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					Edema:
 Incr fluid in interstitial spaces
 Hydrothorax, hydropericardium, and hydroperitoneum (ascites)
 Anasarca = severe and generalized edema with profound sub-q tissue swelling

Non-inflammatory categories of edema:
1. Incr hydrostatic pressure
2. Reduced plasma osmotic pressure
3. Lymphatic obstruction
4. Sodium Retention

Factors that govern movement of water b/c vascular and interstitial spaces:
 Vascular hydrostatic pressure
 Plasma colloid osmotic pressure

 Incr capillary pressure or decr colloid osmotic pressure  incr interstitial fluid
 Excess interstitial fluid is drained away by lymphatics
 Lymphatic obstruction can cause edema

 Edema fluid in hydrodynamic derangements is usually a protein-poor transudate
 Inflammatory edema is a ptn-rich exudate

Increased Hydrostatic Pressure:
 Local increases in HP – may result from impaired venous outflow
    Deep venous thrombosis in lower legs  edema

 Generalized increases in HP  systemic edema
    Occur most frequently in CHF
       CHF affects R vent cardiac fx
       Assoc w/ decr CO  decr renal perfusion  triggers renin-angiotension-aldosterone axis  Na and water retention
       Designed to incr intravascular volume  improve CO  restore renal perfusion
       Heart cannot incr CO  extra fluid load  incr venous P  incr transudation  edema
       Cycle of renal fluid restriction and worsening edema
       Edema of dependent parts of the body – prominent feature of CHF, esp of R ventricle

 Constrictive pericarditis, ascites (liver cirrhosis), venous obstruction or compression, arteriolar dilation

Reduced Plasma Osmotic Pressure:
 Results from excessive loss or decr production of albumin
 Albumin = serum ptn = most resp for maintaining colloid pressure

 Nephrotic Syndrome
    Leaky glomerular capillary wall, generalized edema
    Decr alb production b/c of diffuse liver pathology (cirrhosis), or from ptn malnutrition
    Decr plasma osmotic pressure  net movement of fluid into interstitium  decr in plasma V  decr in renal perfusion
    Also have decr in CO b/c of decr in plasma V
    Decr in renal perfusion  secondary aldosteronism  Na and water retention by kidneys
    Na and water retention cannot correct plasma V b/c still have low serum ptns
    Initial edema ppt by hypoproteinemia is made worse by secondary salt and water retention
    Edema caused by renal dysfx or nephrotic syndrome is generally more severe, affects all parts of the body equally

 Liver cirrhosis, malnutrition, ptn-losing gastroenteropathy

Lymphatic Obstruction:
 Impaired lymphatic drainage and resulting lymphedema is usually localized
 Can result from inflamm or neoplastic obstruction
 Parasitic infection filariases
    Often causes massive lymphatic and lymph node fibrosis in inguinal region  edema of external genitalia and lower limbs
    Edema called elephantiasis

 Cancer of breast
    Can be tx by removal/irradiation of breast and axillary lymph nodes  resection of lymph nodes and scarring  severe edema
      of the arm

 Inflammatory, Neoplastic, Postsurgical, Postirradiation

Sodium and Water Retention:
 Either primary or secondary causes of edema
 Incr salt with obligate accompanying water:
     Incr intravascular fluid volume  incr hydrostatic P
     Decr vascular colloid pressure
 Excessive salt intake w/ renal insufficiency, incr tubular reabs of sodium (renal hypoperfusion, incr R-A-Aldosterone secretion)

Morphology of Edema:
 Most easily recognized grossly
 By LM manifests as subtle cell swelling, w/ clearing and separation of the ECM components
 Most commonly found in sub-q tissues, lungs, and brain

Subcutaneous edema:
 Can be diffuse or more conspicuous at sites of highest hydrostatic pressures
 More conspicuous: called dependent edema, distribution largely dependent on gravity
    Edema of dependent parts of the body – prominent feature of CHF, esp of R ventricle

 Edema caused by renal dysfx or nephrotic syndrome is generally more severe, affects all parts of the body equally
 May initially be seen in tissues w/ soft tissue matrix; ex – eyelids, causing periorbital edema

 Pitting edema – finger pressure on edematous areas leaves a finger-shaped depression

Pulmonary Edema:
 Common clinical concern, most often in left ventricular failure
 Also in renal failure, adult respiratory distress syndrome, pulm infections, and hypersensitivity rxns
 Lungs go to 2X to 3X their normal weight
 Sectioning: frothy, blood-tinged fluid – represents a mixture of air, edema fluid, and extravasated RBCs

Edema of the Brain:
 May be localized to sites of injury (abscess, neoplasm), or may be generalized (encephalitis, hypertensive crises, obstruction to
brain’s venous outflow)
 Trauma can cause local or generalized edema, depending on nature and extent of injury
 Generalized edema
     Brain is grossly swollen, narrowed sulci, distended gyri
     Shows signs of flattening against skull


Clinical Correlation:
 Sub-q tissue edema - can impair wound healing or clearance of infection
 Pulmonary edema – can cause death by interfering w/ gas exchange; fluid in alveoli create favorable place for bacterial infection
 Brain edema – serious, can be rapidly fatal; brain herniation or brain stem vascular supply can be compressed injure vent centers


Hyperemia and Congestion:
 Indicate a local incr volume of blood in a part tissue

 Hyperemia – active process; incr tissue inflow b/c of arteriolar dilation – skel mm during exercise or at sites of inflammation
    Tissue is redder b/c of more oxygenated blood in tissue
 Congestion – passive processes; impaired outflow from a tissue
    Systematically in cardiac failure or local b/c of isolated venous obstruction
    Tissue has a blue-red color (cyanosis); have accumulation of deoxy Hgb in tissues

 Congestion of capillary beds is closely related to development of edema; congestion and edema commonly occur together

 Chronic Passive Congestion
    Stasis of poorly oxygenated blood  chronic hypoxia   cell death, sometimes w/ microscopic scarring
    Capillaries rupture at sites of chronic congestion  small foci of hemorrhage
    Breakdown and phagocytosis of RBC debris   small clusters of hemosiderin-laden macrophages

 Morphology:
 Cut surfaces are hemorrhagic and wet
 Acute pulmonary congestion – alveolar capillaries engorged with blood
        May have assoc alveolar septal edema or focal intra-alveolar hemorrhage

 Chronic pulmonary congestion
    Septa are thick and fibrotic, alveolar spaces have hemosiderin-laden macrophages (= heart failure cells)

 Acute hepatic congestion
    Central vein and sinusoids are distended w/ blood; may be more central hepatocyte degeneration
    Periportal hepatocytes are relatively better oxygenated b/c of their proximity to hepatic arterioles  develop fatty change

 Chronic Passive Congestion of the liver
    Central regions of hepatic lobules are grossly red-brown and slightly depressed
    Surrounding areas are uncongested and tan-colored (nutmeg liver)
    Centrilobular necrosis w/ hepatocyte dropout and hemorrhage including hemosiderin-laden macrophages
    Severe long, standing hepatic congestion, assoc w/ heart failure
       May have grossly evident hepatic fibrosis = cardiac cirrhosis

 Centrilobular necrosis
    Central portion of hepatic lobule is last to receive blood
    Can also occur when there is decr hepatic blood flow – includes shock of any cause

Hemorrhage:
 Extravasation of blood b/c of vessel rupture
 Capillary bleeding can occur in chronic congestion
 Rupture of large artery or vein is usually due to vascular injury – trauma, artherosclerosis, inflamm or neoplastic erosion of wall

 Hemorrhage diatheses: incr tendency to hemorrhage from usually insignificant injury
 Hematoma – hemorrhage is external or is enclosed w/in a tissue; range from bruise or can accumulate enough blood to cause death
 Petechiae – minute hemorrhages into skin, mucous mbrs, or serosal surfaces
    Assoc w/ locally incr intravascular pressure, thrombocytopenia, defective platelet fx, or clotting factor defects
 Purpura – slightly larger hemorrhages, have similar pathology, as well as trauma, vasculitis, or incr vascular fragility (amyloidosis)
 Ecchymoses – larger (1-2 cm) sub-q hematomas; typical after trauma, can be made worse by above conditions
    RBCs are degraded and phagocytoses by macrophages
    Hbg, red-blue color  bilirubin, blue-green   hemosiderin, gold-brown
 Hemothorax, hemopericarduim, hemoperitoneum, hemarthrosis
    Large accumulations of blood in body cavity
    Pts sometimes have jaundice b/c of breakdown of lots of RBCs

 Clinical significance:
    Depends on volume and rate of blood loss
    Rapid removal of up to 20% of blood volume, or slow losses of even more blood – may have little impact on adults
    Greater losses  hemorrhagic shock
    Site of hemorrhage – may cause death if in brain
    Chronic or recurrent external blood loss – may have problem w/ iron-def anemia
Embolism:
 Detached intravascular solid, liquid, or gaseous mass, carried by blood away from pt of origin
 About 99% of emboli are from dislodged thrombus  called thromboembolus
 Rare forms of emboli:
     Droplets of fat, bubbles or air or nitrogen, tumor fragments, bits of bone marrow, foreign bodies (bullets)
     Cholesterol emboli – atherosclerotic debris
 Lodge in too-small vessels  complete or partial vascular occlusion  infarction
 Infarction – ischemic necrosis of tissue distal to a vascular occlusion

Pulmonary Thromboembolism:
 Majority of cases – thrombi are from deep leg thrombi above the level of the knee   right side of hrt  pulm vasculature
     Can occlude main pulmonary artery, bifurcation, or smaller arterioles
 Saddle embolus = occludes the bifurcation of pulm arteries
 Often have multiple emboli
 Pt who has had one pulm embolus  high risk for another embolus

 Most pulm emboli are clinically silent b/t they are small  organization  recanalized  incorp into vascular wall
     Organization of thrombus may leave behind delicate, bridging fibrous web
 If 60% or more of pulm circulation occluded  sudden death, right-sided heart failure (cor pulmonale), CV collapse
 Obstruction of medium-sized arteries  pulm hemorrhage, does not cause pulm infarction b/c of dual blood flow
 Obstruction of medium-sized arteries w/ Left-sided hrt failure  large infarct b/c of sluggish bronchial artery flow
 Obstruction of small end-arteriolar pulm branches  associated infarct
 Multiple emboli over time  pulm hypertension w/ right heart failure

Systemic Thromboembolism:
 Emboli in arterial circulation
 Most from intra-cardiac mural thrombi
    Most of these assoc w/ left ventricular wall infarcts
    Some assoc w/ dilated left atria (secondary to rheumatic valvular disease)
 Remainder from aortic aneurysms, thrombi on atherosclerotic plaques, or fragmentation of valvular vegetation

 Paradoxical emboli – embolus passes t/ interatrial or interventricular defect to gain access to the systemic circulation

 Can travel to large variety of sites; major sites are:
    Lower extremities and brain
    Kidneys, spleen, and upper extremities involved to a lesser extent

 Consequences – depend on any collateral blood supply, vulnerability to ischemia, caliber of vessel occluded
 Generally cause infarction of tissues in the distribution of obstructed vessels


Fat Embolism:
 Microscopic fat globules after fractures of long bones or in setting of soft tissue trauma and burns
 Begins 1-3 days after injury
 Sudden onset of tachypea, dyspnea, and tachycardia; neurologic symptoms – irritability, can progress to coma
 Diffuse petechial rash in nondependent areas

Air Embolism:
 Gas bubbles in circulation  obstruct vascular flow, and cause infarcts
 B/c of obstetric procedures or chest wall injury
 Need in excess of 100 cc of air
 Decompression sickness – sudden changes in atm pressure; problems for divers, unpressurized airplanes
    Incr amounts of gas dissolve in tissues  depressurize too quickly  gas expands in tissues and bubbles out of solution
 Can cause focal ischemia in tissues, including brain and heart
 Lungs – edema, hemorrhages, emphysema may appear  respiratory distress, called the chokes
Amniotic Fluid Embolism:
 Complication of L&D, and in immediate postpartum period
 Sudden sever dyspnea, cyanosis, and hypotensive shock  seizures and coma  pulm edema, DIC
 Tear in placental mbr and rupture of uterine veins  amniotic fluid and its contents enter maternal circulation

Infarction:
 Area of ischemic necrosis caused by occlusion of arterial supply or venous drainage in a particular tissue
 99% of infarcts are from thrombotic or embolic events
 Almost all result from arterial occlusion
 Other causes:
    Local vasospasm
    Expansion of atheroma due to hemorrhage w/in a plague
    Extrinsic compression of the vessel – tumor
    Twisting of vessels – testicular torsion, bowel volvulus
    Compression of blood supply by edema or entrapment in hernial sac
    Traumatic rupture of blood supply

 Venous thrombosis – more often causes venous obstruction and congestion
     Bypass channels rapidly open  provides outflow from area  improves arterial inflow
 Infarcts caused by venous thrombosis more likely in organs w/ single venous outflow channel – testis, ovary

 Infarcts are classified on color and bacterial infection

Red infarcts:
 Hemorrhagic; usually venous, but can be arterial in certain setting
 Occur w/
   1. Venous occlusions (ex – ovarian torsion)
   2. Loose tissues that allow blood to collect in infarcted zone – lung
   3. Tissues w/ dual circulation that permits flow of blood from unobstructed vessel into necrotic zone
   4. Tissues that were previously congested b/c of sluggish venous outflow
   5. When flow is reestablished to site of previous arterial occlusion and necrosis occurs

White infarcts:
 Anemic
 Occur w/ arterial occlusions or in solid organs (heart, spleen, kidney)
 Solidity of tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adj capillary beds
 In solid organs, the few extravasated RBCs are lysed, so white infarcts become more pale and sharply defined w/ time
 Over course of a few days, it becomes more firm and brown (b/c of Hgb  hemosiderin)

 All infarcts tend to be wedge-shaped
    Occluded vessel at apex, periphery of organ forms the base
 When base is serosal surface, tends to be a fibrinous exudate
 Lateral margins may be irregular; reflects pattern of vascular supply from adjacent vessels

 Outset – all infarcts are poorly defined, tend to be better defined w/ time by a rim a hyperemia (b/c of inflammation)

 Dominant histological characteristic is ischemic coagulative necrosis
 Inflamm rxn along margins of infarcts w/in a few hrs; well-defined by 1-2 days
 Can see degradation of dead tissue  phagocytsosis by neutrophils and macrophages
 Followed by reparative response beginning in preserved margins
 Most infarcts replaced by scar tissue
 Infarct in brain  liquefactive necrosis

 Septic infarctions:
    Embolization occurs by fragmentation of bacterial vegetation from a heart valve or seen microbes seed necrotic tissue
    Infarct  abscess w/ greater inflammatory response
Factors that Influence Development of an Infarct:
 Nature of vascular supply
    Availability of alternate blood supply is most important factor
    Lungs have dual pulmonary and bronchial artery blood supply
    Liver – dual hepatic and portal vein circulation
    Hand and forearm – radial and ulnar arteries
    Kidney and spleen – end-arterial

 Rate of development of occlusion
    Slowly developing  less likely to cause infarction; provide time for alternate blood supply
    Coronary artery slowly occluded  flow in collateral circulation may incr sufficiently

 Vulnerability to hypoxia
    More susceptible to hypoxia  incr likelihood of infarction
    Neurons undergo irreversible damage when deprived of blood supply for 3 to 4 minutes
    Myocardial cells also quite sensitive

 Oxygen content of blood
    Anemic or cyanotic pt more susceptible to vessel obstruction
    CHF w/ compromised flow and ventilation  cause infarction in the setting of otherwise inconsequential blockage

Shock:
 Cardiovascular collapse, final common pathway for a number of events
 Systemic hypoperfusion b/c of decr in CO or decr in effective circulating blood volume
 Three main categories of shock, additional categories

Cardiogenic shock         Failure of myocardial pump b/c of intrinsic myocardial damage,           MI
                         extrinsic pressure, or obstruction to outflow                              Ventricular rupture
                                                                                                    Arrhythmia
                                                                                                    Cardiac tamponade
                                                                                                    Pulm embolism

Hypovolemic shock        Loss of blood or plasma volume                                             Hemorrhage
                                                                                                    Fluid loss (vomiting, diarrhea,
                                                                                                      burns, trauma)

Septic shock              Systemic microbial infection                                             Overwhelming septic shock
                          Peripheral vasodilation and pooling of blood                             Endotoxic shock
                          Endothelial activation/injury                                            Gram-positive septicemia
                          Leukocyte-induced damage                                                 Fungal sepsis
                          DIC, activation of cytokine cascades                                     Superantigens

Neurogenic shock          Anesthetic accident, spinal cord injury
                          Loss of vascular tone and peripheral pooling of blood

Anaphylactic shock        Initiated by generalized IgE mediated hypersensitivity response
                          Systemic vasodilation, incr vasc permeability
                          Hypotension, tissue hypoperfusion, cellular anoxia


Pathogenesis of Septic Shock:
 Results from spread and expansion of an initially localized infection
 Most cases are from endotoxin-producing gram-negative bacilli  endotoxic shock
 LPS binds as a complex w/ a circulating blood ptn to leukocytes, endothelial cells, and other cells
 LPS-binding ptn complex can activate vascular wall cells and leukocytes or initiate a cascade of cytokine mediators
 LPS can activate complement
 High levels of LPS:
    Cytokine-induced secondary effectors (NO and PAF) become significant
    Systemic effects of TNF and IL-1  fever, incr synthesis of acute phase reactants
    Causes endothelial cell injury  triggers coagulation cascade

 Super-high levels of LPS  septic shock

Stages of Shock:
1. Initial nonprogressive phase; reflex compensatory mechanisms are activated, perfusion of vital organs is maintained
        Variety of neurohumoral mechanisms help maintain CO and BP
        Tachycardia, periph vasoconstriction, renal conservation of fluid
2. Progressive stage – tissue hypoperfusion, worsening circulatory and metabolic imbalances, acidosis
        Widespread tissue hypoxia; blood pools in microcirculation; vital organs begin to fail, urinary output decr, pt confused
3. Irreversible stage – sets in after body has incurred cellular and tissue injury so severe that survival is not possible
        Lysosomal enzyme leakage, decr myocardial function
        May have endotoxic shock
        Pt has complete renal shutdown b/c of acute tubular necrosis

Morphology:
 Shock characterized by failure of multiple organ systems
 Especially evident in brain, heart, lungs, kidneys, adrenals, and GI tract

 Brain
    Ischemic encephalopathy

 Heart
    Focal or widespread coagulation necrosis or may have widespread coagulation necrosis
    May show subendocardial hemorrhage or contraction band necrosis
    Usually more extensive in cases of shock

 Kidneys
    Extensive tubular ishemic injury – acute tubular necrosis
    Oliguria, anuria, and electrolyte disturbances are major clinical problems

 Lungs
    Seldom affected in pure hypovolemic shock, b/c they are resistant to hypoxic injury
    Bacterial sepsis or trauma – changes in diffuse alveolar damage = shock lung

 Adrenal changes
    Cortical cell lipid depletion
    Conversion of relatively inactive vacuolated cells to metabolically active cells that use stored lipids for the synthesis of steroids

 GI tract
    Patchy mucosal hemorrhages and necroses = hemorrhagic enteropathy

 Liver
    May develop fatty change and central hemorrhagic necrosis

Clinical course:
 Depend on ppt insult
 Hypovolemic and cardiogenic shock  pt has hypotension, weak and rapid pulse, cool, clammy, cyanotic skin
 Septic shock – skin may be initially warm and flushed b/c of periph vasodilation
 If pt survives initial complications  second phase marked by renal insufficiency, progressive fall in urine output, severe fluid and
electrolyte disturbances
 Prognosis varies w/ the origin of shock and its duration
 80 to 90% of young, otherwise healthy pts w/ hypovolemic shock survive w/ appr management
 Cardiogenic shock assoc with extensive MI and gram-negative shock  mortality rates of up to 75%

				
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