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HEMODYNAMIC DISORDERS Manar hajeer, MD University of jordan Faculty of medicine, pathology departement EDEMA The term edema signifies increased fluid in the interstitial tissue spaces. Fluid collections in different body cavities are variously designated: Hydrothorax: in the pleural cavity. Hydropericardium: in the pericardial cavity. Hydroperitoneum (ascites): in peritoneal cavity. Anasarca is a severe and generalized edema with profound subcutaneous tissue swelling. CAUSES OF EDEMA I. Increased hydrostatic pressure and results from impaired venous return 1. Local increase: such as deep venous thrombus in the lower extremity causes edema in the affected leg. 2. Generalized increase in venous pressure, such as in heart failure. 3 II. Reduced Plasma osmotic pressure - Causes 1. Loss of albumin from kidney. 2. Reduced albumin synthesis : Occurs in cirrhosis and protein malnutrition. 3. Protein losing enteropathy. III. Lymphatic Obstruction: 1. Parasitic infection (filariasis) : causes inguinal lymph node fibrosis; so results in massive edema of the lower extremity and external genitalia (elephantiasis). 2. Axillary lymph node resection in breast cancer can obstruct lymphatic drainage, resulting in lymphedema of the arm. IV. Sodium and water retention: can occur with any compromise of renal function, as in poststreptococcal glomerulonephritis and acute renal failure . V. Inflammation: Acute and chronic, due to increase blood flow and hydrostatic pressure. (Localised edema) The edema fluid occurring with volume or pressure overload, or under conditions of reduced plasma protein, is typically a protein-poor transudate. Conversely, because of the increased vascular permeability, inflammatory edema is a protein-rich exudate. HYPEREMIA AND CONGESTION The terms hyperemia and congestion both indicate a local increased volume of blood in a particular tissue. 1.Hyperemia: is an active process resulting from augmented blood flow due to arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise). The affected tissue is redder than normal because of engorgement with oxygenated blood. 2.Congestion is a passive process resulting from impaired venous return out of a tissue. Systemic congestion, as in cardiac failure. Local congestion, as in isolated venous obstruction. The tissue has a blue-red color (cyanosis), as worsening congestion leads to accumulation of deoxygenated hemoglobin. HEMORRHAGE Hemorrhage is extravasation of blood from vessels into the extravascular space. May be: 1. External hemorrhage. 2. Within a tissue (hematoma) 3. Large bleeds into body cavities; a. Hemothorax: Blood in the pleural cavity. b. Hemopericardium: Blood in pericardium. c. Hemarthrosis : Blood in in joints. 4. Small bleeds I. Petechiae are minute 1-2 mm bleeds in skin or mucous membranes, Causes: A-Low platelet counts (thrombocytopenia), B-Defective platelet function (Aspirin) C-Localy increased intravascular pressure. D-Clotting factor deficiency. II. Purpura are 3 to 5 mm bleeds results from above causes in addition to trauma, vascular inflammation (vasculitis), or increased vascular fragility. III. Ecchymoses : Larger (1- to 2-cm) subcutaneous hematomas (bruises). CLINICAL SIGNIFICANCE OF HEMORRHAGE DEPENDS ON: 1. The volume of and Rate of bleeding a. Rapid loss of up to 20% of the blood volume, or slow losses of even of larger amounts, may be insignificant. b. Greater losses can cause hemorrhagic (hypovolemic) shock . 2. Site of bleeding: Bleeding that would be trivial in the subcutaneous tissues can cause death if located in the brain . Note: Chronic or recurrent external blood loss ( peptic ulcer or menstrual bleeding) may result in iron deficiency anemia. HEMOSTASIS AND THROMBOSIS Hemostasis : tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury. The pathologic form of hemostasis is thrombosis. Thrombosis: blood clot (thrombus) formation in uninjured vessels or thrombotic occlusion of a vessel after relatively minor injury. Both hemostasis and thrombosis involve three components: the vascular wall, platelets, and the coagulation cascade. CAUSES OF THROMBOSIS Virchow's triad: (1) endothelial injury, (2) stasis or turbulence of blood flow, (3) blood hypercoagulability. 1- ENDOTHELIAL INJURY exposes highly thrombogenic subendothelial extracellular matrix, allowing platelets to adhere and be activated (aggregation) Intact endothelial cells maintain liquid blood flow by actively inhibiting platelet adherence, preventing coagulation factor activation, and lysing blood clots that may form. Endothelial cells can be stimulated by direct injury. Such stimulation results in local thrombus formation. Examples of endothelial injury: 1. Endocardial injury in myocardial infarction (thrombus formation within the cardiac chambers) 2.Ulcerated plaques in atherosclerotic arteries. 3.At sites of traumatic or inflammatory vascular injury (vasculitis) 2- ALTERATIONS IN NORMAL BLOOD FLOW Turbulence contributes to arterial and cardiac thrombosis by causing endothelial injury or dysfunction. Stasis is a major contributor to the development of venous thrombi. CAN BE SEEN IN SEVERAL CLINICAL SETTINGS: 1- Ulcerated atherosclerotic plaques (turbulent) . 2- Abnormal aortic and arterial dilations, called aneurysms (stasis). 3- Acute myocardial infarction results in focally noncontractile myocardium; can lead to aneurysm formation. 4- Hyperviscosity syndromes (such as polycythemia;) increase resistance to flow and cause small vessel stasis. 5- Deformed red cells in sickle cell anemia cause vascular occlusions, with the resultant stasis also predisposing to thrombosis. 3- HYPERCOAGULABILITY Primary (genetic) and secondary (acquired) disorders . A- Inherited causes of hypercoagulability: Mutations in the factor V gene and the prothrombin gene are the most common. Deficiencies of anticoagulants such as protein C or protein S (rare) B. Acquired hypercoagulability 1.Oral contraceptive use and hyperestrogenic state of pregnancy . 2.Prolonged bed rest or immobilization . 3.Myocardial infarction. 4. Disseminated cancers, release of mucin in adenocarcinoma predisposes to thrombus formation (migratory thrombophlebitis, or Trousseau's syndrome). FATE OF THE THROMBUS 1. Propagation: Thrombus enlargement by accumulation of additional platelets and fibrin. 2. Embolization: Fragment of thrombus is transported elsewhere in the vasculature. 3. Dissolution: In newly formed thrombus,, activation of fibrinolysis may lead to its rapid shrinkage and complete dissolution. Note: older thrombi, are more resistant to plasmin-induced lysis . 4. Organisation and recanalization: Older thrombi become fibrosed and capillary channels may form and establish the continuity of the original lumen. 5. Bacterial seeding of thrombus serve as a culture medium, and the resulting infection may weaken the vessel wall, leading to formation of a mycotic aneurysm. CLINICAL CORRELATIONS: VENOUS VERSUS ARTERIAL THROMBOSIS 1- Venous thrombi by obstructing the venus drainage can cause swelling and edema, but are most worrisome because they can embolize to the lungs and cause death. 2- Arterial thrombi can embolize. However, they mainly obstruct vessels (in coronary and cerebral arteries ) to cause myocardial and cerebral infarction. Also cardiac thrombi in the setting of myocardial infarction can give systemic embolization (brain, kidneys, and spleen). VENOUS THROMBOSIS 1. Superficial venous thrombi: - Arise in the saphenous vein particularly in varicose veins; these rarely embolize but can cause edema from impaired venous outflow, leading to varicose ulcers. II. Deep venous thromboses ("DVTs") : Occur in the larger leg veins at or above the knee ( popliteal, femoral, veins). May be asymptomatic. Serious because they can embolize. EMBOLISM An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. Virtually 99% of all emboli represent some part of a dislodged thrombus, hence the term thromboembolism. Rare forms: Air embolism, fat embolism, amniotic fluid embolism. The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue. Two forms: 1.Pulmonary thromboembolism. 2.Systemic thromboembolism. PULMONARY THROMBOEMBOLISM In 95% of cases, venous emboli originate from thrombi within deep leg veins, above the knee. They are carried through progressively larger channels and pass through the right side of the heart before entering the pulmonary vasculature. CLINICAL FEATURES OF PULMONARY THROMBOEMBOLISM: a. Clinically silent: 60% to 80% of emboli esp. small ones. b. Sudden death or right sided heart failure (acute cor pulmonale):A large embolus that blocks a major pulmonary artery or pulmonary trunk (saddle embolus) c. Pulmonary hemorrhage: embolic obstruction of medium-sized arteries and subsequent rupture of capillaries, with no infarction since the area also receives blood through bronchial arteries. d- Pulmonary hypertension and chronic right ventricular failure (chronic cor pulmonale): Multiple emboli occurring over time. SYSTEMIC THROMBOEMBOLISM 80% arise from intra cardiac thrombi. The remainder originate from aortic aneurysms and thrombi overlying ulcerated atherosclerotic plaques. Common arteriolar embolization sites : a. The lower extremities (75%). b. Central nervous system (10%). c. Intestines, kidneys, are less common. Note: Arterial emboli often cause infarction FAT EMBOLISM Caused by: - Soft tissue crush injury or long bone fractures, with release of microscopic fat globules into the circulation. Note: Fat embolism occurs in some 90% of individuals with severe skeletal injuries, but less than 10% show fat embolism syndrome. FAT EMBOLISM SYNDROME a. Pulmonary insufficiency (tachypnea, dyspnea,) b. Neurologic symptoms (irritability and restlessness to coma) c. Anemia, thrombocytopenia. AIR EMBOLISM Gas bubbles within circulation can coalesce and obstruct vascular flow. a. Small venous gas emboli have no deleterious effects, but sufficient air that enter the pulmonary circulation during obstetric procedures or due to a chest wall injury can cause hypoxia. b. Large venous gas emboli may arrest the heart . INFARCTION An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Nearly 99% of all infarcts result from thrombotic or embolic events, and almost all result from arterial occlusion. Although venous thrombosis can cause infarction, it more often merely induces venous obstruction and congestion. 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) White (anemic) Either septic or bland. RED INFARCTS (1) With venous occlusions (such as in ovarian torsion). (2) In loose tissues (such as lung). (3) In tissues with dual circulations such as lung and small intestine. (4) In tissues that were previously congested because of sluggish venous outflow. (5) When flow is re-established to a site of previous arterial occlusion. WHITE INFARCTS Arterial occlusions or in solid organs (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage.