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.
LOCALIZED EDEMA
Limited to a particular organ or
vascular bed;
easily distinguished from generalized edema. Unilateral
extremity edema is usually
due to venous or lymphatic obstruction (e.g.,deep venous
thrombosis, tumor
obstruction,primary lymphedema). Stasis edema of a
paralyzed lower extremity
may also occur. Allergic reactions (“angioedema”) and
superior vena
caval obstruction are causes of localized facial edema.
Bilateral lower extremity
edema may have localized causes,e.g.,inferior vena caval
obstruction, compression
due to ascites,abdominal mass. Ascites (fluid in
peritoneal cavity) and
hydrothorax (in pleural space) may also present as
isolated localized edema,
due to inflammation or neoplasm.
GENERALIZED EDEMA Soft tissue swelling of most or all
regions of
the body. Bilateral lower extremity swelling,more
pronounced after standing
for several hours,and pulmonary edema are usually cardiac
in origin. Periorbital
edema noted on awakening often results from renal disease
and impaired Na
excretion. Ascites and edema of lower extremities and
scrotum are frequent in
cirrhosis or CHF. In CHF,diminished cardiac output
and effective arterial blood
volume result in both decreased renal perfusion and
increased venous pressure
with resultant renal Na retention due to renal
vasoconstriction,intrarenal blood
flow redistribution,direct Na-retentive effects of
norepinephrine and angiotensin
II,and secondary hyperaldosteronism.
In cirrhosis,arteriovenous shunts lower effective
renal perfusion, resulting
in Na retention. Ascites accumulates when increased
intrahepatic vascular resistance
produces portal hypertension. Reduced serum albumin and
increased
abdominal pressure also promote lower extremity edema.
In nephrotic syndrome,massive renal loss of
albumin lowers plasma oncotic
pressure,promoting fluid transudation into interstitium;
lowering of effective
blood volume stimulates renal Na retention.
In acute or chronic renal failure,edema occurs if
Na intake exceeds kidney’s
ability to excrete Na secondary to marked reductions in
glomerular filtration.
Severe hypoalbuminemia [_25 g/L (2.5 g/dL)] of any cause
(e.g.,nephrosis,
nutritional deficiency states,chronic liver disease) may
lower plasma oncotic
pressure sufficiently to cause edema,if accompanied by
low levels of nonalbumin
proteins [total protein _54 g/L (5.4 g/dL)].
Less common causes of generalized edema: idiopathic
edema,a syndrome
of recurrent rapid weight gain and edema in women of
reproductive age; hypothyroidism,
in which myxedema is typically located in the pretibial
region;
drugs such as
glucocorticoids,estrogens,thiozolidinediones, and vasodilators;
pregnancy; refeeding after starvation.
TREATMENT
Primary management is to identify and treat the
underlying cause of edema
(Fig. 47-1).
Dietary Na restriction (_500 mg/d) may prevent further
edema formation.
Bed rest enhances response to salt restriction in CHF and
cirrhosis. Supportive
stockings and elevation of edematous lower extremities
will help mobilize interstitial fluid. If severe hyponatremia (_132 mmol/L) is
present,water intake
should also be reduced (_1500 mL/d). Diuretics (Table
47-1) are indicated for
marked peripheral edema,pulmonary edema,CHF,inadequate
dietary salt restriction.
Complications are listed in Table 47-2. Weight loss by
diuretics should be limited to 1–1.5 kg/d. Distal (“potassium sparing”)
diuretics or metolazone
may be added to loop diuretics for enhanced effect. Note
that intestinal edema
may impair absorption of oral diuretics and reduce
effectiveness. When desired
weight is achieved,diuretic doses should be reduced.
In CHF (Chap. 126),avoid overdiuresis because it
may bring a fall in
cardiac output and prerenal azotemia. Avoid
diuretic-induced hypokalemia,
which predisposes to digitalis toxicity.
In cirrhosis and other hepatic causes of
edema,spironolactone is the diuretic
of choice but may produce acidosis and hyperkalemia.
Thiazides or
small doses of loop diuretics may also be added.
However,renal failure may
result from volume depletion. Overdiuresis may result in
hyponatremia,hypokalemia,
and alkalosis,which may worsen hepatic encephalopathy.
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