Hemodynamic derangement. Komson Wannasai, M.D.,FRCPath. Department of Pathology Faculty of Medicine Chiang Mai University

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1 Hemodynamic derangement Komson Wannasai, M.D.,FRCPath. Department of Pathology Faculty of Medicine Chiang Mai University

2 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

3 Contents Body fluid compartments Edema Hyperemia and congestion Hemorrhage Thrombosis Embolism Infarction

4 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

5 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

6 Robbins 9 th edition

7 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

8 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

9 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

10 Pleural effusion library.med.utah.edu

11 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

12 Pathophysiology of edema (2) Alteration in Starling pressure Decreased vascular plasma oncotic pressure (hypoalbuminemia) 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

13 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

14 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.

15 Pitting edema cirrhosistreatment reviews.com

16 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

17 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

20 secure.health.utas.edu.au

22 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

23 Severe ascites due to cirrhosis

24 Edema in the nephrotic syndrome Decreased plasma albumin Decreased plasma osmotic pressure Decreased blood volume Increased aldosterone and ADH Increased sodium and water reabsorption

25 Localized edema Obstruction of venous return Lymphatic obstruction Increased vascular permeability Inflammation Urticaria External pressure

26 Deep vein thrombosis (more explanation in vascular diseases II)

27 Brain edema (1) Causes Cerebrovascular accident Trauma Venous obstruction Inflammation; meningitis, abscess, encephalitis Complications Increased intracranial pressure Cerebral herniation

28 Brain edema (2) Morphology Grossly swollen Narrow sulci and distended, flat gyri state.edu

29 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

30 Hyperemia and congestion Congestion Passive process Outflow tract obstruction Blue red tissue Both hyperemia and congestion occur together

31 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

32 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

33 Acute pulmonary congestion Robbins 7 th edition

34 chronic pulmonary congestion Robbins 7 th edition web.squ.edu.om

35 Hyperemia and congestion Morphology Acute hepatic congestion Distended central vein and sinusoids filled with blood Chronic hepatic congestion (more details in pathology of HF)

36 Normal hemostasis 1. Integrity of small blood vessels 2. Adequate numbers of platelets 3. Normal amounts of coagulation factors 4. Normal amounts of coagulation inhibitors 5. Adequate amounts of calcium ions in the blood

37 The vessels constituents and coagulation Endothelial cells are antithrombotic Antiplatelet effects Anticoagulant effects Fibrinolytic effects

injury Platelet adhesion Platelet aggregation

38 Hemostasis and platelets Platelets Cytoplasmic fragments from megakaryocytes After vascular injury Platelet adhesion Platelet aggregation Degranulation Platelet plug

39 Robbins 9 th edition

40 Robbins 9 th edition

41 Robbins 9 th edition

42 The coagulation cascades A series of enzyme reactions ultimately resulting in the formation of thrombin which converts fibrinogen into fibrin Robbins 7 th edition

43 Robbins 9 th edition

44 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

45 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 9 th edition

46 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)

47 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

48 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

49 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.

50 library.med.utah.edu healthfixit.com

51 Hemorrhage Clinical significance Volume Rate Site Patient status Robbins 9 th edition

52 Thrombosis Inappropriate activation of the hemostatic process in uninjured vasculature OR Formation of thrombus in the setting of relatively minimal vascular injury

53 Virchow s triad Robbins 9 th edition

54 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)

55 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

56 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

57 Venous thrombi: Clinical Robbins 7 th edition

58 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 7 th edition

60 Arterial Thrombi : Morphology Adherent masses of blood that demonstrate areas of pale alternating with areas of red Lines of Zahn Mural thrombi Robbins 9 th edition

61 pathhsw5m54.ucsf.edu library.med.utah.edu

62 Arterial Thrombi Outcome Similar to venous thrombi Resolution Organization/Incorporation/ Recanalization Embolization (arterial) Propagation

63 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

64 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

65 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

66 Robbins 7 th edition library.med.utah.edu

67 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

70 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

71 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

72 Embolism Amniotic fluid embolism In complicated labor Sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma Pulmonary edema and DIC

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74 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

75 Infarction Morphology Red (hemorrhagic infarct) Venous occlusion Loose tissue Tissue with dual circulation Tissue previously congested Established flow

76 Infarction White (anemic) infarct Arterial occlusion Solid organs with end arterial circulation Wedge shaped Ischemic coagulative necrosis

77 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

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HEMODYNAMIC DISORDERS

HEMODYNAMIC DISORDERS Normal fluid homeostasis requires vessel wall integrity as well as maintenance of intravascular pressure and osmolarity within certain physiologic ranges. Increases in vascular volume