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Infraction . Dr. Abhinav Golla , Associate Professor , Lab Director & Consultant Pathologist . Aadhya Medicure Pathlabs .
- 1. INFARCTION 2 Dr.Abhinav golla Assistant Professor ConsultantPathologist Aadhya Medicure Pathlas
- 2. CONTENTS Definition Etiology Types Pathogenesis Pathologic changes Infarcts ofdifferent organs References
- 3. DEFINITION Localized area ofischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainageā¦ā¦ā¦ā¦ā¦ā¦ā¦.ROBBINS
- 4. ETIOLOGY ā¢Most Commonly,Infarcts arecaused by Interruption in arterial blood supply, called ischemic necrosis ā¢Less commonly,Venous obstruction can produce infarcts termed stagnant hypoxia
- 12. ā¢ Depending onAge a.Recent or fresh. b.Old or healed. ā¢Presence or absence of infection. a.Bland ā when free of bacterial contamination b.Septic ā when infected.
- 13. 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
- 14. PATHOLOGIC CHANGES ā¢Grossly, infarcts ofsolid organs -wedge-shaped ā¢ apex -pointing towards occluded artery wide base - on the surface of the organ. ā¢Infarcts due to arterial occlusion -pale venous obstruction - hemorrhagic. ā¢Most infarcts become pale later as the red cell are lysed but pulmonary infarcts never become pale due to extensive amount of blood.
- 15. ā¢Cerebral infarcts :poorly defined with central softening (encephalomalacia). ā¢Recent infarcts : slightly elevated over the surface ā¢Old infarcts : shrunken , depressed under the surface of the organ.
- 16. Microscopically ā¢The pathognomic cytologicchange in all infarcts is coagulative (ischaemic) necrosis of the affected area of tissue or organ. ā¢In cerebral infarcts- characteristic liquefactive necrosis.
- 17. 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).
- 18. INFARCTS OF DIFFERENT ORGANS LocationGross appearanc e 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
- 19. LUNG INFARCTION ā¢Embolism of thepulmonary arteries ā¢ May occur in patients who have inadequate circulation : Chronic lung diseases ā¢ Congestive heart failure.
- 21. 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.
- 22. Microscopically ā¢Characteristic histologic feature: coagulative necrosis of the alveolar walls. ā¢Initially: infiltration by neutrophils and intense alveolar capillary congestion hemosiderin, phagocytes and granulation tissue.
- 23. 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.
- 24. 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
- 25. Microscopi cally ļµ Characteristic: ļµ affectedarea shows coagulative necrosis of renal parenchyma i.e. ghosts of renal tubules and glomeruli without intact nuclei and cytoplasmic content. ļµ The margin of the infarct shows inflammatory reaction ā initially acute but later macrophages and fibrous tissue predominate.
- 26. INFARCT SPLEEN ā¢Common sitefor infarcts ā¢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)
- 27. ā¢Less frequently byobstruction of microcirculation (e.g. in myeloproliferative diseases, sickle cell anemia, arteritis, Hodgkin's disease, bacterial infections). ā¢Grossly, splenic infarcts are often multiple. ā¢Characteristically pale or anemic, wedge-shaped ā¢ ā¢ base - at the periphery apex -pointing towards hilum.
- 28. ā¢Features are similarto those found in anemic infarcts in kidney. ā¢Coagulative necrosis and inflammatory reaction are seen. ā¢Later, the necrotic tissues is replaced by shrunken fibrous scar. M ICROSCOPI CALLY
- 29. INFARCT LIVER ā¢ Uncommon ā¢Dual blood supply ā¢Obstruction of the portal vein is usually secondary to other diseases : Hepatic cirrhosis, IV invasion of primary CA of liver, CA of pancreas ā¢Generally does not produce ischemic infarction but instead reduced blood supply to hepatic parenchyma causes non-ischemic infarct called infarct of Zahn.
- 30. ā¢Obstruction of thehepatic artery or its branches: arteritis, arterio-sclerosis, bland or septic emboli. ā¢Grossly, anemic but sometimes hemorrhagic due to stuffing of the site by blood from the portal vein. ā¢Infarcts of Zahn (non-ischemic infarcts) produce sharply defined red-blue area in liver parenchyma.
- 31. Microscopically Infarcts of Zahnoccurring due to reduced portal blood flow result in atrophy of hepatocytes and dilatation of sinusoids .
- 32. CEREBRAL INFARCTION ā¢Local vascularocclusion ā¢Occasionally, non-occlusive cause compression of the cerebral arteries.
- 33. ā¢Clinically, the signsand symptoms depend upon the region infarcted. ā¢In general, the focal neurologic deficit termed stroke, is present. ā¢However, significant atherosclerotic cerebrovascular disease may produce transient ischemic attacks (TIA).
- 34. PATHOLOGIC CHANGES ā¢ Anemicor hemorrhagic ā¢ Affected area : soft and swollen blurring of junction between grey and white matter.
- 35. ā¢Within 2-3days, theinfarct undergoes softening and degeneration. ā¢ Central liquefaction with peripheral firm glial reaction ā¢ thickened leptomeninges, forming a cystic infarct. ā¢Hemorrhagic infarct : red and superficially resembles a hematoma
- 36. MYOCARDIAL INFARCTION Most Importantconsequence 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 butmore common inelderly.
- 37. PREDISPOSINGFACTORSFOR CORONARY ARTHEROSCLEROSIS Hyperlipidaemia Hypertension DM Cigarette smokingetc DOCUMENTED WELL BY AUTOPSY STUDIES AND CORONARY ANGIOGRAPHIC STUDIES.
- 38. ETIOPATHOGENESIS 1.Mechanism of myocardialischemia 2.Role of platelets 3.Complicated plaques 4.Non ā atherosclerotic causes 5.Transmural versus subendocardial infarcts
- 39. MECHANISM OF MYOCARDIAL ISCHEMIA DIMINISHEDCORONARY BLOODFLOW Coronary artery disease,shock ā¢ MYOCARDIAL OXYGEN DEMAND ā¢Exercise,emotion HYPERTROPHY OF HEART W/O SIMULTANEOUS INCREASE INCORONARY BLOOD FLOW Hypertension,Valvular heart disease
- 40. 1 Feature Transmuralinfract Subendoc ardial infarct 1Definition Full-thickness, solid Inner third to half, patchy 2 Frequency Most frequent (95%) Less frequent 3 Distribution Specific area ofcoronary supply Circumferent ial 4 Pathogenesis >75%coronarystenosis Hypoperfusio n of myocardium 5 Coronary thrombosis Common Rare 6 Epicarditis Common None
- 42. 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. 50
- 43. REFERENCES 1.Robbins and Cotran- Pathologic basis of diseases. 8th edition. 2. Harsh Mohan ā Text book of pathology. 3rd edition. 3.Mc Gee, Isaacson and Wright ā Oxford text book of Pathology. Principles of Pathology volume 1. 4.Andersonās Pathology ā 10th edition
- 44. ..ā¦ā¦. To heal thewounds of the world