Circulatory Disturbance PDF

Circulatory disturbance Prepared by : Dr. Rasha Arafa Abd-elmaksoud Pathology Department Port said University  Circulatory disturbances Means: disturbances of blood flow and body fluids. Edema Normal (Physiological) movement of interstitial fluid: 1...

Circulatory disturbance Prepared by : Dr. Rasha Arafa Abd-elmaksoud Pathology Department Port said University  Circulatory disturbances Means: disturbances of blood flow and body fluids. Edema Normal (Physiological) movement of interstitial fluid: 1) Vascular factors: a- Forces the fluid extravascularly; - Intra-capillary hydrostatic pressure. Capillary permeability b- Attracts the fluid from tissue spaces into blood - Colloidal osmotic pressure of plasma proteins. - Opened veins and lymphatic vessels. 2) Tissue factors: Osmotic pressure of the tissue (Na CL, proteins) derives fluid exxtrvascular. Causes of edema:  Classification of edema Localized (Unilateral) Generalized Miscellaneous 1- Inflammatory 1- Cardiac 1- Angioneurotic (Allergic) 2- Obstructive 2- Renal 2- Milroy’s edema Venous Nephritic lymphatic Nephrotic 3-Nutritional (Famine) What is the distribution of each type of edema? Pathological features of edema: - All tissues except bone may be the seat of edema. - Common sites are the S.C. tissue, mucous membranes, serous sacs, lung alveoli, brain, areolar connective tissue. N / E: - edematous tissue is swollen, pale, heavy, moist and soft. - The cut section drips fluid. - Edema of the skin and S.C. tissue may be pitting or non pitting. 1) Pitting (soft) edema: - The accumulated fluid is present free in the tissue spaces and can be moved by pressure, so the affected part pits on pressure. Pitting edema occurs in all varieties of generalized edema and in localized obstructive venous edema. 2) Non pitting (Hard) edema: - The edematous part does not pit on pressure. - Occurs in inflammatory edema and obstructive lymphatic edema. M / E: - Edema fluid is pale red homogenous or fine granular material. - It separates the tissue cells and may enter them (intracellular). Hyperemia and congestion General venous congestion It occurs due to total (congestive) heart failure. Congestion occurs all over the body. Total heart failure means both right sided and left sided heart failure. It may by acute or chronic. 1. A cute general venous congestion: Terminal condition in acute heart failure. All organs show acute congestion. 2- Chronic general venous congestion: Definition: gradual venous congestion affecting the whole venous system. Causes: both right sided and left sided. Right Sided heart failure.: shows venous congestion all over the body except lungs. Left sided. heart failure.; shows chronic venous congestion of lungs. I- General effects: 1- Congested neck veins: due to dilatation of the vena cava and draining systemic veins to accommodate more blood 2- Cyanosis: It is purple- blue coloration of lips, bed of nails … etc. caused by increased reduced HB and inadequate tissue perfusion and decreased oxygenation. 3- Cardiac edema: Accumulation of serous fluid in the interstitial spaces, caused by chronic Right Sided heart failure.  II- Local effects (Pathological features in different organs): * Liver: In the early stages (Nutmeg liver): In late stages (cardiac cirrhosis). Chronic venous congestion lungs (Brown induration) increase Blood In the capillaries leads to rapture and disintegration of R.B.Cs leads to release of hemosiderin which is taken by macrophages that appears swollen and brown and is called heart failure cells.  (A) Local venous congestion Definition: Localized congestion in any part of the body whose venous out flow becomes obstructed. (1) Acute local V.C. Causes: Sudden complete venous obstruction due to: Thrombosis, Ligature, Twisting of the pedicle of movable organ as ovary &Strangulated hernia. Pathology: Rapid severe dilatation of the veins and capillaries which may rupture. Edema occurs rapidly. Fate: (1) Sufficient venous anastomosis: No harmful effect (2) Insufficient venous anastomosis as in mesenteric veins: Venous infarction of intestine. (2) Chronic local venous congestion Causes: gradual incomplete venous obstruction due to compression by: 1- Tumour 2- Enlarged lymph node. 3- Pregnant uterus 4- Liver cirrhosis and fibrosis Pathology:(1) The veins, venules and capillaries distal to obstruction become dilated and congested resulting in edema. (2) Gradual opening of the collaterals and anastomotic veins. Hemorrhage Purpura Thrombosis Definition: It is the process by means of which a solid mass called (thrombus) is formed from circulating blood elements mainly platelets and fibrin in the C.V.S. during life. Causes of thrombosis: (Vircow’s triad) 1) Damage of the vascular endothelium i.e. roughness of the intima. *Normally prostacyclin secreted by the vascular endothelium inhibits thrombosis. This damage may be: a- Mechanical due to Trauma, pressure (as ligature). b- Inflammatory as phlebitis, arteritis, endocarditis c- Degenerative as atheroma 3) Changes of composition of blood (hypercoagulability): 1- Excessive increase in number of blood elements. a. Platelets: After severe hemorrhage new platelets provides by the bone marrow especially after major operations. The new platelets are more sticky. They agglutinate in small masses and adhere to the vascular endothelium. Their lysis release factors which starts thrombosis. b. Red cells: Increase in polycythemia causing increased viscosity and stasis. c. White cells: Increase in leukemia causing increase viscosity and stasis. d. All blood elements: In dehydration due to decrease plasma volume causing increased viscosity. 2- Blood chemical factors causing systemic activation of clotting system as in disseminated intravascular coagulation “DIC” in which wide spread thrombosis of small blood vessels occurs due to endotoxins, septicemia, liver and kidney diseases …….etc. Mechanism of thrombus formation: 1) Platelets adhere to the damaged endothelium. The damaged platelets release thromboxane A2 helps their aggregation. 2) More platelets are deposited in columns across blood stream perpendicular to blood vessel wall. These columns appear as homogenous reddish streaks called Lines of Zahn. 3) Stasis of blood occurs between the lines of Zahn with deposition of fibrin threads and blood corpuscles.  Types of thrombosis: Thrombi are classified according to 1. Presence of organism i.e. infection: - Septic (contains pyogenic bacteria). - Aseptic (no microorganism). 2- Color: a. Pale thrombus; pale grayish white with granular surface, firm and adherent to the intima, consists of platelets and fibrin. b. Red thrombus; dark red with smooth surface soft, adherent to the pale thrombus not to intima mainly of erythrocytes and fibrin. c. Mixed or laminated thrombus; consists of alternating layers of red and white thrombi commonly found in aneurysms. 3- Extension: a. Mural thrombus: thrombus adherent to the wall. b. Occluding thrombus: Thrombus occlude the lumen. Propagating thrombus: The red thrombus may extend to reach the next venous tributary, thrombosis starts again as the blood once more will be in motion, thrombosis occurs in moving blood, clotting in stagnant blood and another red thrombus is produced and the process is repeated and the propagating thrombus extends in the direction of the heart Thrombus Clot * Blood in motion * Stagnant blood * Platelets are essential * Not essential * Lines of Zahn * No. * Platelets and fibrin * Fibrin and red cells. * pale or red or both * Dark red or yellow red. * Firm, friabloode * Soft moist * Firmly adherent to the wall * Not adherent to the wall * Rough surface * Smooth surface  Fate of thrombus: 1. Septic thrombus: Fragments by the proteolytic enzymes into septic emboli causing pyemic abscess. 2. Aseptic thrombus: i. If small dissolved by fibrinolysis and absorbed. ii. Contraction or shrinkage. iii. Organization with or without canalization. iv. Calcification (Phlebolith). v. Detached to form emboli Embolism A) Thrombo- embolism: A detached thrombus may originate from: 1. Veins: - A detached thrombus from systemic veins reaches the right side of heart, then lungs. It impacts in the pulmonary arteries leading to pulmonary Embolism - If the embolus bypassed the lungs due to atrial or ventricular septal defect and passes from right to the left side of the heart it is then carried by the systemic arterial circulation to any tissue. - Detached thrombus from the portal vein or its branches passes to the liver (portal embolism) emboli originating in the liver reach the systemic veins through hepatic veins and impact in the lung. 2- Cardiac thrombi: - Usually in the left side of the heart - They are carried by the systemic arterial circulation to impact in any organ. 3- Arteries: Emboli originating from arteries are uncommon due to: i. Arterial thrombosis is rare. ii. Arteries get narrow in their course and the thrombus does not move. Effects of emboli of thrombotic origin: Depends on: 1. Size of embolus. 2. Nature of the embolus, septic or aseptic: Aseptic embolus: produces transient ischemia if the collateral circulation is good, and infarction when poor. Septic embolus: produces pyaemic abscess at the site of its impaction. 3. State of the collateral circulation in the affected organ. B) Fat embolism: Causes: Is common in sites containing fat as: 1. Cutaneous burns. 2- Bone fractures. 2. In abdomen due to acute pancreatitis. 4- Fatty change liver. Fat globules enter through the ruptured veins and produce pulmonary and systemic embolism. The fatty acids from broken down fat damage the capillaries leading to hemorrhagic edema. C) Tumour emboli: Malignant cells pass as emboli in the circulation and give metastases in the organs. D) Parasitic emboli: As billharzial ova and worms. E) Air embolism: Sudden admission of 100 cc air in the blood stream may lead to sudden death. The air may block the right ventricle or the pulmonary arteries leading to acute heart failure. Causes: 1. Injury of large neck veins leads to their gaping as they are embedded in fascia which prevent their collapse. Air is sucked into the heart 2. Faulty technique in doing artificial pneumothorax and in blood transfusion. 3. Air passes into the uterine veins in criminal abortion. F) Amniotic fluid embolism: Occurs during delivery. It may result in fatal pulmonary embolism.  Ischemia Definition: Decrease blood supply to a part or tissue due to occlusion of its artery. Types: Sudden (acute) ischemia: Cause: Sudden complete arterial occlusion by: a. Thrombosis or embolism. b. Surgical ligature of the artery. c. Twisting of the pedicle of an ovarian cyst. d. Arterial spasm as in ergot poising. Effects: depends on: 1) Collateral: a- Sudden occlusion of end arteries (arteries with inefficient collaterals) leads to infarction then gangrene. b- Sudden occlusion of arteries with efficient collaterals may not cause tissue damage. 2) Nature of the affected tissue: related to its metabolic rate i.e. Highly specialized cells are easily killed as ganglion cells of nervous system die in few minutes. Connective tissue cells and skin withstand ischemia for a longer period. Gradual (chronic) ischemia: Causes: Gradual incomplete arterial occlusion by: a. Pressure on the artery by tumour, enlarged lymph node, fibrosis …. Etc. b. In the wall of the artery as atheroma, endarteritis as in syphilis. Effects: Gradual occlusion gives chance for the collaterals to open up so: 1. With inefficient collaterals some necrosis and replacement fibrosis occur 2. With efficient collaterals; no tissue damage occurs.  Infarction Definition: It is an area of necrosis due to acute ischemia in an organ with endarteries (brain, retina, heart, spleen, kidney and intestine). - An end artery has few or no anastomosis with neighboring arteries. - An infarct is an example of ischemic necrosis which is coagulative in all organs and liquifactive in the brain. Types of infarction: 1- Red (hemorrhagic infarct: 2- Pale (anemic) infarct: Occurs in firm and less vascular organs as the kidneys and heat. 3- Infarction of the brain and spleen may be pale or red Fate of infarct: a. Small infarct: Necrotic tissue is removed by macrophages. Granulation tissue fills the defect followed by fibrosis. b. Large infarct: is surrounded by fibrous capsule and its substances may show dystrophic calcification. In the brain due to high lipid content, it leaves a cyst surrounded by glial tissue.  Gangrene Definition: Necrosis with putrefaction. Causes: 1- Necrosis is caused by: a- Acute ischemia (Secondary gangrene) b- Bacterial infection (Primary gangrene) 2-Putrefaction: is caused by saprophytic bacteria which become active in necrotic tissue. They digest the various components of necrotic tissue liberating hydrogen sulphide (H2S) that gives the tissue a foul odour. Hydrogen sulphide unites with iron of hemoglobin forming iron sulphide that stain the gangrenous tissue black. * Examples of Dry gangrene: A) Senile gangrene of the lower limb. It affects old males. Predisposing factors: a. Atherosclerosis which is common in old age, predispose to thrombosis. b. Weak heart action and low blood pressure causes stasis of blood c. Low body resistance due to nutritional disturbances. (B) Diabetic gangrene: Similar to senile gangrene but: a. It occurs at younger age as diabetes predisposes to atheroma followed by arterial occlusion. b. Gangrene starts dry and passes to a wet gangrene as tissue hyperglycemia is a good culture medium for saprophytic bacteria.  The gangrenous process follows the following steps: 1-Arterial occlusion occurs either due to thrombosis in atherosclerotic artery or spontaneously as a result of wearing tight shoes which cuts the blood supply in dorsalis pedis artery. This leads to necrotic area in the big toe manifesting as a non healing ulcer. 2- Later on the necrotic area stains red by blood escaped from the necrotic vessels. Drainage and evaporation of blood and tissue fluids causes dryness of the dead part It becomes shrunken and mummified. 3- Saprophytic bacteria invade the necrotic tissue and cause putrefaction. They act on the blood proteins liberating hydrogen sulphide which causes bad odour. Hydrogen sulphide unites with iron from hemoglobin to form iron sulphide which stains the gangrenous part black. 4-The gangrenous process advances slowly along the limb because of the toxic products of putrefaction irritates the living one and initiates inflammation of its tissue with thrombosis of its vessels, and further tissue necrosis and extension of the gangrene. 5-When gangrene reaches a level with good blood supply is stops (seldom above the knee). The toxic products of putrefaction act as an irritant and cause a zone of acute inflammation in the neighboring healthy tissue. It appears as a narrow red line between the healthy and gangrenous part called Line of demarcation. 6-The line of separation is formed of granulation tissue below the line of demarcation. It produces a groove that slowly deepens to separate the gangrenous part leaving a cone shaped stump (natural amputation). The stump is conical as the gangrenous process spreads higher up in the skin and subcutaneous tissue than in muscles and bone because the blood supply of the skin and subcutaneous tissue is less abundant. Parameters Dry gangrene Wet gangrene 1- Sites Extremities e.g. lower limb Internal organs e.g. intestine, lung. Extremities in crush injury and diabetes. 2- Cause Gradual arterial obstruction Sudden arterial and venous obstruction. 3- Progress Slow Rapid 4- Line of demarcation Present Absent 5- Gangrenous part Black, Dry, and mummified Swollen, edematous with ulcerated skin. 6- Putrefaction and bad Minimal Maximal odour 7- Toxemia Mild Severe and marked (2) Gas gangrene: It is moist gangrene mainly of muscles. - It occurs in deep wounds contaminated by manured soil containing anaerobic spores. - Muscle necrosis is caused by aerobic pathogenic bacteria or by trauma. - Putrefaction is produced by contaminating anaerobic saprophytes (intestinal commensals from animals and man) -Saprophytes are of 2 types. (1) Saccharolytic: Clostridium Welchii, Clostridium Edematients, Clostridium Septicum. They produce enzymes and exotoxins as: *Lecithinase which lyses the cell membrane. *Necrotoxin which kills the muscle cells. *Hyaluronidase which digest ground substance (2) Proteolytic: CI. Histolyticum , CI. Sordelli ,CI.Bifermentans. They liquefy the dead tissue producing foul smelling gases. N.E: The muscle is swollen; pink stained by liberated HB due to hemolysis of red cells by toxins with bubbles of Co 2. Gas produces an emphysematous crackling on palpation. - Subcutaneous tissue and skin are involved. Prognosis: Highly fatal due to severe toxemia and acute hemolysis by lecithinase leading to shock. What is the Bed Sores?