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FLUID ANDHEMODYNAMIC DERANGEMENTS
SOCORRO CRUZ – YANEZ MD, FPSP
Course objectives •Understand and define terms
•Demonstrate knowledge and understanding of etiopathogenesis and pathophysiology of disorder
•Recognize , describe its morphologic features
• Identify presenting clinical features and providing correlation and explanation
•List outcomes , complications
Learning activities
• Lectures ( Part 1 – Mon and 2- Thurs )
• Laboratory : ( Tues and Thurs )• Guided projection of glass slides • Gross • Microscopic slides
• Evaluation• Formative : SRS• Summative : ( Long exam and
practical exam )
FLUID AND HEMODYNAMIC DERANGEMENTS :
Edema Hyperemia / congestion Hemorrhage Thrombosis / DIC Embolism Infarction Shock
Normal fluid hemeostatic
balance
Normal distribution of body Normal distribution of body
waterwater
2/3
BODY WATER(60% of lean body
weight)
INTRACELLULAR EXTRA-
CELLULAR
1/3
INTERSTITIAL
95%
INTRAVASCULAR5%
• The exchange of fluid is between the vascular and interstitial compartments
• The exchange occur at the capillary level
• No net gain or loss of fluid
• Lymphatic drainage plays a part in maintaining this equilibrium
“THE NORMAL SITUATION”
Normal Fluid Homeostasis •Normal fluid homeostasis is
maintenance within physiologic ranges by :
o endothelial / vessel wall integrity
o intravascular pressure
o plasma osmolarity
TWO TYPES OF FORCES DRIVE THE NORMAL FLUID EXCHANGE
• Hydrostatic pressure o Affected by : cardiac output, vessel wall
elasticity, vascular tone, and blood volume.
• Oncotic or osmotic pressureo Maintained by protein level in the bloodo Serum Albumin level
Normal Microcirculation
Capillary Arterial VenousHydrostatic Pressure + 36 + 16Oncotic Pressure - 26 - 26Net filtration Pressure + 10 mmHg - 9 mm Hg
(leak-out) (Reabsorb)
“The abnormal situation”- Excessive accumulation of fluid in the interstitium and
body cavities EDEMA
EDEMA : definition
Increase accumulation of fluid in the interstitium and body cavities
TYPES OF EDEMA :
A. Inflammatory edema increased vascular permeability
B. Non- inflammatory edema changes in hemodynamic
forces
INFLAMMATORY VERSUS NON-INFLAMMATORY EDEMA
INFLAMMATORY
• Protein-rich fluid because of altered permeability of endothelial cells
• Fibrin-rich fluid• Inflammatory cells
typical• Specific gravity > 1.020• Usually a localized
process
NON-INFLAMMATORY
• Lower protein content no alteration in endothelial permeability
• No fibrin in fluid• No inflammatory cells in
fluid• Specific gravity < 1.012• Often a generalized
process
(These differences can be used in analyzing fluid from tissue cavities.)
D.TRANSUDATE
E. EXUDATE
S.G < 1.012 > 1.020
PROTEIN Low High
CELLCONTENT
few cells high cells
PATHOGE-NESIS
Hydrostatic imbalance
inc vascular permeability
TYPES OF EDEMA cont..
C. Localized• Hydropericardiu
m• hydrothorax• hydroperitoneu
m ( ascitis )
HYDROTHORAX
LOCALIZED SUB EPIDERMAL BULLAE
TYPES OF EDEMA cont..
D. Generalizedaka : Anasarca
• CHF• NS• Malnutrition
ANASARCOUS - HYDROPS FETALIS
Pathophysiologic categories of edema
1. Increased hydrostatic pressure
2. Reduced plasma osmotic pressure
3. Lymphatic obstruction4. Sodium retention5. Inflammation
Edema : Increased HP
1. Impaired venous return/Inc venous pressure
CHF Constrictive pericarditis Liver cirrhosis Venous obstruction / compression
2. Arteriolar dilatation Heat Neurohumoral regulation
CAPILLARY LUMEN(BLOOD)
INTERSTITIAL SPACE
ARTERIOLAR END
VENULEEND
INCREASED MOVEMENT OF FLUIDINTO INTERSTITIUM DUE TOINCREASED HYDROSTATIC PRESSURE
MOVEMENT OF FLUIDBACK INTO BLOODBASED ON DIFFERENTIALOSMOTIC PRESSURE
EXCESS FLUID REMOVEDBY LYMPHATIC DRAINAGE
MECHANISMS OF EDEMA – INCREASED HYDROSTATIC PRESSURE
NOTE: The lymphatic system attempts to compensate by increasing drainage.
Pathogenesis of edema in CHF
Inc plasma volume transudation EDEMA
Pathogenesis of edema in cirrhosis
Edema : Decreased OP
Nephrotic syndromeLiver cirrhosisMalnutritionProtein losing enteropathy
CAPILLARY LUMEN(BLOOD)
INTERSTITIAL SPACE
ARTERIOLAR END
VENULAREND
MOVEMENT OF FLUIDINTO INTERSTITIUMBASED ON DIFFERENTIALHYDROSTATIC PRESSURE
DECREASED MOVEMENT OF FLUID INTO BLOOD DUE TO DECREASED OSMOTIC PRESSURE
EXCESS FLUID REMOVEDBY LYMPHATIC DRAINAGE
MECHANISMS OF EDEMA – DECREASED OSMOTIC PRESSURE IN
BLOOD
NOTE: The lymphatic system attempts to compensate by increasing drainage.
Pathogenesis of Nephrotic Syndrome
Edema : Lymphatic obstruction Tumor
infiltrationInflammatory
scarring ex. filariasisPostsurgical
complicationPostradiation
complication
FILARIASIS
Edema : Na / H2O retention
Acute renal failure Increase salt intake Increased tubular reabsorption
Edema : Inflammation
Acute inflammation Chronic inflammation Angiogenesis
LOCALIZED SUBEPIDERMAL BULLAE
LARYNGEAL EDEMA
Edema : morphology
1. GROSS : increase weight organomegaly moist , wet , glistening subcutaneous edema -
dependent / pitting
DEPENDENT PITTING EDEMA
PITTING EDEMA
URINARY BLADDER – MUCOSAL EDEMA
Edema : morphology
2. Histologic loosening / separation of
extracellular matrix accumulation of poor
staining extracellular material ( water )
PULMONARY EDEMA
Assoc Ds : LV failure , renal failure , ARDS,
infections S/S : dyspnea , PND, orthopnea Morphology :
= distended alveoli with pink, proteinaceous fluid
= septal congestion
NORMAL LUNG PULMUNARY EDEMA
PULMONARY EDEMA
Pulmonary edema
PULMONARY EDEMA
NORMAL LUNG
AIR SAC
ALVEOLAR WALL
CONGESTED SEPTAL VESSELS
PULMONARY EDEMA
PULMONARY EDEMA
CEREBRAL EDEMA
Assoc Ds : brain tumors, infection, HPN , injury S/S : stupor , coma death CX : herniation Morphology : enlargement , swelling , narrowing of sulci, distension of gyri
CEREBRAL EDEMA
CEREBRAL EDEMA
WIDENED GYRI
FLATTENED SULCI
CEREBRAL EDEMA
TONSILLAR HERNIATION
EDEMA : CLINICAL SIGNIFICANCE
Edema of vital organs a. Lungs respiratory
insuff/ failure b. Brain increase ICP
brain herniation
HYPEREMIA AND CONGESTION
Definition : local increased volume of blood in an affected organ or tissue
Hyperemia and Congestion
Hyperemia ( Active Hyperemia )increase blood flow to capillaries
secondary to arterial / arteriolar dilatation
Ex : blushing Congestion ( passive hyperemia ) Retention of blood secondary to
impaired venous drainage Ex : CHF
PATHOGENESIS
MORPHOLOGY
ACTIVE HYPER-EMIA
Art dilatation 2 o SNS stim /vasoactive subs
Bright red discolorationEx. Blushing , exercise, inflam
PASSIVE HYPER- EMIA /
CONGES-TION
Impaired outflow Venous obstruction
Blue – red discoloration ( cyanotic )
TYPES OF CONGESTION
1.Acute congestion – passive hyperemia 2. Chronic congestion- long standing congestion
Acute pulm congestion : Morphology
Heavy , dark red, violaceous
Septal capillary engorged and thickened with blood
Assoc septal edema, alveolar hge and edema
PULMONARY CONGESTION
SEPTAL CAPILLARY CONGESTION
Chronic Passive Congestion of Lung : Morphology
Thickened , fibrotic alveolar septal wall
Alveolar congestion/ septal Hge
Heart failure cells Long standing : pulm HPN
HEART FAILURE CELLS
CPC OF THE LUNG
ACUTE HEPATIC CONGESTION
Central venous congestionCentral hepatocytic necrosis and hgesSparing of periportal hepatocytes
NORMAL HEPATOCYTE LOBULE
CENTRILOBULAR
MID-ZONAL
PERI-PORTAL
CENTRAL CONGESTION
SPARRING OF PERI-PORTAL AREA
ACUTE HEPATIC CONGESTION
CPC OF LIVER
“ Nutmeg “ liver Centrilobular necrosis , hemosiderin
macrophages Long standing
complication : cardiac cirrhosis
NORMAL LIVER
NORMAL LIVER
NUTMEG SPICE NUTMEG LIVER
CPC OF THE LIVER - NUTMEG LIVER
CPC OF THE LIVER
C. V
CENTRAL VEIN
CENTRAL HEPATOCYTIC CONGESTION
LIVER CELL NECROSIS
HEMOSIDERIN MACROPHAGES
CONGESTIVE SPLENOMEGALY
CONGESTIVE SPLENOMEGALY
HEMORRHAGE
DEFINITION : Extravasation of RBCsecondary to blood vessel rupture
HEMORRHAGE : TYPES
1. AS TO SITE : Hemothorax Hemopericardium Hemoperitoneum Hemarthrosis
HEMOPERICARDIUM
HEMOTHORAX
HEMORRHAGES : TYPES
2. AS TO SIZE :a. Petechiae - 1-2 mm b. Purpura - > 3 mm c. Ecchymosis - > 1-2 cm d. Hematoma - large
pools of blood
PETECHIAE
PETECHIAE
PURPURIC HGES
ECCHYMOTIC HEMORRHAGES
ECCHYMOSIS
SUB-UNGAL HEMORRHAGES
SUBDURAL HEMATOMA
INTRACEREBRAL HEMATOMA
Subcapsular hematoma - liver
hematoma
HGE : PATHOGENESIS
1. Trauma, laceration2. Atherosclerosis3. Inflammatory4. Neoplastic erosion of
blood vessel5. Hgic diathesis
HEMORRHAGE : CLINICAL SIGNIFICANCE
1. Significant blood loss hgic / hypovolemic shock
2. Bleeding into vital organs like brain, lung and pericardium (cardiac tamponade )
3. External blood loss iron def anemia
4. Internal blood loss jaundice
GOOD DAY!
UNILATERAL EDEMA
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