Hemodynamic derangement Komson Wannasai, M.D.,FRCPath.
Department of Pathology
Faculty of Medicine
Chiang Mai University Objective
•The students should be able to
• Explain normal body fluid homeostasis
• Explain definition of edema, congestion, hyperemia, hemorrhage, thrombosis, embolism and infarction
• Explain pathophysiology of edema, congestion, hyperemia, hemorrhage, thrombosis, embolism and infarction
• Explain pathological finding of edema, congestion, hyperemia, hemorrhage, thrombosis, embolism and infarction
• Apply basic knowledge to clinical application Contents •Body fluid compartments
•Edema
•Hyperemia and congestion
•Hemorrhage
•Thrombosis
•Embolism
•Infarction Body fluid compartments • Total body water (TBW)
• 60% of the body weight in kg • 2/3  intracellular fluid
• 1/3  extracellular fluid
• Sodium (Na+)
• Major extracellular fluid (ECF) cation
• Potassium (K+)
• Major intracellular fluid (ICF) cation
• ECF is subdivided into the interstitial and vascular compartments
Normal water homeostasis •Hydrostatic pressure
•Plasma oncotic pressure •The exit of fluid into the interstitium is nearly balanced by inflow at the venular end
•A small residuum of excess interstitial fluid is drained by the lymphatics Robbins 9th edition
Edema •Presence of increased fluid in the interstitial space of the ECF compartment •Causes of edema • Increased hydrostatic pressure • Reduced plasma osmotic pressure
• Lymphatic obstruction • Sodium and water retention Types of edema fluid • Transudate • Protein‐poor (<3 g/dL) and cell‐poor fluid • Produces dependent pitting edema and body cavity effusions • Exudate • Protein‐rich (>3 g/dL) and cell‐rich (neutrophils) fluid • Produces swelling of tissue but no pitting edema • Lymphedema • Protein‐rich fluid • Nonpitting edema Related trems •Hydrothorax (pleural effusion)
•Effusions involving the pleural cavity
•Hydropericardium (pericardial effusion)
•Effusions involving the pericardial cavity
•Hydroperitoneum (ascites)
•Effusions involving the peritoneal cavity
Pleural effusion
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Pathophysiology of edema (1) •Alteration in Starling pressure • Produces a transudate • Increased vascular hydrostatic pressure
• Pulmonary edema in left‐sided heart failure • Peripheral pitting edema in right‐sided heart failure • Portal hypertension in cirrhosis producing ascites Pathophysiology of edema (2) •Alteration in Starling pressure • Decreased vascular plasma oncotic pressure (hypoalbuminemia)
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Malnutrition with decreased protein intake Cirrhosis with decreased synthesis of albumin Nephrotic syndrome with increased loss of protein in urine Malabsorption with decreased reabsorption of protein • Renal retention of sodium and water • Increases hydrostatic pressure (increased plasma volume) • Decreases oncotic pressure (dilutional effect on albumin) • Examples‐acute renal failure, glomerulonephritis Pathophysiology of edema (3) • Increased vascular permeability • Produces an exudate • Example‐acute inflammation (e.g., tissue swelling following a bee sting) • Lymphatic obstruction • Produces lymphedema • Examples • Lymphedema following modified radical mastectomy and radiation • Filariasis due to Wuchereria bancrofti
Morphology of edema •Most easily recognized grossly
•Microscopically
•Cell swelling with clearing and separation of the extracellular matrix elements
•Edema is most commonly encountered in subcutaneous tissues, the lungs, and the brain. Pitting edema
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Pulmonary Edema (1) • Increased fluid in the alveolar spaces and interstitium of the lung. • Most common cause: left ventricular failure
• Increase perfusion pressure in the pulmonary capillaries and block effective lymphatic drainage
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Pulmonary Edema (2) •Gross morphology: lung
• Two or three times of their normal weight
• Tense, firm consistency
•Microscopic findings
• Congested capillaries and damaged alveoli with debris‐containing and extravasated RBC
• Proteinaceous fluid within alveolar spaces
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Edema in Cirrhosis of the Liver •Cirrhosis
• Chronic disease in which liver parenchyma deteriorates; the lobules become infiltrated with fat and dense connective tissue. • Decreased albumin production
• Decreased plasma osmotic pressure
• Increased portal hydrostatic pressure
• Increased sodium and water reabsorption
Severe ascites due to cirrhosis www.pathologyoutlines.com
Edema in the nephrotic syndrome •Decreased plasma albumin
•Decreased plasma osmotic pressure
•Decreased blood volume
•Increased aldosterone and ADH
•Increased sodium and water reabsorption Localized edema •Obstruction of venous return
•Lymphatic obstruction
•Increased vascular permeability
•Inflammation
•Urticaria
•External pressure
Deep vein thrombosis
(more explanation in vascular diseases II) www.dvtvictims.com
Brain edema (1) •Causes •Cerebrovascular accident •Trauma •Venous obstruction •Inflammation; meningitis, abscess, encephalitis •Complications
•Increased intracranial pressure
•Cerebral herniation
Brain edema (2) •Morphology
•Grossly swollen
•Narrow sulci and distended, flat gyri
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Hyperemia and congestion •Both indicated a local increased volume of blood in tissues.
•Hyperemia
• Active process
• Increase tissue inflow due to arteriolar dilatation
• Red tissues
• Exercise, inflammation
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Hyperemia and congestion •Congestion
• Passive process
• Outflow tract obstruction
• Blue‐red tissue
•Both hyperemia and congestion occur together www.???
Hyperemia and congestion •In long‐standing congestion
•Called CHRONIC PASSIVE CONGESTION
•Stasis of deoxygenated blood cause hypoxia and cell death
•Capillary rupture: hemorrhage
•Hemosiderin‐laden macrophage
Hyperemia and congestion •Morphology
•The cut surface is hemorrhagic and wet
•Acute pulmonary congestion
• Engorged capillary vessels
• Alveolar septal edema
• Focal intra alveolar hemorrhage
•Chronic pulmonary congestion
• Thickening of septa
• Numerous hemosiderin‐laden macrophage
Acute pulmonary congestion
Robbins 7th edition
chronic pulmonary congestion
Robbins 7th edition
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Hyperemia and congestion •Morphology
•Acute hepatic congestion
• Distended central vein and sinusoids filled with blood
•Chronic hepatic congestion (more details in pathology of HF)
Normal hemostasis 1.
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Integrity of small blood vessels
Adequate numbers of platelets
Normal amounts of coagulation factors
Normal amounts of coagulation inhibitors
Adequate amounts of calcium ions in the blood
The vessels constituents and coagulation •Endothelial cells are antithrombotic
• Antiplatelet effects
• Anticoagulant effects
• Fibrinolytic effects
Hemostasis and platelets •Platelets
• Cytoplasmic fragments from megakaryocytes
• After vascular injury
• Platelet adhesion
• Platelet aggregation
• Degranulation
• Platelet plug www.wadsworth.org
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Robbins 9th edition
Robbins 9th edition
Robbins 9th edition
The coagulation cascades •A series of enzyme reactions ultimately resulting in the formation of thrombin which converts fibrinogen into fibrin
Robbins 7th edition
Robbins 9th edition
How do we stop this ? •Fibrinolytic system
•Predominantly by action of plasmin
• Plasmin formed by action of tissue plasminogen activator and urokinase
• Lead to breakdown of fibrin into fibrin degradation products
How do we stop this ? •Fibrinolytic system
•Predominantly by action of plasmin
• Plasmin formed by action of tissue plasminogen activator and urokinase
• Lead to breakdown of fibrin into fibrin degradation products
Robbins 9th edition
Hemorrhage •Extravasation of blood due to vessel rupture
•Hemorrhagic diatheses •Capillary bleeding can occur under conditions of chronic congestion
•Rupture of a large artery or vein is almost always due to vascular injury
•Manifested in a variety of patterns (size, extent, and location of bleeding)
Hemorrhage •External or may be enclosed within a tissue
•Hematoma ‐‐ accumulation of blood within tissue •Petechiae ‐‐ minute 1‐ to 2‐mm hemorrhages into skin, mucous membranes, or serosal surfaces
• Locally increased intravascular pressure
• Low platelet counts (thrombocytopenia)
• Defective platelet function
Hemorrhage •Purpura : Slightly larger (≥3 mm) hemorrhages •Associated with many of the same disorders that cause petechiae
•Occur secondary to trauma, vascular inflammation, or increased vascular fragility Hemorrhage • Ecchymoses : Larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises) • Red‐blue color  bilirubin (blue‐green color) 
hemosiderin (gold‐brown color) • Hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis
• Patients with extensive hemorrhage occasionally develop jaundice.
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Hemorrhage •Clinical significance
• Volume
• Rate
• Site
• Patient status
Robbins 9th edition
Thrombosis •Inappropriate activation of the hemostatic process in uninjured vasculature OR
•Formation of thrombus in the setting of relatively minimal vascular injury
Virchow’s triad Robbins 9th edition
Factors predisposing to thrombosis (1) •Hypercoagulability
•Any alteration of the coagulation pathway that predisposes to thrombosis
•Primary (genetics)
•Secondary (acquired)
• Bed rest – immobilization, obesity, cancer, atrial fibrillation, myocardial infarction, tissue damage (surgery, burns)
Factors predisposing to thrombosis (2) •Abnormalities of blood flow
•Turbulance
• Endothelial injury
• Local areas of stasis
• Disrupt laminar flow
• Moves platelets from center of flow to the vessel wall
• Prevent dilution of activated clotting factors by flowing blood
• Slow down the inflow of clotting factor inhibitors
• Promotes endothelial cell activation Thrombi Morphology •Venous thrombi
• Usually occlusive
• Red (because they form in stasis syndrome and have more associated enmeshed RBCs)
• Long ‐ forming a cast of vein with markings on them from venous valves
• Red blood cells alternating with peripheral areas of fibrin
Venous thrombi: Clinical Robbins 7th edition
Venous thrombi: Fates • Organization
• Ingrowth of cells into thrombus with incorporation into wall
• Resolution • It goes away
• Embolization
• Travels from its site of origin to a distal part of circulation
Robbins 7th edition
Arterial Thrombi : Morphology •Adherent masses of blood that demonstrate areas of pale alternating with areas of red
• Lines of Zahn Robbins 9th edition
Mural thrombi
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Arterial Thrombi Outcome •Similar to venous thrombi
•Resolution
•Organization/Incorporation/ Recanalization
•Embolization (arterial)
•Propagation
Embolism •A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin.
•Related terms
• Embolus/Emboli
• Thromboembolis
• Saddle embolism
Embolism •Pulmonary embolism
•Clinically silent (most)
•Sudden death, right heart failure (cor
pulmonale), or cardiovascular collapse •Embolic obstruction of medium‐sized arteries may result in pulmonary hemorrhage
Embolism •An embolus in the setting of left‐sided cardiac failure may result in a large infarct
•Embolic obstruction of small end‐arteriolar pulmonary branches usually does result in associated infarction
•Multiple emboli over time may cause pulmonary hypertension with right heart failure
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Robbins 7th edition
Embolism •Fat embolism
• After fractures of long bones ‐‐ microscopic fat globules in the circulation
• Fat embolism syndrome ‐‐ pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia
• Sudden onset of tachypnea, dyspnea, and tachycardia
• Neurologic symptoms ‐‐ irritability and restlessness, progression to delirium or coma www.wikidoc.org
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Embolism •Air embolism
•Decompression sickness •Gas emboli may also induce focal ischemia in a number of tissues
•A more chronic form of decompression sickness is called Caisson disease Embolism •Persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis
•The more common sites are the heads of the femurs, tibia, and humeri Embolism •Amniotic fluid embolism
•In complicated labor
•Sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma
•Pulmonary edema and DIC library.med.utah.edu
Infarction •An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue
•Causes
• Thrombotic or embolic event
• Arterial occlusion
• Local vasospasm
• Compression of vessels
• Entrapment Infarction •Morphology • Red (hemorrhagic infarct)
• Venous occlusion
• Loose tissue
• Tissue with dual circulation
• Tissue previously congested
• Established flow www.uaz.edu.mx
Infarction •White (anemic) infarct
• Arterial occlusion
• Solid organs with end arterial circulation
•Wedge‐shaped
•Ischemic coagulative necrosis
Infarction •Factor that influence development of an infarct
•Nature of the vascular supply
•Rate of development of occlusion
•Vulnerability to hypoxia
•Oxygen content of blood www.proprofs.com
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