombosis.
- #36 Initially, eosinophilic neuronal necrosis and lipid vacuolization produced by breakdown of myelin. Simultaneously, the infracted area is infiltrated by neutrophils 2. After the first 2-3days, there is progressive invasion by macrophages and there is astrocytic and vascular proliferation.
- #37 3. In the following weeks to months, the macrophages clear away the necrotic debris by phagocytosis followed by reactive astrocytosis, often with little fine fibrosis. A hemorrhagic infract has some phagocytes containing haemosiderin. 4. Ultimately, after 3-4 months and old cystic infract is formed which shows a cyst transversed by small blood vessels and has peripheral fibrillary gliosis. Small cavitary infracts are called lacunar infracts and are commonly found as a complication of systemic hypertension.
- #48 Region of infraction depends upon the area of obstructed blood supply by one or more of three coronary arterial trunks,