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Similar to Embolism (Dr. MURALEEDHARA)
Embolism (Dr. MURALEEDHARA)
- 2. EMBOLISM Process of obstructionof CVS by any mass carried in the circulation Embolus:transported intravascular mass (solid liquid or gas) detached from its site of origin Ninety percent of emboli are Thromboemboli originating from Thrombi or their parts detached from the vessel wall
- 3. TYPES OF EMBOLI Content : Solid: Thrombi, atheromatous material, tumor cell / bacterial clumps, parasites, foreign bodies, tissue fragments Liquid ; fat globules, amniotic fluid, bone marrow Gaseous : air, other gases
- 4. TYPES OF EMBOLI Source : Cardiac : Left side of heart eg, from atrial appendages, infarct in left ventricle, vegetations of endocarditis Arterial : Systemic arteries in brain, kidney spleen, small intestine Venous ; Pulmonary vessels Lymphatic emboli can also occur
- 5. Septic (infected) or Bland ( sterile) Paradoxical : from arterial to venous or vice versa through septal defects in heart, patent foramen ovale, AV shunts Retrograde : opposite to flow of blood eg, Carcinoma metastatis to spine
- 6. THROMBOEMBOLISM Arterial (systemic ) thromboembolism : Heart – mural thrombi, vegetations , valves ,cardiomyopathy Arteries : atheromaous plaques, aortic aneurysms, pulmonary veins Effects : Infarction(MI,brain,kidney,spleen) Gangrene, Arteritis & Mycotic aneurysm ( bacterial endocarditis ), sudden death
- 7. Venous thromboembolism Deep veins of lower limbs – common Pevic veins, upper limb veins, cavenous sinus in brain, thrombi in right side of heart. Most significant effect – obstruction of pulmonary arterial circulation leading to sudden death, infarction of lung, Cor Pulmonale, Pulmonary hypertension
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- 10. PULMONARY THROMBOEMBOLISM Occlusionof pulmonary arterial tree by thromboemboli 95 % from large veins of lower limbs( iliac femoral, popliteal ) Other sources : Varicosities of superficial veins of legs,peri prostatic,peri ovarian, uterine, broad ligament veins Common in hospitalised & bedridden
- 11. Detached thrombusfrom these sites go to right side of heart If large – impacted at bifurcation of main Pulmonary artery ( saddle embolus ) Commonly multiple fragments or small emboli to many vessels espl lower lobes Paradoxical – rare
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- 13. Consequences : Sudden death Acute Cor Pulmonale leading to acute right sided heart failure Pulmonary infarction Pulmonary haemorrhage Pulmonary hypertension, chronic cor pulmonale
- 14. FAT EMBOLISM Obstructionof arterioles & capillaries by fat globules Traumatic : fracture long bones, post orthopaedic surgical procedures, laceration of adipose tissue, puerperium Non traumatic : burns, D.M. pancreatitis, sickle cell anaemia, fatty liver Mechanical ( trauma ), emulsion instability, intravascular coagulation, toxic injury
- 15. PULMONARY FAT EMBOLISM Fat globules in capillaries of pts with long bone fractures Lungs : hyperemia,oedema, petechial haemorrhages & changes of ARDS Fat stains : Frozen sections stained with Sudan Black, 3 & 4, Oil red O & Osmic acid
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- 18. SYSTEMIC FAT EMBOLISM Fat globules pass through patent Foramen Ovale, AV shunts in lungs & vertebral venous plexuses. Capillaries of brain ,kidneys, skin Brain : petechiaes,microinfarcts, oedema Delirium, convulsions, coma, death Kidney : < GFR, tubular damage Petechiae in skin,conjunctaivae, serosa
- 19. AIR EMBOLISM (VENOUS ) Surgeries & wounds of head/ neck Obstetric surgeries & trauma, IV infusions Angiography 100 to 150 ml entry is fatal Entrapment of air emboli in pulmonary arterial tree & right heart Autopsy : heart & pulmonary artery opened insitu under water – escaping froth of mixed air & blood
- 20. AIR EMBOLISM (ARTERIAL) Cardiothoracic surgery / trauma, paradoxical embolism,Arteriography Marble skin ; blockage of skin vessels Pallor of tongue : occlusion of Lingual art Retinal vessels : air bubbles Death : Coronary or Cerebral arteies
- 21. AIR EMBOLISM –BRAIN
- 22. DECOMPRESSION SICKNESS Gasembolism : Caisson’s disease, Diver’s palsy , aeroembolism When individual decompresses suddenly from high atmospheric pressure to normal level or from normal to low atmospheric pressure Diver’s, Offshore drilling, tunnel workers: increased Nitrogen, O2 ,CO2 is dissolved in blood b’cos high atmospheric pressure
- 23. When suchperson ascends too rapidly, comes to normal pressure too soon – gases bubble out which merge to form emboli. Nitrogen – fatty tissue Aeroembolism ; those who ascend to high altitudes (hot air balloon ), air flights in unpressurised cabin – exposed to sudden decompression Effects : Acute form & Chronic form
- 24. ACUTE CAISSON’S DISEASE Acute obstruction of small vessels of joints & skeletal muscles Bends : person doubles up in bed due to acute pain in joints, ligaments,tendons Chokes : accumulation in lungs causing respiratory distress Cerebral effects : Vertigo, Coma, death
- 25. CHRONIC CAISSON’S DISEASE Ischaemic necrosis in skeletal system Avascular necrosis of head of femur,tibia Neurological : paraesthesias, paraplegia Lungs : haemorrhage,oedema, atelectasis causing dysponea,cough,chest pain Skin ; itching,patchy erythema, cyanosis Lipid vacuoles in cells of Liver, pancreas
- 26. AMNIOTIC FLUID EMBOLISM Most serious, unpredictable and unpreventable cause of maternal mortality During labour, immediate post partum period amniotic fluid can enter uterine veins & reach right side of heart Enter through tears in myometrium or endocervix or forced into uterine sinuses by vigorous uterine contractions
- 27. In Pulmonary/ uterine veins : squames, vernix caseosa, lanugo hair, bile,mucus Lungs : haemorrhages,congestion, oedema ARDS, dilated right heart Respiratory distress,dyspoena,Cyanosis, Cardiovascular shock, coma ,death ? Mechanical blockage of Pulmn circln,DIC Anaphylactoid reaction, haemorrhages due to thrombocytopenia , < fibrinogen
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- 29. ATHEROEMBOLISM Aortic atheromatousplaques get eroded , lodged in medium & small arteries Emboli consist of cholestrol crystals, hyaline debris,calcified material Ischaemia , atrophy & necrosis – distal Infarcts in kidneys , spleen, brain, heart Gangrene of lower limbs Hypertension if widespread renal invlvmt
- 30. SEPTIC EMBOLI INBRAIN
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- 32. INFARCTION Process oftissue necrosis due to some form of circulatory insufficiency Infarct – the localised area of necrosis Interruption in arterial blood supply – ischaemic necrosis Venous obstruction – stagnant hypoxia Sudden , complete occlusion by thrombi or emboli
- 33. TYPES OF INFARCTS Colour : Pale(anaemic) –arterial occlusion of compact organs e.g kidney,heart, spleen Red ( haemmoragic) – soft loose tissues lungs, intestine Age : Fresh ( recent ) , old ( healed ) Infection : Bland , Septic
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- 35. PATHOGENESIS OF INFARCTION Localised hyperemia– haemorrhage / oedema – cellular changes – necrosis (12 – 48 hrs) – proteolysis of necrotic tissue – inflammatory reaction – lysis of rbcs – deposition of blood pigments – ingrowth of granulation tissue – fibrous scar Gross – solid organs: wedge shaped, apex pointing to occluded artery, wide base on the surface of the organ
- 36. Infarcts ofarterial occlusion : pale Infarcts of venous occlusion : haemorragic Pulmonary infarcts never become pale Cerebral infarcts poorly defined with central softening Recent : elevated over surface old : depressed & shrunken Microscopy : coagulative necrosis except brain – liquefactive necrosis
- 37. Some amountof haemorrhage + Inflammatory reaction at periphery, initially neutrophils later macrophages Fibrosis, dystrophic calcification Cerebral infarcts : necrosis followed by gliosis microglial cells distended with fatty material ( glitter cells ) Myocardial infarct : transluminal , sub endocardial
- 38. INFARCT LUNG Embolismof pulmonary artery(dual blood supply of lungs saves it), but patients with CCF, chronic lung infections – at risk Wedge shaped, base on pleura, vary in size ,haemorrhagic, lower lobes, fibrinous pleuritis on surface C/S : dark purple,blocked vessel at apex Micro : coagulative necrosis, inflammation, scarring, granulation tissue, pigments
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- 41. INFARCT KIDNEY Thromboembolifrom mural thrombi of left atrium ,vegetations, aortic aneurysm renal artery atheroma, sickle cell anaemia Gross : multiple, may be bilateral, pale, wedge shaped with apex towards medulla C/S : first 2-3 days red, centre pale yellow by 4 th day, I week – anaemic & depressed Microscopy : Ghosts of glomeruli & tubules, margin shows inflammation
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- 45. INFARCT SPLEEN Occlusionof splenic artery or branches Thromboemboli from left side of heart or obstruction to microcirculation e.g, SCA Myeloproliferative diseases, Hodgkin’s disease, bacterial infections Gross : multiple, anaemic, wedge shaped base at periphery & apex towards hilum Microscopy : coagulative necrosis , later shrunken fibrous scar
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- 48. INFARCT LIVER Uncommondue to dual blood supply Obstruction of Portal vein – cirrhosis, carcinoma liver, ca pancreas, pylephlebitis non ischemic infarct of Zahn Obstruction of Hepatic artery – arteritis, atherosclerosis, bland or septic emboli ischaemic infarcts Gross : anaemic, infarcts of Zahn–red blue Micro : atrophy, necrosis, dilated sinusoids
- 49. MYOCARDIAL INFARCTION Myocardialischaemia :coronary artery disease, shock, exercise, hypertension,valve disease Atherosclerosis : thrombosis, haemorrhage Coronary spasm, arteritis, embolism Types : Transmural , Sub endocardial Gross : 4 – 10 cms,left venticle ,? age of infarct Micro : 6 hrs no change, later oedema, 12 hrs coagulative necrosis of fibres, neutophils
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- 52. CEREBRAL INFARCTION Obstructionto major arteries e,g. middle cerebral artery by emboli or thrombosis Stroke ; paralysis, hemiplegia,coma, death Gross: Haemorrhagic or pale Microscopy : Liquefactive necrosis , centre cystic with necrotic debris, wall - inflammatory cells , proliferating capillaries , gliosis
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