EDEMA

Pendrik Tandean
Internal Medicine, Medical Faculty of
Hasanuddin University, Makassar
Definition :
 Soft tissue swelling due to abnormal
expansion of interstitial fluid volume.
 Edema fluid is a plasma transudate that
accumulates when movement of fluid from
vascular to interstitial space is favored.
 Since detectable generalized edema in the
adult reflects a gain of >3 L,renal retention
of salt and water is necessary for edema to
occur. Distribution of edema can be an
important guide to cause.
 Types of edema
• Dependent bilateral edema
(usually“pitting”)
• Lymphedema
• Localized edema
• Myxedema
 Pitting dependent
edema:
causes :
• Decreased serum protein
• Increased systemic venous pressure
• Capillary edema (increased permea-
bility).
Edema due to hypoalbuminemia:

common causes
1. Impaired protein synthesis
– Decreased protein intake: starvation, kwashiokor
– Decreased absorption of proteins: malabsorption
– Impaired hepatic synthesis due to liver disease
2. Increased loss of protein
– Skin loss: burns, weeping skin diseases
– Urinary loss: nephrotic syndrome
– Fecal loss: bowel disease
Edema due to venous pressure:

Common causes
1. Systemic venous hypertension
– Congestive heart failure
– Pericardial diseases, tricuspid valve
disease
2. Regional venous hypertension
– Inferior vena cava syndrome
– Venous thrombosis
– Lower extremity venous insufficiency
 Edema due to capillary permeability
• Vasculitis
• Idiopathic cyclic edema of women
– Varies with menstrual cycle
• Post-anoxic encephalopath
Pitting recovery time

• Technique:
– Press firmly to bone
– Shine light and determine time resolution
of shadow
• Interpretation
– Acute edema (< 3 months)
– < 40 seconds associated with low serum
albumin
 Rapid pitting recovery:
< 40 seconds
1. Decreased of protein synthesis :
– protein intake: dietary history
– Rapid pitting recovery: < 40 seconds
absorption of proteins: diarrhea
– hepatic synthesis due to liver disease:
History: alcohol, other hepatotoxins, hepatitis
Physical findings: spider angiomata
2. Increased loss of protein :
– Skin loss: skin lesions such as burns, ulcers
– Urinary loss: foamy urine with high protein
– Fecal loss: diarrhea, sticky, oily stools
 Edema with rapid
pitting recovery:

Evaluation of etiology
• Impaired protein synthesis
– ↓protein intake: starvation, kwashiokor
– ↓absorption of proteins: malabsorption
– ↓hepatic synthesis due to liver disease
• Increased loss of protein
– Skin loss: burns, weeping skin diseases
– Urinary loss: nephrotic syndrome
– Fecal loss: bowel disease.
Slow pitting time (> 40 seconds)
normoalbuminemic edema

• Systemic venous hypertension

– Congestive heart failure
– Pericardial diseases, tricuspid valve disease

• Regional venous hypertension

– Inferior vena cava syndrome
– Venous thrombosis
– Lower extremity venous insufficiency
 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 to be
special forms of edema.
 PATHOGENESIS

 About one-third of the total-body water

is confined to the extracellular space.
Approximately 25% of the latter, in
turn, is composed of the plasma
volume, and the remainder is
interstitial fluid.
 STARLING FORCES
 The forces that regulate the disposition
of fluid between these two components
of the extracellular compartment are
frequently referred to as the Starling
forces.
 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.
 On the other hand, the colloid oncotic
pressure contributed by the plasma
proteins and the hydrostatic pressure
within the interstitial fluid, referred to
as the tissue tension, promote the
movement of fluid into the vascular
compartment.
 Consequently there is a movement of
water and diffusible solutes from the
vascular space at the arteriolar end of
the capillaries.
 Fluid is returned from the interstitial
space into the vascular system at the
venous end of the capillary and by way
of the lymphatics.
 Unless these channels are obstructed,
lymph flow rises with increases in net
movement of fluid from the vascular
compartment to the interstitium
 The development of edema then
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.
Edema due to increase in capillary pressure may
result from an elevation of venous pressure due to
obstruction in venous drainage.
 This increase in capillary pressure may be
generalized, as occurs in congestive heart
failure. The Starling forces may be
imbalanced when the colloid oncotic
pressure of the plasma is reduced, owing to
any factor that may induced
hypoalbuminemia, such as saline
expansion,malnutrition, liver disease, loss of
protein into the urine or into the
gastrointestinal tract, or a severe catabolic
state.
 Hydrostatic pressure
 Causes fluids moving through a semi
permeable membrane to flow from higher
pressure side to lower pressure side of the
membrane.
 Plasma pressure>interstitial fluid pressure
at capillary end.
 Blood plasma pressure at the arteriole end
of a capillary ~25mmhg & 10mmHg at
venule
 Therefore this pressure within the capillary
forces fluids out into the interstitial
 Interstitial pressure
 Normally negative pressure ~ -
5.3mmHg.
 Negative pressure tends to act as a
suction: thus negativity on the
interstitial side of the membrane also
favors fluid out of the capillary in to the
interstitial space.
 Hydrostatic and
Interstitial pressures
 So far both force fluids out of the capillary
into the interstitial space.
 1. Cap pressure = 25mmHg arteriole and 10
mmHg venule
 2. Interstitial pressure= -5.3 mmHg arteriole
and venous ends
 These combine for a pressure gradient of
30.3 mmHg at the arteriole end and
15.3mmHg at the venule. Forcing fluids out
 Pressure out is 15mmHg greater at arteriole
end
 Osmotic pressure
 Pressure that causes fluids to pass
from lower concentration to greater
concentration of Osmotic substances.
 Causes of edema
 1. Increased HP of blood
 2. Decreased Osmotic Pressure of
blood
 3. Increased Capillary permeability

 4. Lymphatic obstruction

 5. Slowed flow of blood and lymph

 Clinical Aspects of
Edema
 Consider:
– Amount
– Acute vs. Chronic
– Consistency of Fluid
– Site
– Size of the edematous area
 Types of Edema
 Cardiac
 Renal

 Starvation

 Traumatic

 Obstructive

 Paralytic
 Consistency of Fluid
 Transudate vs. Exudate
 Pitting vs. Nonpitting

 Site and Size

 Anasarca/ dropsy
`
 Edema is defined as a clinically apparent
increase in the interstitial fluid volume,
which may expand by several liters before
the abnormalityis evident. Therefore, a
weight gain of several kilograms usually
precedes overt manifestations of edema,
and a similar weight loss from diuresis can
be induced in a slightly edematous patient
before “dry weight” is achieved.