EDEMA

PATHOPHYSIOLOGY AND CLINICAL

APPROACH
 DEFINITION
• Edema is defined as a clinically apparent increase in
the interstitial fluid volume.

 may expand by several liters before the abnormality

is evident.
 Anasarca refers to gross, generalized edema.
• Ascites and hydrothorax refer to accumulation of
excess fluid in the peritoneal and pleural cavities,
respectively, and are considered special forms of
edema.
 TYPES OF EDEMA
• Localized or Generalized
• Pitting or Non-pitting
PATHOPHYSIOLOGY

TOTAL BODY
WATER

2/3rd
75% interstitial INTRACELLULAR
25% intravascular
 MECHANISMS

i. Imbalance of Starling forces

ii. Capillary damage
iii. Activation of RAAS and AVP
• STARLING FORCES
• The forces that regulate the disposition of fluid
between the two components of the extracellular
compartment are referred to as the Starling forces.
• These include:Hydrostatic pressure
Colloid oncotic pressure

• The hydrostatic pressure within the vascular system

and the colloid oncotic pressure in the interstitial
fluid tend to promote movement of fluid from the
vascular to the extravascular space
• By contrast, the colloid oncotic pressure of plasma
contributed by plasma proteins and the hydrostatic
pressure within the interstitial fluid promote the
movement of fluid into the vascular compartment.
• These flows are usually balanced so that there is a
steady state in the sizes of the intravascular and
interstitial compartments
• The development of edema depends on one or
more alterations in the Starling forces so that there is
increased flow of fluid from the vascular system into
the interstitium or into a body cavity.
 DECREASE IN DECREASE IN
HYDROSTASTIC PLASMA
PRESSURE OF ONCOTIC
INTERSTITIUM PRESSURE

INCREASE IN
COLLOID ONCOTIC
PRESSURE OF EDEMA
INTERSTITIUM

INCREASE IN
VASCULAR
HYDROSTATIC
PRESSURE
• INCREASE IN VASCULAR HYDROSTATIC PRESSURE:
Venous obstuction
Lymphatic obstruction

• DECREASE IN PLASMA COLLOID ONCOTIC

PRESSURE:
Hypoalbuminemia:such as in severe
malnutrition, liver disease, loss of protein into the
urine or into the gastrointestinal tract, or a severe
catabolic state
• CAPILLARY DAMAGE
Can also lead to edema
Capillary damage increases its permeability and
permits the transfer of proteins into the interstitial
compartment.
Can result from drugs, viral or bacterial agents,
and thermal or mechanical trauma.
Increased capillary permeability also may be a
consequence of a hypersensitivity reaction.
• Damage to the capillary endothelium is responsible
for inflammatory edema, which is usually nonpitting,
localized, and accompanied by other signs of
inflammation .
• REDUCTION OF EFFECTIVE ARTERIAL VOLUME
Stimulates the Renin-angiotensin-
aldosterone system and AVP, resulting in salt
and water retention and consequent edema.
 CAUSES OF EDEMA
• Generalised edema:
Cardiac edema-CCF
Renal edema-Nephrotic syndrome,CKD
Hepatic edema-Cirrhosis
Nutritional edema-Hypoproteinemia,Beri-
beri
Cyclic-Premenstrual
Idiopathic
• Cardiac edema pathogenesis
 Increased back pressure on venous side of
circulation leading to transudation of fluid into
interstitium .
 Decreased intravascular volume leading to
decreased renal blood flow and thereby stimulation
of RAAS.
Characteristic:
Dependent edema found over ankles in
ambulant patients and over sacrum in bed ridden
patients.
• Renal edema pathogenesis
 Primary increase in sodium and water retention by
the kidneys.
 Decrease in plasma oncotic pressure due to
increased loss of albumin in urine.
Characteristic:
Involves loose connective tissue,
especially over periorbital region.
More prominent when the patient
wakes up in the morning.
• Hepatic edema pathogenesis
 Increased portal venous pressure
 Obliteration of lymphatic drainage of the liver.
 Decreased in intravascular volume and activation
of RAAS
 Secondary hyperaldosternism leading to salt and
water retention
 Hypoalbuminemia due to decreased albumin
production from liver.
• Edema of nutritional deficiency
 Hypoprotinemia: decreased plasma oncotic pressure
 Thiamine deficiency:
Peripheral vasodilatation resulting from
lactate and pyruvate accumulation.
High output cardiac failure
• LOCALISED EDEMA:CAUSES
 Venous edema
i. DVT
ii. Trombophlebitis
iii. Varicose veins
iv. SVC/IVC obstruction
 Lymphatic edema
i. Chronic Lymphangitis
ii. Regional lymph node resection
iii. Filariasis
iv. Radiotherapy , v. Milroy’s disease
 Inflammatory/Allergic edema
i. Cellulitis
ii. Bee or Wasp Sting
• Drug-Induced Edema
A large number of widely used drugs can
cause edema . Mechanisms include
 renal vasoconstriction (NSAIDs and
cyclosporine),
 arteriolar dilation (vasodilators),
 augmented renal Na+ reabsorption (steroid
hormones), and
 capillary damage (interleukin 2).
•
 APPROACH TO EDEMA
• History
• Physical examination: Localized or Generalized
• Laboratory testing
CBC
Blood urea, Serum creatinine
Liver function Test
Cardiac evaluation
Urine examination
Imaging studies
•
• Treatment
 Management of underlying cause
 Diuretics provide temporary benefit in cardiac
and renal failure.
 Renal replacement therapy in renal failure.
 Protein supplementation in hypoproteinemia .
 Aldosterone receptor antagonist: Spironolactone
in cirrhosis and cardiac failure
 Liver transplantation in cirrhosis.