Edema

Allergic, cardiac, cirrhotic, nephrotic, and nephritic edema states are discussed below. Expanded discussions of nephrotic and nephritic edema may be found, with links to recent articles reviewing the other types of edema.

Cardiac Edema

Cirrhotic Edema

Allergic Edema

Lymphedema

Renal Edema

Prep Questions

Question 142 2006

Question 158 2006

In pediatrics, edema is an uncommon physical finding. A thoughtful history and examination may allow the practitioner to identify the etiology of the edema state.

Edema may be brought about through a variety of mechanisms. An understanding of the pathophysiology of edema may allow the practitioner to identify the disease state in the patient and to formulate an initial plan of management.

A 3-year-old boy develops edema, and his general pediatrician obtains laboratory results revealing hypoalbuminemia, proteinuria, and hypercholesterolemia that are consistent with nephrotic syndrome. He sends the patient to the emergency department because the boy has not voided for 12 hours. On physical examination, he has anasarca and abdominal distention. His mucous membranes are dry, and his skin turgor is decreased. He is less active than normal but arousable. His heart rate is 145 beats/min and blood pressure is 70/40 mm Hg.

Of the following, the MOST appropriate initial therapy for this child is intravenous

A. albumin

B. albumin and furosemide

C. furosemide

D. lactated Ringer solution

E. 0.9% sodium chloride solution

Nephrotic syndrome (NS) is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. A variety of diseases cause NS, including minimal-change NS, focal segmental glomerulosclerosis, postinfectious acute glomerulonephritis, and membranoproliferative glomerulonephritis. Generally, any disease of the glomerulus can result in massive proteinuria and NS. Although the type of NS eventually determines chronic management and patient prognosis, the most important initial step is to assess the patient’s current intravascular volume status. Most patients who have NS have euvolemia despite the presence of edema. However, hypovolemia or hypervolemia may be present. The serum albumin is always low (usually <2.0 g/dL [20 g/L]) at the presentation of NS, but the degree of hypoalbuminemia may be helpful to determine the volume status. Additionally, the patient’s vital signs and findings on physical examination are important clues to assess the volume status. Using the patient’s change in weight can be misleading because some volume is not lost from the body but displaced out of the intravascular space. The child described in the vignette is showing obvious signs of hypovolemia, indicating the need for albumin infusion (1 mg/kg of body weight of 25% albumin) to help restore volume in the intravascular space and reduce the edema. This may be repeated up to four times per day, as needed. Furosemide therapy will result in loss of intravascular volume, which would exacerbate his hypovolemia. Normal saline alone may restore some intravascular volume temporarily, but the infusion will leak out into the interstitium rapidly and worsen the edema. Patients who have hypervolemia have a loss of albumin and decrease in oncotic pressure, with concomitant reduced glomerular filtration rate and subsequent retention of excess salt and water that requires diuresis. This can be difficult if there is severe hypoalbuminemia because albumin delivers diuretics such as furosemide to the kidney, so high doses (1.0 to 1.5 mg/kg) of furosemide may be required. Finally, severe anasarca in patients who have euvolemia can be treated with albumin infusion followed by furosemide. The goal in these patients is to maintain the current volume status but reduce the edema and its potential adverse effects (eg, peritonitis). The most commonly used diuretics for patients who have NS are the loop (eg, furosemide) and thiazide diuretics (eg, hydrochlorothiazide). Loop diuretics block sodium, potassium, and chloride reabsorption in the kidney and may cause hyponatremia, hypokalemia, and hypochloremia. Other potential adverse effects include alkalosis and hypercalciuria.Thiazide diuretics block sodium and chloride transport and may induce hyponatremia and hypochloremia. They also may cause hypercalcemia. In addition to albumin or diuretics, many patients who have NS require treatment of the underlying inflammatory disease. Oral or intravenous steroids almost always are prescribed. Other medications used depend upon the underlying pathology.

References:

Bircan Z, Kervancioglu M, Katar S, Vitrinel A. Does albumin and furosemide therapy affect plasma volume in nephrotic children? Pediatr Nephrol. 2001;16:497-499

Hodson EM, Knight JF, Willis NS, Craig JC. Corticosteroid therapy for nephrotic syndrome in children. Cochrane Database Syst Rev. 2004:CD001533

Roth KS, Amaker BH, Chan JCM. Nephrotic syndrome: pathogenesis and management. Pediatr Rev. 2002;23:237-248

A previously healthy 10-year-old boy presents with facial and leg edema. He has had increasing swelling for about 2 weeks. He claims that he has been unable to tie his shoes completely and feels tired. He reports no history of abdominal pain, gross hematuria, or decreased urine output. Measurement of serum electrolytes reveals:

• Sodium, 132 mEq/L (132 mmol/L)

• Potassium, 4.6 mEq/L (4.6 mmol/L)

• Chloride, 92 mEq/L (92 mmol/L)

• Bicarbonate, 21 mEq/L (21 mmol/L)

• Blood urea nitrogen, 21 mg/dL (7.5 mmol/L)

• Creatinine, 1.8 mg/dL (159 mcmol/L)

His serum albumin concentration is 1.6 g/dL (16 g/L). His urinalysis reveals moderate blood and 4+ protein. Measurement of serum complements (C) reveal: C3, 41 mg/dL (low) and C4, 3 mg/dL (low). Of the following, the MOST likely cause of this boy’s symptoms is

A. acute postinfectious glomerulonephritis

B. focal segmental glomerulosclerosis

C. immunoglobulin A nephropathy

D. membranoproliferative glomerulonephritis

E. membranous nephropathy

The edema, decreased renal function, hypoalbuminemia, hematuria, and proteinuria described for the child in the

vignette indicate that he has nephrotic syndrome (NS). The low serum complement levels reported suggest that he has membranoproliferative glomerulonephritis (MPGN). With postinfectious acute glomerulonephritis (PIAGN), only the complement 3 (C3) level is low. Patients who have focal segmental glomerulosclerosis (FSGS), immunoglobulin A nephropathy (IgAN), and membranous nephropathy (MGN) may present with NS, but their serum complement levels are normal. The features of NS are proteinuria, hypoalbuminemia, edema, and hypercholesterolemia. There are many causes of NS (Item C158A). Determining the cause of NS requires a through a history and physical examination. The patient’s age and clinical features usually provide valuable clues. First, certain diseases are more common in younger children (eg, minimal-change nephrotic syndrome [MCNS]) versus older children (eg, MGN). Second, associated features may be helpful. For example, although many patients who have NS may exhibit elevated blood pressure, this is unusual in patients who have MCNS and almost always is present in patients who have PIAGN. Laboratory tests also aid in the diagnosis. For example, patients who have MCNS usually present with normal renal function. Serum complement levels may be very helpful. Serum C3 always is low at the onset of PIAGN, MPGN, and in most cases of LN. C4 is normal in PIAGN, but generally is low in patients who have MPGN and lupus nephritis (LN). In PIAGN, the C3 level returns to normal by 3 months; in NPGN and LN, this generally does not occur. Thus, a persistently low C3 value raises the suspicion of LN or MPGN. The prognosis in MCNS and PIAGN is generally excellent; it is variable in IgAN and MGN. Aggressive treatment of FSGS, MPGN, and certain forms of LN has improved the prognosis of these diseases, but the outcome remains guarded.

References:

2006 PREP SA on CD-ROM

page 33

Eddy AA, Symons JM. Nephrotic syndrome in childhood. Lancet. 2003;362:629-639

Fakhouri F, Bocquet N, Taupin P, et al. Steroid-sensitive nephrotic syndrome: from childhood to adulthood. Am J Kidney Dis. 2003;41:550-557

Hiraoka M, Tsukahara H, Matsubara K, et al, West Japan Cooperative Study Group of Kidney Disease in Children. A randomized study of two long-course prednisolone regimens for nephrotic syndrome in children. Am J Kidney Dis. 2003;41:1155-1162