4 Edema Normal body water distribution:- Two compartments: Intracellular – comprising of two- thirds of total body fluid.Extracellular – comprising of one- third of total body fluid.1. Interstitial compartment- 75%2. Intra vascular compartment – 25%
5 Normal fluid exchange There are two ends for a capillary 1. Arteriolar end2. Venous endThe pressure is high in the arteriolar end then the venous end.Normally the fluid moves out from the vessel in arteriolar end into interstitial tissue. From interstitial tissue same fluid moves back into vessel at venous end.The small amount of fluid which is left in interstitial space is cleared by lymphatics.
9 Normal fluid pressures 1. Osmotic pressureIs exerted by the chemical constituents of the body fluidsEg. Electrolytes – crystalloid osmotic pressureproteins (albumin)- oncotic osmotic pressure.2. Hydrostatic pressurePressure within the blood vessel.
10 EdemaIs accumulation of excessive fluid in the interstitial spaces.
11 Classification of edema according to distribution of fluid Localized edemainvolving one organ or part of the body.eg-pleural effusion,ascitis,pericardial effusion ,etc.2. Generalized edemaInvolving the entire body- ANSARCA
12 Pathogenesis of edema:- Increased hydrostatic pressureIncreased permeability of the vessel wallDecreased oncotic pressureSodium retention in the kidneysObstruction of lymph flow
13 1. Hydrostatic edemaResults from increased intra vascular pressure (hydrostatic pressure).
15 2. Increased vascular permeability Commonest cause is inflammation.Release of inflammatory mediators like histamine, bradykinin, PAF & others leads to increased permeability.Other causes: Injury,
16 3.Decreased plasma oncotic pressure 1.Decresed synthesis in the liver – end stage liver disease.2.Incresed loss in urine(nephrotic syndrome) or stool (protein losing enteropathy)3.Inadequte intake-kwashiokar
37 Clinical Features of Oedema Considerable quantities must accumulate before clinically apparent (oedema can be assessed by weighing the patientapprox. 5 litres)GeneralisedCardiac Oedemagravitational distributionpitting oedema holds depression for a few minutesRenal Oedemafluid retentiongenerally distributed in C.T. puffy face/eyelidsSerous Cavitiese.g. hydrothorax/ascitesBrain Oedemaswollen; narrow sulci & flattened gyriPulmonary Oedemaexudateprone to infection e.g. bronchopneumoniarales
39 HemorrhageIndicates extravasation of blood due to rupture of vessel.
40 Classification based on origin 1. Cardiac- penetrating woundrupture of ventricles in MI2. Arterial – traumarupture of aneurysm3. Capillary – trauma, surgery4. Venous – trauma, surgery
41 Petechiae, Pupura, Ecchymoses Refers to the hemorrhage into the skin & mucosae.Petechiae- pinpoint hemorrhage ( < 1mm)Purpura- 1mm- 1cm in diameterEchymoses- >1cm
42 PetechiaeCaused by abnormalities in number or function of platelets or abnormalities in capillary wall (e.g. scurvy)
43 PurpuraThe palpable purpura on the foot of this nearly 3-year-old boy are associated with the disease Henoch-Schönlein Purpura.Henoch-Schönlein Purpura involves small vessels, not capillaries. Another common cause of purpura is vasculitis induced by an allergic reaction to drugs.
44 EcchymosisThe purpura and ecchymosis on the skin of this 12-year-old boy were the presenting symptoms of his acute myelogenous leukemia.The hemoglobin is converted to bilirubin (greenish) and hemosiderin (brown)
45 HematomaIs grossly visible accumulation of extravasted blood in tissue.First it is red, then as the blood is deoxygenated it becomes dusky & bluish red.
46 Body cavity hemorrhage Hemothorax – accumulation of blood in pleural cavityHemopericardium – in pericardial cavityHemoperitonium – in peritonial cavityHemoarthrosis – in intra – articular spaceHematocephalus – in ventricles of brain
47 Hematuria Is appearance of blood in urine. Microscopic – detectable by microscopic examination of urine.Macroscopic – visible to naked eyeHematuria signifies disease of kidney or urinary tract
48 Hematemesis Is vomiting of blood. Sign of esophageal & gastric hemorrhage like rupture of esophageal varices & peptic ulcer bleeding.
49 Hematochezia Bleeding through rectem. Sign of diseases in large intestine.
50 Melena Black colored blood in stools. Indicates bleeding in upper GIT. Blood is partialy digested by HCLof gastric juice & transformed into a black pigment called hematein.This pigmentis not digested in the intestines & is passed in the feces.
51 Epistaxis & Hemoptysis Epistaxis is bleeding from the nose.Hemoptysis is bleeding from lungs.
52 Menorrhagia & Metrorrahagia Menorrhagia is heavy menstrual bleeding.Metrorrhagia occurs at any time & is not related to menstrual cycle.
53 Effects of Hemorrhage Site of hemorrhage Rate of blood loss brain, pericardium, pleural spacRate of blood lossacuteloss of > 20% of blood volume may cause hypotension or hypovolemic shockhemoglobin concentration not alterednon-acutevolume loss compensated by shift of fluid from extravascular to intravascular compartmenthemoglobin concentration decreased
54 HYPEREMIA & CONGESTION Is increase in volume of blood in a particular tissue.Hyperemia is an “active process” , the increased blood influx results from arteriolar dilatation.Congestion, also known as “passive hyperemia”, results due to stagnation of blood because of venous obstruction.
58 Examples:- Hyperemia:- Inflammation Blushing – adrenergic stimulation Exercise – incresed blood flow to the muscle.Congestion:-Obstruction of veins due to thrombi or backward pressure due to heart failure.
59 Color of hyperemic & congested tissue:- Hyperemic tissue contains increased amounts of oxygenated blood & therefore the tissue appears bright red.Congested tissue contains increased amounts of deoxygenated blood & appears blue.Hyperemic tissue is warm, while congested blood is cold & clammy.
60 Chronic venous congestion (CVC):- In CVC there is long standing there is accumulation of deoxygenated blood & hence there is damage to the tissue.
61 Mechanism heart failure left heart failure right heart failure Pressure into pressure into thePulmonary vein systemic venous systemCVC LUNGS CVC LIVER SPLEEN KIDNEY
62 CVC Lung Causes:- Left heart failure Gross :- The lungs are heavy. Lungs appear brown- BROWN INDURATION OF LUNGS.
63 CVC LungsMicro:-Rupture of congested vessel results in edema & hemorrhage. Lysis of RBC’s releases hemosiderin pigment which is taken up by macrophages – HEART FAILURE CELLS.
64 View of pulmonary congestion and edema View of pulmonary congestion and edema. Often caused by an increase in hydrostatic pressure, a protein poor transudate seeps into interstitial and alveolar spaces. Note the engorged alveolar wall capillaries. If capillaries rupture, RBCs will escape into the alveolar space
65 Heart failure cells are hemosiderin laden macrophages Heart failure cells are hemosiderin laden macrophages. Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst. Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.
66 CVC Liver Causes:- Right heart failure Occlusion of inferior vena cava or portal vein.GROSS APPEARANCE:-NUTMEG APPEARANCE – Alternate areas of red & yellow .
68 CVC Liver (MICRO)Blood fills up the central vein & sinusoids around it. Followed by centrilobular hepatocytes necrosis.In the long standing cases the necrotic area is replaced by fibrous tissue.The areas with blood appears red & areas with fibrosis appears whitish yellow- NUTMEG APPEARANCE.
69 Nutmeg liver compared with actual nutmeg. Courtesy of Dr. Ed Friedlander
70 This view shows a close up of hemorrhagic central necrosis This view shows a close up of hemorrhagic central necrosis. Necrotic cells in the central area have been removed (cell dropout) and been replaced by cellular debris and hemorrhge. There is evidence that the passive congestion and hemorrhage is chronic, as many of the RBCs have been degraded into hemosiderin.