- increased volume of blood within vessels

- active (deliberate dilation) and passive (obstruction)

- Acute and chronic

- heavy, red, may have grossly visibile dilated vessels

- Commonly also associated with hemorrhage

Hyperemia (Congestion)

- inflammation

- hormonal or neural stimulation of vessels producing dilated arterioles and capillaries w/ enhanced perfusion

- exercise, need to dissipate heat, response to local heat, psychogenic (blushing)

Acute active hyperemia

- rapid obstruction of venous return

- acute MI leading to heart failure

- String around finger

Acute passive congestion

- any prolongation of acute passive congestion

- gradually developing process which impedes venous return

- lungs (chronic left-sided failure)

- liver ("nutmeg") w/ pattern of light and dark due to accumulation of blood in terminal hepatic veins/sinusoids

Chronic passive congestion

- excess fluid in interstitial spaces

- caused by increased capillary hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, sodium retention, and increased capillary permeability

- localized and generalized

- organs become enlarged, pale, tense capsule, w/ pitting

- microscopically look pink (more protein) like hyaline

Edema

- tends to encourage water to enter the interstitium

- greater pressure inside capillary

- influenced by venous back pressure, tissue tone, muscular activity, and gravity

Capillary hydrostatic pressure

- tends to encourage water to leave the interstitium

- leads to reabsorption of fluid back into the capillary

- small molecules diffuse freely, large molecules are trapped

- major contributor is albumin

Plasma oncotic pressure

- allows water and proteins to leave the interstitium

- begin as blind-ended capillaries in the interstitium

- collect excess fluid and protein that accumulates

- eventually returned to venous circulation

Lymphatic drainage

- moves freely between intravascular & interstitial compartment

- major determinant of osmolality of extracellular fluid

- major influence in total ECF volume

- primarily controlled by renal excretion

Sodium

- commonly associated with impeded outflow thru the venous system (heart failure, venous obstruction)

- increased total blood volume, sodium retention

- increased rate of fluid loss into the interstitium

Increased capillary hydrostatic pressure

- reduced plasma proteins lead to reduced oncotic reabsorption of interstitial fluid back into capillaries

- less common than edema due to sodium retention

- may produce more severe anasarca

Decreased Plasma Oncotic Pressure

- lymphatic obstruction and increased capillary permeability cause this

Localized edema

- extreme generalized edema especially of subcu tissues

Anasarca

- fluid with high specific gravity and high protein count

- often associated w/ inflammation

Exudate

- fluid with low specific gravity and low protein content

- generalized edema

Transudate

- escape of blood from the vascular system into surrounding tissues

Hemorrhage

- large flat diffuse hemorrhage

Ecchymosis

- large lump/mass of blood in tissue

Hematoma

- 1 mm diameter, flat hemorrhages

Petechia

- many ecchymoses in skin

- commonly associated with hemorrhagic diseases

Purpura

- rapid loss of circulating blood volume (shock)

- chronic loss outside of body (iron deficiency anemia)

- mechanical effects (hemopericardium-> tamponade, intra-cranial -> "space-occupying lesion")

Consequences of Hemorrhage

- Resorption (hemosiderin), Organization (fibrous scar), elevated levels of bilirubin

Fate of hemorrhage within the body

- localized area of ischemic necrosis

- tissue death due to sudden loss of blood supply

- caused by thrombosis, embolism, strangulation, torsion (arterial or venous)

Infarction

- dead tissue corresponds to the distribution of the affected vessel

- cone or wedge shaped

- pale infarcts (tan-yellow to white with red border)

- red (hemorrhagic) infarcts (subsequent hemorrhage into dead tissue)

- coagulative necrosis (except brain)

Description of Infarction

- loss of function of infarcted organ

- massive hemorrhage due to rupture of infarcted organ

- elevated plasma enzyme levels

- activation of intravascular coagulation from "thromboplastins"

- survivors may heal with scar tissue

Sequelae of Infarct

- ischemic necrosis plus putrefaction due to invasion by saprophytic micro-organisms

- usually close or easy access to fecal contents

- "dry", "wet", "gas"

Gangrene

- mummification of lower extremities

- technically not really gangrene, no bacterial putrefaction

- occurs due to long-term peripheral ischemia

Dry gangrene

- true, classic gangrene

- associated with bowel ischemia/infarction allowing contamination by fecal contents

- infected wounds: especially those contaminated by dirt or fecal material

"Wet" gangrene

- necrotic tissue, contaminated with clostridia sp., require avascular (anaerobic) conditions

- characterized by production of multiple gas bubbles in the tissue ("crepitation")

- elaborate a necrotizing toxin and produce an advancing wave of necrosis

- treatment is extensive surgery and suitable antitoxin

Gas gangrene