EDEMA/ ANASARCA/ ANGIOEDEMA
†††† The accumulation of fluid in the intercellular space of subcutaneous tissue or in body cavities is referred to as edema.† Anasarca refers to a diffuse generalized edema of multiple organ systems.† Ascites and hydrothorax are special forms of edema that accumulate in the peritoneal and pleural cavities, respectively.† Pulmonary edema may present as an acute, life-threatening condition.† When evaluating patients for edema, remember that it is a dependent phenomenon, so in bed ridden patients, it is important to assess the sacral area for fluid accumulation.
†††† When associated with damage to the endothelial lining of the vasculature, an inflammatory edema forms as the result of an abnormal increase in the loss of a protein-rich exudate into the surrounding tissues.† This protein-rich fluid also has a higher osmotic pressure than the intravascular fluid and this serves to further increase the tendency towards edema formation.† This form of inflammatory edema occurs secondary to trauma or infection (cellulitis).† Edema that forms secondary to underlying disease is generally a transudative edema (low in protein content) that occurs secondary to either an increase in the intravascular hydrostatic pressure or a decrease in the intravascular oncotic pressure (hypoproteinemia).† Unilateral edema of an extremity may occur as a result of blockage of venous or lymphatic outflow such as with a deep venous thrombosis (DVT) or following surgical disruption of lymphatic channels (lymphedema).† Painless, unilateral lower extremity edema in a diabetic patient may also be the initial presentation of Charcot foot.
†††† Primary edema may result from lymphatic agenesis, hypoplasia, or obstruction.† Common etiologies for secondary edema include: congestive heart failure (CHF), hepatic cirrhosis, acute or chronic renal failure (usually associated with significant oliguria or anuria), protein-losing glomerulopathies (nephrotic syndrome), pulmonary hypertension, hypoproteinemia, hypoalbuminemia (serum albumin less than 2.5 g/dL), DVT, lymphatic obstruction, inferior vena cava obstruction or compression, and idiopathic edema.† Other causes of specific forms of edema include hypothyroidism (periorbital or diffuse myxedema), Graveís disease (pretibial myxedema), trichinosis (periorbital and facial edema), and dermatomyositis (periorbital edema associated with a heliotrope-colored rash).† The yellow nail syndrome is a condition characterized by the triad of lymphedema, pleural effusion, and slow, growing yellow nails.† Medication side effect (estrogens, nifedipine, amlodipine, thiazolidinediones, steroids, etc) should always be considered a possible cause of edema in patients receiving medications.† ACEI therapy may result in angioedema of the face, neck, or abdominal viscera.
The work up for bilateral edema should start with a determination of the patientís serum protein/ albumin level. If the serum albumin level is less than 2.5 gm/dL, then hypoalbuminemia resulting in a decrease in intravascular oncotic pressure may be the cause of the edema, and a further investigation into the cause of the hypoalbuminemia is warranted.† If the serum albumin level is greater than 2.5 gm/dL, then further work up should include determination of liver and kidney function studies, a chest radiograph, and a urinalysis to screen for underlying proteinuria.† If proteinuria is present, then an evaluation of the degree of proteinuria should include either a 24 hour urine protein determination or a random urine collection for protein/creatinine ratio. Levels of proteinuria greater than 3.5 grams/day with associated edema and hypoalbuminemia are diagnostic of the nephrotic syndrome.† If the work up is unrewarding at this point, further studies may include an echocardiogram, to determine the cardiac ejection fraction and to evaluate for signs of pulmonary hypertension, and a renal sonogram.† B-type natriuretic peptide may also be a useful screening test used in patients with edema that is suspected to bew secondary to CHF. Abdominal and pelvic CT scanning may be useful to exclude mass lesions causing extrinsic compression of the inferior vena cava.† If there is unilateral edema of a lower extremity, then the possibility of an underlying DVT should be considered and evaluation with a duplex scan or impedance plethysmography along with serum D-dimer assay should be initiated.† Post-operative edema secondary to lymphatic disruption may occur acutely or even years after the surgery.† This form of edema is often seen in the ipsilateral upper extremity of women who have undergone axillary lymph node dissection as part of breast cancer surgery.† Ascites and pleural effusions each have their own work ups which start with fluid analysis.
†††† Localized, recurrent edema without an identifiable etiology should raise the possibility of hereditary angioedema or acquired angioedema.† The edema is generally nonpitting and without associated pruritus.† The face, extremities, and genitalia are frequently involved.† Associated gastrointestinal symptoms include pain, nausea, vomiting, and watery diarrhea.† Laryngeal involvement may be life-threatening.† Angioedema may also be a complication of ACEI therapy.
†††† Therapy for edema is best accomplished by treating the underlying etiology.† If this cannot be accomplished, then instituting a sodium-restricted diet is often all that is needed.† If this fails, treatment with diuretics may prove effective.† Loop or thiazide diuretics are often used, but aldactone may be effective in cases of refractory edema secondary to itís aldosterone antagonistic effect which serves to decrease renal sodium and water retention.† Physical therapy may be offered in the form of instructing patients to keep the edematous portion of the body elevated as much as possible or in the form of Ted hoses or graded compression stockings.† Cerebral edema and pulmonary edema may be life threatening and in such cases should be treated emergently.