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Fluid Compartments

Intracellular Fluid (ICF) : 40% Interstitial Fluid (ISF) : 15%} Intravascular Fluid (IVF) : 4% } 20% Transcellular Water (TCW) : 1-2%} (joints, CSF, pleural cavity, peritoneal cavity; eye, GI secretions)

Fluid Movement
Hydrostatic Pressure: Moves fluid across a pressure gradient (Fluid moves from capillaries to ISF by hydrostatic pressure) Will not move if BP

Fluid Movement
Osmotic Pressure Moves from an area of lesser solute concentration to greater concentration. Low serum protein shift to ISF

DEFINITION OF EDEMA
The Accumulation of Abnormal Amounts of Extravascular

ANASARCA: Severe, widely distributed pitting edema.

Classification
1) Interstitial pitting edema 2) Intracellular edema non pitting edema

Interstitial Edema
Edema Fluid in interstitial tissue Occurs when hydrostatic pressure or osmotic pressure moves fluid into third space.

Edema
Causes: Colloid osmotic pressure (kidney disease) Capillary permeability (inflammation; burns) Capillary hydrostatic pressure (congestive heart disease) Lymphatic obstruction (cancer) Sodium & water excess (renal failure)

TYPES OF EDEMA
GENERALIZED LOCALIZED
Inflammation Lymphatic Obstruction Venous Obstruction Thrombophlebitis Chronic lymphangitis Resection of reg lymph nodes Filariasis CARDIAC HEPATIC RENAL NEPHROTIC SYNDROME ACUTE GN CRF IDIOPATHIC Malnutrition Other Cyclic Myxedema Vasodilator-induced Pregnancy-induced Capillary leak syndrome

Pathogenesis of edema
Starling forces Capillary damage Reduction of effective arterial volume Reduced cardiac output Renal factors The renin-angiotensin-aldosterone (RAA) system Arginine vasopressin (AVP) Endothelin Natriuretic peptides

MECHANISMS OF EDEMA FORMATION

(Capillary Permeability) nterstitial Space


Filtration < or = Lymphatic Drainage Filtration > Lymphatic Drainage

odema

DEMA

CARDIAC EDEMA Diagnosis History of Heart Disease Cardiac enlargement Evidence of Pulmonary Edema Orthopnea Exertional Dyspnea Basilar rales Evidence of Volume Expansion Venous distention Hepatic Congestion Hepatojugular Reflux Ventricular Gallop Rhythm

CARDIAC EDEMA Pathophysiology


HEART DISEASE
Left Ventricular Dysfunction Right Ventricular Dysfunction

Increased Pulmonary Venous Pressure

Hypotension Renal Na Retention Systemic Edema

Pulmonary Edema

HEPATIC EDEMA Diagnosis History of Liver Disease Evidence of Chronic Liver Disease Spider Angiomas Palmar Erythema Jaundice Hypoalbuminemia Evidence of Portal Hypertension Venous Pattern on Abdominal Wall Esophogeal Varices Ascites

LIVER DISEASE
Liver Cirrhosis

HEPATIC EDEMA Pathophysiology

Increased Pressure in Hepatic Sinusoids Neurohumoral Activation (Increased Volume Hormones)

Exudation of Fluid Into Peritoneal Cavity

Ascites

Functional Renal Insufficiency (Hepatorenal Syndrome)

Renal Na Retention

Systemic Edema

RENAL EDEMA Diagnosis History of Renal Disease Evidence of Albumin Loss Proteinuria Hypoalbuminemia

Renal Imaging Enlarged Kidneys Shrunken Kidneys

Nephrotic Syndrome or AGN CRF

RENAL EDEMA Diagnosis Nephrotic Syndrome Hyaline Casts Oval Fat Bodies Lipid Droplets/Casts Acute Glomerulonephritis Hematuria Erythrocyte Casts Leukocyte Casts Pyuria

Urinalysis

RENAL EDEMA Pathophysiology


RENAL DISEASE
Urinary Loss of Albumin Reduced GFR

Hypoalbuminemia

Renal Na Retention

Altered Starling Forces

Systemic Edema

CARDIAC

HEPATIC

RENAL

Facial Edema Ascites Hypoalbuminemia Proteinuria

Absent

Absent

Severe/Moderate

Absent/Mil Severe Absent/Mil d d Absent Moderate/Mild Severe


Absent/Trace

Absent/Trace

Severe

DISTRIBUTION OF EDEMA Important guide to the cause One leg or to one or both arms Venous and/or lymphatic obstruction Resulting from hypoproteinemia generalized especially in eyelids and face Facial edema : trichinosis, allergic reactions, myxedema Associated with heart failure : more extensive in the legs

Additional factors in diagnosis


Measurement estimation of the venous pressure is of importance in evaluating edema - an isolated part of the body = reflects localized venous obstruction - generalized elevation of systemic venous pressure usually indicates the presence of congestive heart failure

Approach to the patient


First question : - localized - generalized - Serious hypoalbuminemia History, PE urinalysis, other lab cirrhosis, severe malnutrition protein -losing gastroenteropathy nephrotic syndrome - hypoalbuminemia ( - )

evidence of CHF Second question : - adequate urine output - oliguria or anuria

ASCITES
DEFINITION FREE FLUID IN THE ABDOMINAL CAVITY

JAMA 1992;267:2645-2648

PATHOPHYSIOLOGY OF ASCITES

HYDROSTATIC PRESSURE
CIRRHOSIS CHF CONSTRICTIVE PERICARDITIS

OSMOTIC PRESSURE
NEPHROTIC SYNDROME MALNUTRITION PROTEIN LOSING ENTEROPATHY

FLUID PRODUCTION EXCEEDING RESORPTIVE CAPACITY


INFECTION TB MALIGNANCY
JAMA 1992;267:2645-2648

SHIFTING DULLNESS

METHOD OF EXAMINATION BEGIN BY PERCUSSING AT THE UMBILICUS AND MOVING TOWARD THE FLANKS. THE TRANSITION FROM AIR TO FLUID CAN BE IDENTIFIED WHEN THE PERCUSSION NOTE CHANGES FROM TYMPANIC TO DULL. ROLL THE PATIENT ON THEIR SIDE AND PERCUSS AS BEFORE. THE AREA OF TYMPANY WILL SHIFT TOWARDS THE TOP AND THE AREA OF DULLNESS TOWARDS THE BOTTOM.
JAMA 1992;267:2645-2648

Reference
Kasper DL, Braunwald E et.al Harrisons Principles of Internal Medicine,16th Ed, Mc-G raw Hill, 2005: 212 - 216