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The circulation and blood supply is very important to the health of all organs. The metabolism of organs and cells dependent on a normal fluid environment and on adequate blood supply. Disturbances or interference with circulation and blood supply to organs lead to a variety of disturbances in metabolism. In this chapter we are going to study hyperemia, thrombosis, embolism, hemorrhage, edema, infarction and shock.
Both terms refer to increased volume of blood in any portion of the circulatory system. The term active hyperemia means increased volume of blood in the arterial side of vascular system.. The passive hyperemia or passive congestion or congestion means increase amount of blood in venous side and resulted from interference with venous drainage.
It is an increased volume of blood in the arterial side of vascular system. Under normal physiological condition, blood may be flowing through a few capillaries in a tissue and may be shunted many capillaries. It depends on the amount of work carried by animal. The amount of blood flow usually corresponds to the amount of work carried out. If however, more blood is needed for a heavy workload, then all the capillaries and shunts open, the vessels dilated and greater amount of blood is present “Hyperemia”. Active hyperemia is usually associated with inflammation .
1. Physiological active hyperemia It is associated with increased function e.g. in. digestive system after meal, in muscles after exercise and in udder during lactation.
It is usually associated with inflammation. Many etiological agents causing active hyperemia. Physical agents as in case of exposure to heat, light and sun rays, chemicals, as counter irritant, mechanical such as trauma and fraction and infection by bacteria, viruses and their toxins are the common causes of active hyperemia. Moreover, paralysis of vasoactive nerve or stimulation of vasodilators and interference with the blood flow as in case of thrombosis, lead to increase volume of blood in collateral branches which called collateral hyperemia.
The affected part is red in color, enlarged, heavier and oozed blood from cut surface (Figure1).
Microscopic picture The arterioles and capillaries are dilated and filled with blood. In case of the cause is inflammatory, leukocytic infiltration is seen (Figs 2 & 3). Significance and result It is of great benefit in an area of inflammation because it brings more blood and oxygen, which is needed, in body defense. It is usually disappear with removal of the cause leaving no permanent alteration.
It is increased volume of blood in the venous side of the vascular system due to interference venous return from tissue.
Active hyperemia may be classified according to duration and affected area into: Acute or chronic general venous congestion. Acute or chronic local venous congestion.
Causes As mentioned before venous congestion occurs due to interference of blood flow. Moreover acute general venous congestion are resulting from any cause interfere with blood flow through heart and lungs. Degeneration and necrosis of myocardium, in animal put to sever exercise after a prolonged rest or in some infectious diseases, beside interference with flow of blood in lungs, in case of pneumonia where exudates compress the capillaries, are the common causes.
The affected organs are swollen, heavier and bluish red in color beside oozing blood from its cut surface
The veins, venules and capillaries are engorged with blood Significance and result Removal of the cause early results in disappear of hyperemia but persistent moderate cardiac or pulmonary affection usually leads to chronic general congestion
Chronic general venous congestion is increased volume of blood in venous side that persists for long time resulting in prominent alteration in different organs. Causes The causes are present in two organs; the first one is the heart and the second is the lungs. In the heart, stenosis and incompetence (insufficiency) in tricuspid pulmonary or aortic valve beside infarction of heart muscle or myocarditis are the common causes. In the lungs diseases as fibrosis, TB, emphysema and malignant tumor of both lungs are recorded as causes of chronic venous congestion.
The defect in heart, or lungs lead to accumulation of blood in venous side with increase of CO2 concentration, which affect on the endothelial lining of capillaries and venules leading to increase its permeability and permits plasma to escape to tissue and serous cavities. Moreover, increase CO2 concentration stimulates fibroblast proliferation. Pressure atrophy results from persist of large amount of blood in venous side.
The affected organ shows enlargement at first then atrophied. The color becomes dark red to brown due to congestion and lysis of RBCs. The consistency of the organs is firm due to proliferation of fibrous connective tissue. The cut section is oozing blood.
The venules and capillaries are congested besides pressure atrophy, fibrosis, hemosiderosis and transudation in the interstitial tissue of parenchymatous organs are noticed. Significance Pressure atrophy and fibrosis are permanent.
It is a temporally increase in the amount of blood in the veins of an organ or portion of an individual.
Sudden obstruction of veins by thrombus or emboli or compression as in case of strangulated hernia or intussusception is the common causes of acute local venous congestion.
The affected part becomes swelling, cyanotic and cold.
Sudden obstruction of the venous blood leads to accumulate of the non oxygenated blood and damage of the endothelium, which permit exudation of plasma.
The venules and capillaries are congested besides pale eosinophilic edematous fluid and blood is seen in interstitial tissue and lumen of organs (Figure 4).
Venous obstruction of short duration usually followed by recovery. Persistent obstruction lead to atrophy, fibrosis and necrosis of the affected organs.
It is a long-standing increase amount of blood in veins of a portion of the body, which results from gradual interference of venous outflow due to external pressure upon the vein or obstruction within the vein
Brown induration of the lungs Cause Myocardial weakness and valvular diseases are the most common causes of chronic venous congestion in human. Moreover, increase intra abdominal pressure as in case of tympany are seen in animals.
The lungs are large, firm in consistency, dark brown in color due to hemosiderosis and oozed blood and fluid from cut surface.
Congestion of peribronchial blood vessels and inter alveolar capillaries are seen • The lumen of alveoli are filled with transudate and RBCs which lysis to give rise to hemosiderin pigment which engulfed by macrophages called heart failure cells. Moreover, thickened inter alveolar septa by congested blood vessels, fibrosis and heart failure cells are noticed (Figure 5, 6).
Congestion of the posterior vena cava and hepatic veins through heart or lungs is the main cause.
The liver is firm, enlarged and dark red, brownish or yellowish in color, which oozed blood from cut surface (Figure 7).
Congestion of central and portal veins beside hepatic sinusoids is seen. The hepatic cells around central vein show pressure atrophy and necrosis while the peripheral hepatocytes show fatty change. Moreover, hemosiderin pigment is seen inside Von Kupffer’s cells besides fibroblast cells proliferation around the center veins are seen (Figure 8).
It is the gravitation of blood in the lowermost portion of the body. It is usually caused by cardiac defect, which fail to maintain sufficient blood pressure to overcome the force of gravity.
In normal condition and for healthy tissue and organs blood must be remain fluid, but at the same time be able to coagulate to arrest hemorrhage. The mechanisms controlling fluidity and coagulation are highly complex depending on endothelium, platelets and the coagulation system.
Normally the endothelial cells insulate the blood elements from the underlying thrombogenic collagen tissue. Endothelium are intrinsically non-thrombogenic so the platelets do not adhere to the surface of intact endothelial cells in vivo. Once the endothelial cells are removed by injury, procoagulant factors become available, including sub-endothelial collagen, tissue factor, and Von Willebrand's factor. The platelets contain a membrane receptor for Von Willebrand's factor and it appears likely that they adhere to the sub endothelium via this factor. The endothelium prevent coagulation through: It insulates the circulating blood elements from the highly thrombogenic sub endothelium connective tissue. Producing a number of factors as heparin like molecules and thrombomodulin, which inhibit platelet aggregations, constrain the coagulation system and favor dissolution of clots.
The platelets play a central role in normal hemostasis and thrombosis. At the site of endothelial injury they are capable of: a. Adhesion to the subendothelial collagen through specific collagen receptors. b. Secret several factors that promote aggregation of platelets to form a temporary plug and initiate the coagulation system as secretion of thromboxane.
The coagulation cascade involves a sequence of transformation of pro enzymes to activated enzymes culminating in the formation of thrombin, which converts soluble fibrinogen to insoluble fibrin. The various factors are listed in table (1).
Extrinsic pathway; begins with binding between tissue factor and factor VII in the presence of calcium leading to activation of factor X which converts prothrombin into thrombin, which convert fibrinogen to fibrin. lntrinsic pathway is initiated by the activation of factor XII by contact with glass, prekallikrein or high molecular weight kininogen. Activated factor XII activates factor XI, which activates factor IX, Activated factor IX in the presence of calcium, activated factor VIII and phospholipids activate factor X which in turn converts prothrombin to thrombin.
There is a system that maintains the fluidity of blood and localizes a clot to the site of injury to prevent a chain of reaction that leading to coagulation of the entire cardiovascular system. It depend on the following: Depletion of clotting factors by active blood flow. Clearance of activated clotting factors by liver and mononuclear cells. Antithrombin III (Protease inhibitor) in the presence of heparin inactivates thrombin. Fibrinolytic system: It depend on the plasmin (fibrinolytic protease) which acts on fibrin and leukocytes leading to dissolution of clots. It is the escape of all of the blood constituents from any portion of the blood vascular system either to outside the body or into a body cavity or into adjacent tissue.
1. According to location Hemorrhage occurs on the body surface called external hemorrhage but the one occurs into a body cavity or into adjacent tissue called internal hemorrhage.
The escape of blood elements through break or cut in the vessel wall is called hemorrhage by rhexis. Meanwhile, when blood leaves a vessel through an apparently intact vascular wall is called hemorrhage by diapedesis.
Petechial hemorrhages means that the diameter of hemorrhagic area is not more than 1 mm and indicates capillary injury (diapedesis) (Figure 9&10). The ecchymotic hemorrhage is the hemorrhage characterized by diameter not more than 10 mm and indicates injury of capillaries, arterioles and venules (diapedesis) (Figure 11). Moreover, suffusion hemorrhages are diffuse flat irregular areas of bleeding and indicates a defect in clotting mechanism (diapedesis). Meanwhile, hematoma or Hematocyst is excessive hemorrhage which form spherical mass in the tissue vary in size from tiny to over a meter in diameter, it indicates injury of large artery (rhexis) (Figure 12). It is usually associated with trauma or a clotting defect. Linear hemorrhage takes the form of lines like Zebra striping on rectal mucosa in cattle plague Paintbrush type refers to extensive streaking with hemorrhage.
Physiological hemorrhages occurs during parturition, estrus and rupture of umbilical vessels. Any mechanical trauma which lead to laceration, incision, contusion and rupture of blood vessels. Moreover passive congestion usually associated with hemorrhage due to increase permeability. Blood vessel diseases as atheroma, aneurysm besides invading of the vessel wall by malignant tumors. Bacterial, viral and neoplastic diseases beside, hemophilic diseases and passive hyperemia are causing hemorrhage. Hemorrhages are seen associate with deficiency diseases as vitamin C and K deficiency besides exposure to many chemicals and poisoning substances as sweat clover, phosphorus, and arsenic.
Epistaxis means hemorrhage from nose while hemoptysis means hemorrhage from lung. Hematomesis indicates hemorrhage from stomach but melaena means hemorrhage from intestine. The hemometra means hemorrhage from uterus. Hematocele indicates hemorrhage from tunica vaginalis. Hemoperitoneum means hemorrhage in abdominal cavity. Hemopericardium means hemorrhage in pericardium while, Hemothorax: It means hemorrhage in thoracic cavity. Agonal hemorrhage is the hemorrhages on epicardium and endocardium caused by labored breathing and terminal muscular activity in the process of dying. The Purpura hemorrhagica means extensive petechial and ecchymotic hemorrhages on serous and mucous membranes. It is a descriptive term and doesn’t mean a specific disease. It is usually associated with disturbances of clotting mechanism due to platelets such as toxic depression, excessive destruction and extensive and diffuse endothelial damage, which consume excessive numbers of platelets. It is usually associated with strangles due to intoxication.
Red cells are clearly visible in tissue outside the blood vessels. Presence of hemosiderin-laden macrophages (sidrocytes) is indication of old hemorrhages (Figures). Moreover, pretences of cholesterol mass of blood.
The factors which share in arresting hemorrhages including, pressure from perivascular tissue, retraction of severed blood vessels leads to reduces the diameter of their lumen, blood clot usually stops hemorrhage beside an low blood pressure.
The extravasated erythrocytes usually break down and liberate hemoglobin, which break into hem and globin. Hem breaks into hematoidin (yellow granules usually are not seen because they dissolve in tissue fluid) and hemosiderin (golden yellow pigment engulfed by macrophages). Phagocytic cells remove small hemorrhages. Large hemorrhages are encapsulated and organized with some sidrocytes.
The importance of hemorrhages is varies according to its size and location as small hemorrhage in brain may lead to paralysis or death. If the cause removed and stopping of hemorrhage, recovery occur, if persist it lead to death.
Thrombosis is the pathologic formation of a solid mass from the blood elements within the cardiovascular system during life of the patient. Thrombus is the solid mass adheres to the vessel lining.
Thrombosis is a dynamic and complex process resulting from the interaction of blood constituents with the altered vessel wall resulted in formation of a blood clot due to the activation of the coagulation sequence similar to occur when blood is poured into a test tube.
It stimulates platelet adhesion and initiates the coagulation cascade. It is the main cause of arterial thrombosis. Cause
Slow of the blood flow lead to disruption of normal laminar flow of blood, which characterized by cellular element in the center separated from endothelium by plasma. It brings platelets in contact with endothelium and encouraging coagulation.
It is seen in aneurysms, cardiac anomalies and venous stasis. 3. Changes in the blood itself Cause Increased viscosity, increased fibrinogen levels and platelets number, bacterial and parasitic emboli. It is the most important factors in venous thrombus.
Changes in the vessel wall (endothelial injury) Damage to endothelial cells exposes the thrombogenic sub endothelium, which initiates thrombosis: Following injury, platelets becoming sticky and adhere, aggregate and release; the extrinsic pathway of blood coagulation is activated and results in fibrin formation.
Slowing blood flow favors thrombosis. The former is a major factor in thrombosis of the leg veins, which is seen primarily in conditions of stasis such as congestive heart failure. Stasis or slower blood flow lead to disrupt laminar blood flow and brings platelets in contact with the vessel lining and it may damage the endothelium. Aneurysms are good examples of altered vascular segments where turbulent flow is associated with thrombosis.
Several clinical conditions as disseminated cancer enhancement thrombosis. When necrosis develops in the setting of rapid tumor growth, these cancers release tissue thromboplastin (tissue factor) and possibly other pro coagulants into the circulation. Hypercoagulability is believed to be an important pathogenic factor in the increased tendency to venous thrombosis among women aged 35-45 who takes oral contraceptives
The thrombi tend to be irregular in shape friable with dull roughened surface. The color usually is a mixture of red and gray or has have a laminated structure in irregular layers or lines of zahn which contain alternating pale lines (composed of platelets and fibrin) and darker strips of (predominantly red blood cells). Thrombi may vary in size from microscopic (such as fibrin thrombi plugging capillaries) to thrombi that occupy large portions of the aorta or fill a cardiac chamber. At least one side attached to the wall of blood vessel (Figure 16).
It composed of blood elements along with fibrin. Platelets are difficult to observe, except perhaps at the points of attachment (Figure 17&18).
I. Classification according to location of thrombus Cardiac thrombi may attach to the valves (valvular thrombi) as in case of infection with streptococcus pyogenes or Erysiplothrix rhusiopathiae. The other one attached to the wall and called mural thrombi. Arterial thrombi occur in case of parasitic thrombus caused by larvae of Strongylus valgaris. Venous thrombi are more frequent in human than animals. Capillary thrombi are usually associated with inflammation. Lymphatic thrombi occur in lymph vessels draining area of inflammation
Mural thrombi are attached to the heart wall while, valvular thrombi are attached to the heart valves. Lateral thrombi are attached to one side of a vessel wall while occluding thrombi are attached to the entire endothelium of the vessel. The saddle thrombi straddle the bifurcation of the blood vessels but canalized thrombi result from partial repair of the clot with formation of a new blood canal. Moreover, obturating thrombi have a free end trailing downstream.
Thrombi classified into septic thrombi, parasitic thrombi and aseptic thrombi IV-Classification according to color of thrombi
N.B. Vegetation thrombi occur when thrombi formed on the heart valves, they are known as vegetation. These are often infected.
1. Contraction The first alteration occurring in thrombi, containing fibrin, is decrease in size due to contraction of fibrin. 2. Lysis of the thrombus by plasmin, which activated by factor VII. 3. Liquefaction: It occurs under the effect of autolytic leukocytic enzymes. 4. Abscessation when pyogenic are present. 5. Organization and recanalization commonly occur in large thrombi. Recanalization occurs by invasion of thrombus mass by newly formed capillaries and does not prevent the acute effects of thrombosis (Figure 19). 6.Mineralization of degenerated and necrotic thrombi usually occur. 7.Thromboembolism: Some time fragment of thrombus is detached and carried in the circulation. Effect of thrombosis Negligible effects if the organ or tissue has a rich collateral circulation. Beneficial effects. Thrombosis of injured vessels which assists in control of hemorrhage. Harmful effect: Thrombosis of major blood vessels in areas with insufficient collateral circulation.
The postmortem clot occurs after death due to release of thromboplastin from damaged endothelium by lack of oxygen. There are two types of postmortem clots. Red or current jelly clot: It occurs when there is a rapid clotting of the blood. The blood components are evenly distributed throughout the clot. Yellow or chicken fat clot. The ventral portion of the clot is red and contains erythrocytes, while the dorsal portion is composed of fibrin and serum. The erythrocytes sedimentation to form red zone is due to prolonged coagulation time or increased sedimentation rate.
It is the widespread development of small fibrin thrombi in the microcirculation throughout the body. It occurs with infectious disease, immunologic injury and snakebite, which lead to diffuse endothelial injury. In animals, it is usually observed with severe burn, extensive trauma and in severe systemic infection as canine hepatitis, blue tongue and hog cholera Effects It is usually fatal due to infarction, sever bleeding and hemolytic anemia.
It is the process of moving of solid, liquid, gaseous foreign body through the circulatory system.
Causes and types of emboli Thromboemboli: It is the most important and common one. More than 99% of all emboli originate in thrombi and are called thromboemboli. It results from fragmentation of thrombi and carried away by flowing blood. They resemble thrombus in microscopic and gross appearance. Thromboembi arise from venous thrombi usually lodge in pulmonary arterial tree, Systemic Embolism: almost always originates in the heart and aorta, travel through the arteries and lodge in various organs, usually causing infarcts.
Gas emboli: It may cause bubbles in blood that may coalesce and obstruct the flow of blood causing infarction. It may occur when traumatic or surgical wounds rupture large blood vessels. In human, gas embolism is seen following a rapid change in atmospheric pressure in deep-sea divers and in construction workers emerging from underwater compartments (Caisson disease). Tumor cell emboli are occasionally seen in patients with cancer. Spodogenous emboli occur due incompatible blood transfusion.
It depends upon several factors. If the blood vessels have efficient collateral circulation, the circulation is maintained and little damage occur, but if there is no efficient collateral circulation as in end artery it lead to infarction. Moreover, the small sizes lead to partial arrest of blood supply and ischemia but the large one lead to obstruction and infarction. Aseptic emboli lead to ischemia and infarction while septic one lead to pyemia with multiple abscess formation.
An infarct is a localized area of ischemic necrosis resulting most often from reduction of its arterial supply or occasionally its venous drainage. The process of development of this lesion is known as infarction.
A. According to color Pale infarct: It occurs in solid organs which lacks significant collateral circulation as heart, kidney, spleen and brain as a result of obstruction of and end artery.
The venous infarcts are intensely hemorrhagic due to congestion and hemorrhage.
In all tissue other than brain infarction usually produce coagulative necrosis of cells, so the infarction is solid. C. Sterile versus septic Most infarcts are sterile. Septic infarcts usually associated with septic thromboemboli or when infarction occur in tissue normally contain bacteria as intestine.
Immediately after obstruction of the artery, the capillaries begin to dilate in an attempt to increase the blood supply. However, blood from adjacent arteries is forced to ischemic area through the anastomosing capillaries. Due to the engorgement of capillaries the affected area is much redder than the surrounding tissue and called red infarct. Blood flow through capillaries in the infarct area become extremely slow and lead to hypoxemia and accumulation of waste products which lead to damaged endothelium and hemorrhage (Hemorrhagic infarct) Within 24 hours the cells in the infarct area shows coagulative necrosis. The erythrocytes in the area of infarction undergo autolytic changes leaving the infarct pale (Pale or anemic infarct) (Figure 23 & 24). Dead tissue is irritating to the body which response by line of defense formed from dilated capillaries and leukocytic infiltration mainly macrophages and neutrophils. Later on the necrotic tissue is replaced by granulation tissue, which mature to form fibrous tissue.
The color is differs from red to pale or white. The infarcts usually red in the first (Figure 25) and then become pale (Figure 26) except in the brain it is usually pale. The infarct of intestine lungs and liver is usually red. It is usually cone shape with the apex at the point of obstruction and the base at the surface of organ. The infarct is swollen in the early stage and shrinkage below the surface with red margin.
The infarct area losses their function of affected area or may be invaded by pyogenic bacteria to form suppuration or by putrefactive micro-organism to form gangrene and kill the animals. Organization and replaced by scar may develop.
It is a syndrome resulting from a disproportion between blood volume and volume of the circulatory system that need to be filled. The fundamental disturbance is that blood volume is too small to fill the vascular system. The cell damage is due to inadequate perfusion of tissues with adequate oxygen and nutrients, which lead to anaerobic metabolism and lactic acidosis resulting in cell damage.
1. Hypovolemic shock It results from a large loss of fluids as in case of extensive hemorrhage, vomiting, and diarrhea or severe burn. The result is marked reduction in blood volume and therefore cardiac output.
It caused by primary cardiac disease (myocardial infarction), which lead to inadequate cardiac systolic output in the presence of adequate intravascular blood volume. It is more common in humans than animals.
It is caused by marked decrease in the peripheral vascular resistance caused by arteriolar dilatation and pooling of blood in dilated capillaries and venules, which effectively reduce blood volume. It caused by several bacterial infection e.g., E. coli, Pseudomonas and streptococcus. It characterized by dilatation of capillaries and venules caused by chemical mediators with destruction of endothelial lining.
It follow sever trauma, pain and restrain which lead to arteriolar dilatation and pooling of blood in capillaries and venules. 5. Anaphylactic shock It mediated through release of histamine and other mediators which lead to pooling of blood in capillaries and venules and increase vascular permeability.
Stage of compensation Increase heart rate (tachycardia) and peripheral vasoconstriction under the effect of sympathetic reflex to compensate the decrease in cardiac output that maintains blood pressure in vital organs.
Prolonged vasoconstriction is harmful because it impairs tissue perfusion, tissue fluid exchange and oxygenation leading to lactic acidosis, cellular degeneration and necrosis.
Widespread vasodilatation of capillaries and venules lead to progressive fall in blood pressure with critical decrease in brain and myocardial perfusion which lead to brain and cardiac dysfunction and death.
Cellular necrosis and degeneration particularly in liver, kidneys, heart and gastrointestinal tract besides petechial hemorrhage are numerous. Severe congestion in most tissue particularly liver, gastrointestinal tract and adrenal gland except in shock due to sever hemorrhage are seen. The capillaries and venules are congested beside transudate in body cavities and among cells. Definition: Edema is the term generally used for the accumulation of excess fluid in the intercellular (interstitial) spaces or body cavities, which has different importance depending on its location.
Water constitutes roughly about 60% of the body weight. One third is extracellular fluid, while the remainder is intracellular. Normal there is a continues flow of fluid from the blood to the interstitial tissue and then back to the blood stream under the opposing effect of osmotic and hydrostatic pressure. Fluid moves from the intravascular to the interstitial compartment at the arteriolar end of microcirculation under the influence of hydrostatic pressure of the blood minus the osmotic pressure of plasma proteins. It returns to the intravascular compartment, at the venular end, under the influence of the osmotic pressure of the blood minus the hydrostatic pressure at the venous end of the capillary. Normally, the outflow of fluid from the arteriolar end is nearly equal to inflow at the venular end. There is a small loss of fluid into the interstitial tissue; this fluid is drained off through lymphatic to be returned to bloodstream. Any disturbances of the delicate balance between the production of interstitial fluid and its return back to blood through either reabsorption or lymphatic drainage will result in edema. The disturbances occur through increase hydrostatic pressure, decrease osmotic pressure or lymphatic obstruction. Moreover, increase permeability associated with inflammation, hypersensitivity and chronic venous congestion lead to leakage of plasma fluid and edema.
As mentioned before, increase permeability due to bacteria and their toxins, snake venom and inflammatory chemical mediators lead to leakage of plasma fluid and edema. Moreover, increase hydrostatic pressure, which occurs, associated with venous congestion due to heart diseases, thrombosis and aneurysm besides decreased colloidal osmotic pressure as in case of intestinal parasitic infestation, malnutrition and kidney diseases are the common causes of edema.. Lymphatic obstruction as in case of tumor, abscess and intravascular parasites lead to accumulation of edematous fluid.
Edema may be localized or generalized, inflammatory or non-inflammatory. A. Local edema
Edema is a cardinal sign of inflammation. It is caused by increased capillary permeability and hydrostatic pressure due to release of chemical mediators.
It is caused by increased capillary permeability and hydrostatic pressure due to release of vasoactive substances as histamine.
When complete obstruction of vein as in case of thrombosis lead to sever edema and hemorrhage resulted from increased hydrostatic pressure at venous side. When venous drainage is partially impaired, edema is less sever.
It is caused by lymphatic damage by surgery, neoplasm, abscess and intravascular parasites.
It is caused by impaired cardiac function leading to increased hydrostatic pressure. Also cardiac failure lead to diminished left ventricular output, which lead to decrease glomerular filtration and stimulate juxtaglomerular cells to secret renin. Renin in turn induces increased aldosterone production leading to retention of sodium and water and generalized edema.
It caused by decreased plasma osmotic pressure due to dietary protein deficiency (malnutrition edema), decrease synthesis of albumin in liver diseases (hepatic edema), renal diseases which lead to loss of plasma protein and increase sodium retention (renal edema) and heavy infestations with intestinal parasites as trichostrongyles (parasitic edema).
The affected organ is edematous, swollen, wet and oozed fluid when cut besides, doughy and firm in consistency. Moreover, the edematous tissues are cool and painless in non inflammatory, but hot and painful in inflammatory edema. The color is pale due to compressed capillaries with transudate in non-inflammatory or red with inflammatory due to hyperemia. The edematous tissue is pitting on pressure when force is applied to the area of non-inflammatory edema.
The intercellular space are larger and numerous than normal due to presence of pale eosinophilic granular material (transudate) (Figure 28), or more eosinophilic contain leukocytes (transudate) in intercellular space (Figure 29). Congested capillaries are seen Moreover, atrophy of parenchymatous organs with hyperplastic fibrous tissue in case of chronic edema.
Hydropericardium is edema in pericardial sac. Hydrothorax is edema in thoracic cavity. Anasarca is generalized edema prominent in subcutaneous tissue and body cavities. Hydrocele means edema in tunica vaginalis. Meanwhile hydrocephalus is edema in brain. Ascites means edema in abdominal cavity. Moreover, Intracellular cytotoxic cerebral edema is an early manifestation of cell injury resulting from failure of normal energy.
Early removal of the cause lead to complete recovery. Chronic edema lead to atrophy and fibrosis of parenchymatous organs. |
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