An active process resulting from arteriolar dilation and increased blood inflow, as occurs at sites of inflammation or in exercising skeletal muscle
Congestion
A passive process resulting from impaired outflow of venous blood from a tissue
Conjunctival hyperaemia
Tortous, dilated conjunctival arterioles
Liver with chronic passive congestion and hemorrhagic necrosis
Central areas are red and slightly depressed compared with the surrounding tan viable parenchyma, creating "nutmeg liver" (so called because it resembles the cut surface of a nutmeg)
Liver with chronic passive congestion and hemorrhagic necrosis
Microscopic preparation shows centrilobular hepatic necrosis with hemorrhage and scattered inflammatory cells
Oedema
An accumulation of interstitial fluid within tissues
Transudate
The edema fluid that accumulates owing to increased hydrostatic pressure or reduced intravascular colloid, typically is a protein-poor fluid with a specific gravity less than 1.012
Exudate
The edema fluid that accumulates due to increased vascular permeability, is a protein-rich fluid with a specific gravity usually greater than 1.020
Pathophysiologic Categories of Oedema
Increased Hydrostatic Pressure
Reduced Plasma Osmotic Pressure (Hypoproteinemia)
Lymphatic Obstruction
Sodium Retention
Inflammation
Increased Hydrostatic Pressure (Local)
Increases in intravascular pressure can result from impaired venous return, e.g. a deep venous thrombosis in the lower extremity can cause edema restricted to the distal portion of the affected leg
Increased Hydrostatic Pressure (Generalized)
Increases in venous pressure, with resultant systemic edema, occur most commonly in congestive heart failure
Increased Hydrostatic Pressure in Congestive Heart Failure
1. Reduced cardiac output leads to hypoperfusion of the kidneys, triggering the renin-angiotensin-aldosterone axis and inducing sodium and water retention (secondary hyperaldosteronism)
2. Failing heart often cannot increase its cardiac output in response to the compensatory increases in blood volume, leading to a vicious cycle of fluid retention, increased venous hydrostatic pressures, and worsening edema
Reduced Plasma Osmotic Pressure
Conditions in which albumin is either lost from the circulation or synthesized in inadequate amounts, e.g. nephrotic syndrome, liver cirrhosis, protein malnutrition
Lymphatic Obstruction
Impaired lymphatic drainage and consequent lymphedema usually result from a localized obstruction caused by an inflammatory or neoplastic condition, e.g. filariasis, breast cancer
Sodium and Water Retention
Excessive retention of salt (and its obligate associated water) can lead to edema by increasing hydrostatic pressure and reducing plasma osmotic pressure, seen in diseases that compromise renal function
Effects of Edema
Can range from annoying to rapidly fatal, e.g. subcutaneous edema can impair wound healing or clearance of infections, pulmonary edema can interfere with normal ventilatory function and create a favorable environment for infections, brain edema can cause herniation and compression of the brain stem vascular supply
Herniation syndromes
Displacement of brain parenchyma across fixed barriers can be subfalcine, transtentorial, or tonsillar (into the foramen magnum)
Haemorrhage
The extravasation of blood from vessels
Haemorrhage
Can occur in a variety of settings, e.g. capillary bleeding in chronically congested tissues, trauma, atherosclerosis, or inflammatory or neoplastic erosion of a vessel wall
May accumulate within a tissue as a hematoma, ranging from trivial (e.g. a bruise) to fatal (e.g. a massive retroperitoneal hematoma from a ruptured aortic aneurysm)
Large bleeds into body cavities are called hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis
Extensive hemorrhages can occasionally result in jaundice from the massive breakdown of red cells and hemoglobin
Petechiae
Minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces, caused by low platelet counts, defective platelet function, or loss of vascular wall support
Purpura
Slightly larger (3 to 5 mm) hemorrhages, resulting from the same disorders that cause petechiae, as well as trauma, vascular inflammation, and increased vascular fragility
Ecchymoses
Larger (1 to 2 cm) subcutaneous hematomas (colloquially called bruises), with characteristic color changes due to the enzymatic conversion of hemoglobin and bilirubin
Clinical significance of hemorrhage
Depends on the volume of blood lost and the rate of bleeding, with rapid loss of up to 20% of blood volume being tolerated in healthy individuals
Haemorrhages
Massive breakdown of red cells and haemoglobin that can occasionally result in jaundice
Petechiae
Minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces; causes include low platelet counts (thrombocytopenia), defective platelet function, and loss of vascular wall support, as in vitamin C deficiency
Purpura
Slightly larger (3 to 5 mm) hemorrhages that can result from the same disorders that cause petechiae, as well as trauma, vascular inflammation (vasculitis), and increased vascular fragility
Ecchymoses
Larger (1 to 2 cm) subcutaneous hematomas (colloquially called bruises); extravasated red cells are phagocytosed and degraded by macrophages, causing characteristic color changes
Clinical significance of hemorrhage
Depends on the volume of blood lost and the rate of bleeding; rapid loss of up to 20% of blood volume or slow losses of even larger amounts may have little impact in healthy adults, but greater losses can cause hemorrhagic (hypovolemic) shock; the site of hemorrhage is also important, as bleeding that would be trivial in the subcutaneous tissues can cause death if located in the brain; chronic or recurrent external blood loss frequently culminates in iron deficiency anemia, while internal bleeding does not lead to iron deficiency
Hemorrhage
Punctate petechial hemorrhages of the colonic mucosa, a consequence of thrombocytopenia
Fatal intracerebral hemorrhage
Outline
Hyperaemia
Congestion
Oedema
Haemorrhage
Thrombosis
Embolism
Infarction
Shock
Hemostasis
A series of regulated processes that maintain blood in a fluid, clot-free state in normal vessels while rapidly forming a localized hemostatic plug at the site of vascular injury
Thrombosis
The formation of blood clot (thrombus) within intact vessels, the pathologic counterpart of hemostasis
Virchow's triad
The three primary abnormalities that lead to thrombus formation: endothelial injury, stasis or turbulent blood flow, and hypercoagulability of the blood
Thrombosis
Venous thrombus
Histological section showing the characteristic laminated or coralline structure of a thrombus
Antemortem clot (Thrombus)
Firm, focally attached to vessel walls, and contain gray strands of deposited fibrin; characterized by lines of Zahn (pale platelet and fibrin layers alternating with darker red cell–rich layers)
Postmortem clot
Gelatinous, usually not attached to the underlying vessel wall, with a dark red dependent portion and a yellow "chicken fat" upper portion
Causes of endothelial injury
Atherosclerosis
Vasculitis
High levels of homocysteine
Causes of stasis or turbulent blood flow
Immobilisation
Cardiac wall dysfunction
Aneurysm
Hypercoagulability
Due to excessive procoagulant or defective anticoagulant proteins, may be inherited or acquired; classic presentation is recurrent DVTs or DVT at a young age; DVT usually occurs in the deep veins of the legs, other sites include hepatic and cerebral veins