Disturbances of Blood Flow- EMBOLISM H.A. MWAKYOMA, MD

Disturbances of Blood Flow Hyperemia and congestion Hemorrhage Ischemia Thrombosis Postmortem clots Disseminated intravascular coagulation Embolism Infarction Edema Shock

Emboli Definition: emboli are solid, fluid or gaseous material carried by the blood stream from the site of their origin or entry into the circulation to a site distant from its site of origin Embolism is the process by which a detached intravascular solid, liquid, or gaseous mass is carried by the blood to a site distant from its point of origin.

Classification of emboli Thromboemboli –commonest: arterial,venous ,paradoxic Air (gas ) Fat Bone marrow Tumour Cholesterol Foreign body Amniotic fluid

Consequences of embolization ↓perfusion distal to embolus Affected by collateral or dual blood supply Possible infarction of tissue

Thromboemboli Most important clinically Detached thrombi cause the commonest type of embolism Venous-originate from veins & carried by venous system to lungs (pulmonary) Arterial originate in large arteries, heart or aorta ,carried by arterial blood into organs e.g. brain, kidney, spleen (systemic) Paradoxical originate in venous system & cross through a heart shunt/foramen ovale to arterial circulation

Common locations in which venous and arterial emboli cause infarction and the anatomical routes by which they reach these organs

Pulmonary(Venous) Thromboembolism Aetiology: deep vein thrombosis Pathogenesis: depends on the size of embolus ,extent of embolization & collateral circulation Occlusion of main pulmonary artery or main branch can cause death by preventing blood going to the lungs “saddle embolus”

Pulmonary Embolus = saddle emboli Figure 4-17 Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM) © 2005 Elsevier

Venous Thromboembolism (cont.) Occlusion of the branches of pulmonary artery . Depending on the degree of collateral circulation (dual blood supply of lungs,pulmonary & bronchial)→Pulmonary infarcts Non occlusive thrombi “silent” May lead to pulmonary hypertension eventually

Systemic (Arterial) Thromboembolism Emboli travelling in arterial circulation Aetio-pathogenesis intracardiac mural thrombi (80%) left atrium: dilation and fibrillation (25%) heart valve vegetations aortic mural thrombi paradoxical Sites of embolization lower extremities (75%) brain (10%) intestine, kidney, spleen

Effects of emboli Depends on the Collateral vascular supply of the affected tissue The vulnerability of the tissue to ischemia Calibre of occluded vessel

Fat Embolism Aetiology : TRAUMATIC CAUSES: Definition : embolism caused by fat in the circulation Aetiology : TRAUMATIC CAUSES: Trauma with multiple fractures of long bones and/or operative manipulation of fractures; Trauma to adipose tissue or fatty liver; :

Fat Embolism—cont-- Acute pancreatitis. Extensive burns NON-TRAUMATIC CAUSES Acute pancreatitis. Extensive burns Diabetes mellitus Fatty liver Sickle cell anaemia Decompression sickness Inflammation of the bones and soft tissue NB: Fat emboli tend to be small and they often cause small infarcts adjacent to capillaries at the sites where they lodge in.

Fat Embolism Pathogenesis: Mechanical theory: Mechanical obstruction by microemboli of neutral fat +platelet &RBC aggregates Intravascular coagulation theory: Chemical irritation (local injury to endothelium) from release of fatty acids + platelet activation & recruitment of granulocyyes –release of free radicals,protease &ecosanoids →DIC

Fat emboli

Sites of embolization lungs: pulmonary insufficiency brain: restlessness, convulsions delirium, coma and sudden death Demonstration of fat embolism Fat globules in capillaries demonstrated in frozen sections of lung, brain .-using fat stains Sudan dyes- Sudan black, Sudan IV or III) Oil red O Osmic acid

Clinical features Asymptomatic (up to 90% of cases) Pulmonary insufficiency Neurological symptoms Anemia Thrombocytopenia—petechial rash Prognosis Asymptomatic (up to 90% of cases) Fatal in severe cases

Air Embolism- Gaseous embolism Definition :embolism caused by entry of air bubbles into circulation Aetiology: Trauma: chest internal jugular vein or SVC Obstetrical procedures Vascular surgery Decompression events- Decompression sickness. Mismanaged intravenous infusions Pathogenesis:Usually more than 150 ml of air needed to produce symptoms Symptoms of ischemia, infarction or DIC

Decompression sickness Is a specialised form of gas embolism Divers (Nitrogen bubbles in decompression) Nitrogen bubbles in blood due to rapid decompression Gas bubbles occlude small vessels In joints ,bones & soft tissues “bends” pulmonary vessels -“chokes” Initiate DIC Treatment -repressurise Caisson disease - chronic decompression sickness Gas emboli in skeletal system → ischemic necrosis especially in the femur,tibia,humeri

Amniotic Fluid Embolism Def: Obstetrical complication with entry of amniotic fluid into uterine venous circulation The uterine contractions that occur during childbirth can sometimes cause amniotic fluid to be driven through the placental bed into the maternal circulation. Incidence: Rare but lethal in 80% cases Pathogenesis: Amniotic fluid contains squamous cells lanugo hair,fat, mucin Amniotic fluid may obstruct pulmonary arteries → sudden death or initiate DIC

Amniotic Fluid Embolism Morphology:post mortem – particulate material in pulmonary arteries / thrombi in small vessels. Pulmonary oedema,diffuse alveolar damage,systemic fibrin thrombi(DIC)

Others Septic thromboemboli: infected thrombi e.g. valvular vegetations in bacterial endocarditis .infarcts become infected by bacteria & transforms into an abscess. Tumour emboli-don’t cause infarcts Foreign body –IV drug users Cholesterol –AS plaques

Infarction Aetiology Thrombosis or embolism 99% 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. Aetiology Thrombosis or embolism 99% Venous outflow obstruction (single outflow organs) Others : Hypotensive,local vasospasm, compression of, vessel by hematoma or tumor, torsion

Morphological Classification of infarcts Colour-Pale/anemic/white Red (hemorrhagic) Infarct Septic or bland

Pale / White Infarct Ischemia following obstruction of nutrient artery or hypoperfusion of tissue Solid organs with end-arterial circulation such as kidney, heart, spleen Wedge shaped.occluded vessel at the apex,base at the serosal surface Better defined with time, paler, hyperemic margins

Microscopy Ischemic coagulative necrosis Demonstrable only >12-18 hrs. Inflammation in response to necrosis Phagocytosis of cellular debris by neutrophils & macrophages 1-2 days Healing response Scar tissue (brain- liquefactive necrosis)

Red (hemorrhagic)infarcts Sites :venous occlusion of organ with single venous outflow e.g. testicular torsion Loose tissues- e.g. lung Tissues with dual circulations: lung and gut Previously congested tissue With reperfusion of previously infarcted tissue

Pulmonary infarcts Ischemic necrosis of lung parenchyma following pulmonary embolism & lack of blood from bronchial arteries. When blood from bronchial arteries reperfuses the ischemic area, blood leaks into the alveolar spaces Appears triangular, red & airless. Becomes more firm &brown with time.

Examples of infarcts Figure 4-19 Examples of infarcts. A, Hemorrhagic, roughly wedge-shaped pulmonary infarct. B, Sharply demarcated white infarct in the spleen. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM) © 2005 Elsevier

In this low power view, the darker pink (eosinophilic)areas are coagulation necrosis (infarcted myocardial cells). The lighter pink areas at the left top and bottom are viable myocardium and the basophilic areas contain acute inflammatory cells entering the necrotic tissue. Note the patchy distribution of the infarcted myocardium. This patient died several days after the infarction occurred. Iowa Histopathology Series

Septic infarct Following fragmentation of a bacterial vegetation from a heart valve or following microbes seeding a necrotic area. Converted into an abscess Greater inflammatory response scarring

Clinical Correlations Nature of blood supply end-artery blood supply dual blood supply Rate of development of occlusion role of collateral circulation Vulnerability of tissue to hypoxia brain: 3-4 minutes heart: 20-30 minutes Oxygen content of blood hemoglobin concentration and saturation