Evaluation and management of edema in children

INTRODUCTION — Edema is a clinical condition characterized by an increase in interstitial fluid volume and tissue swelling that can be either localized or generalized. Severe generalized edema is known as anasarca. More localized interstitial fluid collections include ascites and pleural effusions.

The diagnostic approach to edema is based upon a thoughtful approach to the pathogenesis of its formation. Once a diagnosis is established, specific treatment of the underlying disorder can be given. If specific therapy is not available, general treatment such as optimization of fluid management can be considered.

The evaluation and management of edema in children will be presented in this topic review. The pathogenesis and etiology of edema in children are discussed separately. (See "Pathophysiology and etiology of edema in children".)

EVALUATION — The goals of the evaluation of a child with edema include the following:

●Determine the underlying cause and character of the edema (localized or generalized), which will guide both evaluation and treatment (table 1). A more detailed discussion on the etiology based on the pathogenesis of the edema is presented separately. (See "Pathophysiology and etiology of edema in children".)

●Identify those conditions that are potentially life-threatening or have serious medical consequences, although most causes of edema are self-limiting disorders. Potentially life-threatening or serious medical disorders include anaphylaxis, hereditary angioedema with laryngeal involvement, decreased cardiac output (especially as a result of myocarditis or restrictive pericarditis), and liver and kidney disease.

History — The evaluation of a child with edema begins with a thorough history. The following should be included:

●Edema location.

●Establish time course (age at onset and duration of symptoms) to distinguish an acquired condition from a congenital condition. For example, edema of the hands and feet of a newborn girl is suggestive of Turner syndrome.

●Associated complaints that suggest systemic disease or major organ dysfunction. As an example, shortness of breath suggests heart failure and/or pulmonary edema.

●Additional concurrent illnesses or signs. A streptococcal infection one to three weeks earlier may point to poststreptococcal glomerulonephritis.

●Past medical and family history. A family history of recurrent angioedema, for example, may suggest hereditary angioedema as a possible diagnosis.

●Weight gain and tight-fitting clothes and shoes. Such changes may have been ignored by parents/caregivers as they were thought to be normal signs of growth, rather than the onset of edema because of nephrosis.

●History of allergies and current medications. Allergies and adverse reaction to certain medications can present as angioedema in childhood. As an example, angiotensin-converting enzyme (ACE) inhibitors are kininase inhibitors that result in high bradykinin levels and increased vascular permeability. ACE inhibitors are a common cause of drug-induced bradykinin-mediated angioedema that is manifested by swelling of the lips, tongue, pharynx, and larynx. Angioedema has also been seen with the use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. (See "An overview of angioedema: Pathogenesis and causes", section on 'ACE inhibitors' and "An overview of angioedema: Pathogenesis and causes", section on 'Aspirin and NSAIDs'.)

Physical examination

General assessment — General assessment includes:

●Measuring the child's growth parameters.

●Fully evaluating the cardiovascular system, including vital signs. Findings of tachycardia, tachypnea, gallop, rales, or hepatomegaly are seen in patients with heart failure, whereas tachypnea and rales alone may be indicative of pulmonary edema, which can be either cardiogenic or noncardiogenic. Increased blood pressure (BP) levels may reflect hypervolemia resulting from acute kidney injury (AKI), chronic kidney disease (CKD) or glomerulonephritis. BP measurements are interpreted in relation to the patient's age, sex, and height percentile (table 2 and table 3). (See "Definition and diagnosis of hypertension in children and adolescents".)

●Characterizing the edema as localized or generalized, and assessing the extent of edema. (See 'Edema' below.)

Edema — The extent of edema (localized or generalized) and character of the edema affects further testing and imaging.

●Generalized edema – If generalized edema is present, the child should be examined and possibly tested for the presence of a pleural effusion, pulmonary edema, ascites, scrotal/labial edema, or evidence of skin breakdown in regions of edema.

•Pulmonary findings of decreased breath sounds and dullness to percussion are consistent with pleural effusion, although pulmonary edema is suggested by adventitial sounds such as rales.

•Ascites is associated with abdominal distention, and shifting dullness and a fluid wave on percussion of the abdomen.

•Patients with the nephrotic syndrome also may have prominent periorbital edema because of the low tissue hydrostatic pressure in this area; this finding is usually worse in the morning and improves with ambulation due to the dependent nature of this type of edema.

●Localized edema – With regional edema, the clinician should localize the area of swelling to help deduce where a region of venous or lymphatic obstruction is likely to be present, or if localized allergen exposure has occurred. Because cellulitis also can manifest with regional edema, assessment of the patient for fever and local signs of inflammation is important. If the edema is localized to the face, the child also should be carefully evaluated for concurrent airway involvement, which can be life-threatening.

In addition, determine the presence of peripheral edema by the presence of pitting after pressure is applied to the edematous area. Pitting reflects movement of the excess interstitial water in response to pressure. Because peripheral edema locates preferentially in dependent areas, it is primarily found in the lower extremities of ambulatory patients and over the sacrum in patients at bed rest.

When the edema is nonpitting, lymphedema (which may also be associated with pitting edema) or pretibial myxedema should be considered. (See "Clinical features and diagnosis of peripheral lymphedema" and "Pretibial myxedema (thyroid dermopathy) in autoimmune thyroid disease".)

Clues from constellations of symptoms and signs — The child with edema must be assessed for associated symptoms or other medical conditions that may help suggest the underlying etiology. The following are groupings of signs and symptoms found in a variety of diseases that cause edema in children.

●A child with diaphoresis, dyspnea on exertion, and/or a history of heart disease may have edema secondary to heart failure. Findings on clinical examination include tachycardia, tachypnea, rales, hepatomegaly, and/or gallop. (See "Heart failure in children: Etiology, clinical manifestations, and diagnosis".)

●A child with a history of food allergies may present acutely with urticaria and angioedema after allergen exposure. If there is airway involvement, this is a medical emergency and requires emergent therapy. (See "Clinical manifestations of food allergy: An overview", section on 'Urticaria and angioedema' and "Anaphylaxis: Emergency treatment" and "Clinical manifestations of food allergy: An overview", section on 'Anaphylaxis'.)

●A history of jaundice, failure to thrive, steatorrhea, or abdominal pain should point the clinician toward a diagnosis of liver failure/disease or possibly a protein-losing enteropathy [1,2]. (See "Acute liver failure in children: Etiology and evaluation", section on 'Physical examination' and "Protein-losing gastroenteropathy", section on 'Clinical features'.)

●A child with progressive anasarca with a significant periorbital component, but minimal systemic complaints, may have nephrotic syndrome. (See "Clinical manifestations, diagnosis, and evaluation of nephrotic syndrome in children", section on 'Edema'.)

●Cola-colored urine with either generalized or facial edema strongly suggests acute glomerulonephritis. These patients also may have hypertension. (See "Glomerular disease: Evaluation in children", section on 'Clinical features'.)

●Edema, anorexia, and growth impairment can be seen in a child with CKD. (See "Chronic kidney disease in children: Complications", section on 'Fluid and electrolyte abnormalities' and "Chronic kidney disease in children: Clinical manifestations and evaluation", section on 'Additional history'.)

●Family history of angioedema favors a diagnosis of hereditary angioedema. (See "Hereditary angioedema: Epidemiology, clinical manifestations, exacerbating factors, and prognosis", section on 'Characteristic features of angioedema attacks'.)

●A newborn girl with edema of the hands and feet, webbed neck, nail dysplasia, high palate, and short fourth metacarpal may have Turner syndrome. (See "Clinical manifestations and diagnosis of Turner syndrome", section on 'Typical features'.)

Initial laboratory evaluation — The initial laboratory evaluation in the child with edema without an apparent cause should include a complete blood count (CBC), serum chemistry tests (serum creatinine, blood urea nitrogen [BUN], albumin, and liver function studies) and urinalysis. The results of these initial tests, the clinical history and physical examination should provide information on the underlying general cause and help to select subsequent tests.

Urinalysis — A urinalysis including a dipstick for proteinuria must be obtained in all children with edema. Dipstick testing principally detects albumin. The finding of a markedly positive dipstick for protein in combination with hypoalbuminemia and clinical edema is virtually diagnostic of the nephrotic syndrome. False-positive results may be obtained with very alkaline or concentrated urines, or when urine is contaminated by some antiseptic agents (such as chlorhexidine or benzalkonium chloride). However, highly positive results (>300 mg/dL) cannot be explained by a concentrated urine. (See "Evaluation of proteinuria in children" and "Treatment of idiopathic nephrotic syndrome in children" and "Congenital nephrotic syndrome".)

Examination of the urine sediment may reveal hematuria, pyuria, and/or cellular casts. In the edematous child with kidney disease, different patterns of urinary findings favor different kidney diseases. (See "Urinalysis in the diagnosis of kidney disease".)

With glomerular diseases, for example:

●Hematuria with red cell casts and dysmorphic red cells, with or without heavy proteinuria, is virtually diagnostic of glomerulonephritis, such as poststreptococcal glomerulonephritis. This constellation of urinary findings is called a nephritic sediment. The absence of red cell casts does not exclude the diagnosis.

●Heavy proteinuria, but few cells or casts, is most consistent with a noninflammatory cause of nephrotic syndrome such as minimal change disease (MCD) or focal segmental glomerulosclerosis (FSGS).

Subsequent testing — Subsequent testing, including additional laboratory studies and imaging, is based on a suspected etiology/category based on results of the initial evaluation.

●Kidney disease – Underlying kidney disease may be suspected based on abnormal kidney function tests (elevated serum creatinine and BUN) or abnormal urinalysis (evidence for either glomerulonephritis or nephrotic syndrome). (See 'Urinalysis' above.)

Further testing may include:

•Suspected glomerulonephritis – Complement testing and serologic testing may identify the specific renal disease.

-Complement testing can classify glomerulonephritis as either hypocomplementemic or normocomplementemic, which helps in making a diagnosis of the underlying etiology (table 4). (See "Glomerular disease: Evaluation in children", section on 'Glomerulonephritis'.)

-Serologic testing may identify specific disorders and includes antistreptococcal antibodies (poststreptococcal glomerulonephritis), antinuclear antibodies (ANA), anti-double-stranded DNA antibodies (lupus nephritis), antiglomerular basement membrane (GBM) antibodies (anti-GBM [Goodpasture]) disease, and antineutrophil cytoplasmic autoantibodies (ANCA vasculitides). (See "Glomerular disease: Evaluation in children", section on 'Glomerulonephritis'.)

-A renal biopsy may be considered in children with suspected glomerulonephritis, particularly in patients with significant renal dysfunction, normocomplementemia, heavy proteinuria without an underlying diagnosis, or to stage the histologic severity to guide approach to treatment for suspected lupus nephritis, ANCA-associated vasculitis, or nephritis associated with Henoch-Schönlein purpura. (See "Glomerular disease: Evaluation in children", section on 'Kidney biopsy'.)

•Suspected nephrotic syndrome – Complement components and serologic tests also are frequently ordered as part of the routine evaluation. These include C3, C4, ANA, and anti-double stranded DNA to screen for underlying diseases such as membranoproliferative glomerulonephritis or systemic lupus erythematosus (SLE).

•Viral infection – Serologic screening for markers of occult viral infection that affects the kidneys include tests for hepatitis B (hepatitis B surface antigen and core antibody), hepatitis C (antibody), and human immunodeficiency virus (HIV) (antibody) infection. However, a positive serology does not prove that the renal disease is a result of the viral infection. (See "Overview of the pathogenesis and causes of glomerulonephritis in children", section on 'Secondary glomerulonephritis' and "Kidney disease associated with hepatitis B virus infection" and "Overview of kidney disease associated with hepatitis C virus infection" and "Overview of kidney disease in patients with HIV".)

•AKI or advanced CKD – Kidney failure results in fluid retention, which may impact on management decisions. The evaluation of AKI and CKD are discussed separately. (See 'General supportive care' below and "Acute kidney injury in children: Clinical features, etiology, evaluation, and diagnosis" and "Chronic kidney disease in children: Clinical manifestations and evaluation".)

•Suspected congenital or acquired structural abnormality – Imaging is used to determine if there is an underlying congenital or acquired structural abnormality of the kidney. The most commonly used modality is kidney ultrasonography, which can determine the presence of one or two kidneys, assess kidney size, and detect cystic kidney disease and hydronephrosis. Examples in which imaging may be useful include:

-An edematous newborn male with a poor urinary stream, in whom an ultrasound may reveal bilateral hydronephrosis with or without a thickened bladder wall. These findings are consistent with obstructive uropathy from posterior urethral valves (PUV). (See "Clinical presentation and diagnosis of posterior urethral valves".)

-A teenager with renal failure in whom an ultrasound may demonstrate small shrunken kidneys. This may have resulted from congenital kidney hypoplasia or scarring from reflux nephropathy.

●Chronic liver disease or protein-losing enteropathy – A diagnosis of chronic liver disease or a protein-losing enteropathy is suspected in the child with hypoalbuminemia, but no proteinuria. In this setting, liver function tests, total serum protein levels, and prothrombin times should be obtained to assess liver function [3]. In addition, stool level of alpha-1 antitrypsin is the best screening test for protein-losing enteropathy. (See "Protein-losing gastroenteropathy" and "Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis".)

●Heart failure – Heart failure may be suspected based on the pattern of general edema with cardiac findings suggestive of heart failure (tachycardia, tachypnea, gallop, rales, or hepatomegaly). In this setting, chest radiography, electrocardiogram, echocardiography, and laboratory tests, including brain natriuretic peptide [BNP] or N-terminal pro-BNP [NT-proBNP are helpful to confirm the diagnosis, ascertain severity of heart failure, and determine the underlying cause. (See "Heart failure in children: Etiology, clinical manifestations, and diagnosis", section on 'Diagnostic evaluation'.)

●Venous thrombosis – Venous thrombosis may be suspected based on the pattern of edema (eg, localized swelling with associated discoloration of the extremity). The diagnosis is established with duplex ultrasonography. The clinical manifestations and diagnosis of venous thrombosis are discussed separately. (See "Venous thrombosis and thromboembolism (VTE) in children: Risk factors, clinical manifestations, and diagnosis".)

●Hemolytic disease of the newborn – Severe hemolysis in the newborn period can result in a hydropic infant with generalized edema. One notable cause for hydrops is hemolytic disease of the newborn, which may be because of ABO blood type incompatibility or Rh disease. To diagnose this disorder, a CBC and serology testing should be obtained. (See "Management of non-RhD red blood cell alloantibodies during pregnancy".)

●Angioedema – With suspected angioedema, plasma levels of the complement components, C1q, C4, C2, and C1 inhibitor may help diagnose inherited or acquired C1 inhibitor deficiency. With the inherited forms, C4 and C2 levels are chronically low in the majority of patients. (See "Hereditary angioedema (due to C1 inhibitor deficiency): Pathogenesis and diagnosis".)

MANAGEMENT

Treatment of underlying disease — The most effective therapeutic intervention is to treat the underlying cause. As an example, corticosteroid therapy for a patient with steroid-sensitive nephrotic syndrome (SSNS) will resolve his/her edema by inducing a remission and correcting the underlying pathogenesis.

For the following causes of edema in children, further discussion concerning the treatment of the edema and, if appropriate, the underlying conditions are discussed in detail elsewhere:

●Nephrotic syndrome (see "Treatment of idiopathic nephrotic syndrome in children")

●Acute and chronic kidney failure (see "Prevention and management of acute kidney injury (acute renal failure) in children", section on 'Hypervolemia' and "Chronic kidney disease in children: Complications", section on 'Sodium and water homeostasis')

●Cirrhosis (see "Acute liver failure in children: Management, complications, and outcomes", section on 'Ascites' and "Ascites in adults with cirrhosis: Initial therapy")

●Venous thromboembolism (see "Venous thrombosis and thromboembolism (VTE) in children: Treatment, prevention, and outcome")

●Heart failure (see "Heart failure in children: Management")

●Protein-losing enteropathy (see "Protein-losing gastroenteropathy", section on 'Management')

●Anaphylaxis (see "Anaphylaxis: Emergency treatment")

●Hereditary angioedema (see "Hereditary angioedema: Acute treatment of angioedema attacks")

●Lymphedema (see "Clinical staging and conservative management of peripheral lymphedema")

General supportive care — General supportive measures may be considered prior to and/or during the implementation of specific therapy based upon the underlying cause. In some cases when specific therapy is not available, general measures may be the only treatment offered and include:

●Sodium restriction

●Diuretic therapy

●Intravenous albumin

Sodium and fluid restriction — Sodium restriction is usually appropriate in the setting of generalized edema, which includes patients with kidney failure, acute glomerulonephritis, heart failure, hepatic ascites, and nephrotic syndrome. A sodium-restricted diet is tailored to provide the child with approximately 2 to 3 mEq of sodium/kg per day, the amount of sodium required for a growing child. A 10 kg child should therefore receive between 20 to 30 mEq of sodium per day or 460 to 690 mg of sodium per day. This strategy is continued up to a maximum sodium intake of 2000 mg/day in larger children.

Fluid restriction can be considered in patients with generalized edema, but must be done cautiously in patients with reduced effective circulating blood volume of noncardiac origin. This includes children with nephrotic syndrome and hepatic cirrhosis. Fluid limitations are based on specific patient characteristics and underlying cause. Patients with edema associated with the nephrotic syndrome who are being managed in the outpatient setting should be treated with sodium restriction, but not fluid restriction. Fluid restriction may result in a compromised intravascular volume, which could exacerbate the thrombotic tendency of this disorder [4].

Diuretics — Children with edema and an associated expanded intravascular volume may be candidates for diuretic therapy, such as in heart failure and kidney failure. However, when diuretics are utilized in patients with either appropriate or depleted intravascular volume, there is a risk of both precipitating acute kidney injury and decreasing perfusion to peripheral tissues. As a result, creatinine and BUN levels should be monitored. In general, a significant decrease in tissue perfusion secondary to excessive diuresis and inadequate mobilization of peripheral edema can be detected simply by an otherwise unexplained rise in the BUN. A stable BUN and creatinine implies that perfusion to the kidneys (and therefore to other organs) is being well maintained and that the diuresis can be continued if the patient is still edematous.

As a result, the use of diuretics varies based on the clinical setting and should be avoided or used cautiously in children with intravascular depletion.

●Heart failure – Children with heart failure with increased hydrostatic pressure and hypervolemia due to water and sodium retention may benefit from fluid removal. This can be achieved with the use of loop diuretics (eg, furosemide). (See "Heart failure in children: Management", section on 'Diuretics'.)

●Kidney disease – Diuretics also are useful in the treatment of edema resulting from kidney dysfunction with acute glomerulonephritis and acute or chronic kidney failure due to hypervolemia.

In the child with nephrotic syndrome, diuretic therapy should be used sparingly and with great caution, as these children typically are hypoalbuminemic and intravascularly volume depleted. Thus, aggressive diuresis may lead to further intravascular volume depletion, thereby possibly precipitating acute kidney injury (AKI) and increasing the risk of thrombosis in this already susceptible group of patients [5,6]. In children with nephrotic syndrome, diuretics should be administered with intravenous albumin as albumin raises the intravascular oncotic pressure and thereby protects the intravascular compartment against volume contraction. (See "Acute kidney injury (AKI) in minimal change disease and other forms of nephrotic syndrome" and "Symptomatic management of nephrotic syndrome in children", section on 'Diuretics' and 'Intravenous albumin infusion' below.)

●Liver disease – Diuretics need to be used cautiously in children with ascites due to cirrhosis as these children have a reduced effective circulatory volume. Aggressive diuresis of these patients may precipitate hepatorenal syndrome and overt kidney failure [7,8]. The clinician must therefore closely monitor the blood urea nitrogen (BUN) and serum creatinine concentration, as any unexplained deterioration of kidney function would imply an untoward effect on kidney blood flow.

In children with liver dysfunction, loop diuretics can induce a hypokalemic metabolic alkalosis, which can lead to increased ammonia production by the kidney tubules and result in a hepatic coma in patients with early hepatic encephalopathy [9]. Thus, in the child with cirrhotic ascites, it is probably most prudent to use sodium restriction and possibly add spironolactone to avoid the risks of hypokalemia. Spironolactone also is occasionally combined with loop diuretics in this setting [7]. If active diuresis is needed, loop diuretics can be administered with intravenous albumin. (See "Acute liver failure in children: Management, complications, and outcomes", section on 'Ascites' and 'Sodium and fluid restriction' above and 'Intravenous albumin infusion' below.)

●Lymphedema – Diuretics are usually of little benefit in chronic lymphedema resulting from obstruction and may promote the development of volume depletion. With lymphatic obstruction, the mobilization of interstitial fluid to replace the diuretic-induced fluid loss from the intravascular space is blocked.

In addition, the use of systemic therapy such as diuretics for a regional problem (lymphedema) may result in untoward effects in unaffected regions of the body, such as effects in the central venous circulation that result in undesirable hemodynamic effects. Therefore, diuretics should not be used in this clinical setting.

Intravenous albumin infusion — Some children with edema secondary to low oncotic pressure may benefit from intravenous albumin infusions in conjunction with loop diuretics. This may include subgroups of the following patients:

●Children with nephrotic syndrome [6] (see "Treatment of idiopathic nephrotic syndrome in children" and "Pathophysiology and treatment of edema in adults with the nephrotic syndrome").

●Children with protein-losing enteropathy or protein malnutrition.

●Children with cirrhosis and severe ascites [10,11].

This therapy is reserved for patients with severe ascites or pleural effusions leading to respiratory embarrassment or infection, a contracted intravascular volume with AKI, or severe edema resulting in impending or actual skin breakdown. This therapy should not be considered for milder cases because of the expense of the therapy and possible complications including hypertension and pulmonary edema [6].

Patients who meet the above criteria can be given salt-poor 25 percent albumin at a dose of 0.5 g/kg infused over four hours in conjunction with intravenous furosemide at a dose of 1 mg/kg (maximum dose of 40 mg). Albumin dose of up to 1 g/kg per dose also has been used [12]. Respiratory status should be monitored in these patients in the event of transient intravascular volume expansion, which could lead to respiratory compromise from pulmonary edema.

SUMMARY AND RECOMMENDATIONS

●Goals of evaluation – The initial goal of the evaluation of a child with edema is to identify and treat potential serious and life-threatening causes of edema. Once life-threatening causes have been excluded, a more detailed evaluation is performed to determine the underlying cause (table 1).

●Initial evaluation – Initial evaluation includes a thorough history, physical examination, and laboratory testing (see 'Evaluation' above):

•History – The history should include the following details (see 'History' above):

-Edema location

-Age of edema onset

-Duration of symptoms

-Associated complaints

-Additional concurrent illnesses or signs

-Medical and family history

-History of allergies and current medications

Clues from constellations of symptoms and signs may help suggest the underlying etiology. (See 'Clues from constellations of symptoms and signs' above.)

•Physical examination – The physical examination should include (see 'Physical examination' above):

-Measurement of the child's growth parameters

-Full evaluation of the cardiovascular system

-Characterization of the edema as localized or generalized (see 'Edema' above)

If generalized edema is present, the child should be examined and possibly tested for the presence of a pleural effusion, pulmonary edema, ascites, scrotal/labial edema, or evidence of skin breakdown in regions of edema.

If localized edema is present, the clinician should focus the evaluation on identifying venous or lymphatic obstruction in the affected area.

•Laboratory testing – Initial laboratory tests to perform in the child with generalized edema without an apparent cause includes (see 'Initial laboratory evaluation' above):

-Complete blood count (CBC)

-Serum chemistry tests (serum creatinine, blood urea nitrogen [BUN], albumin, and liver function studies)

-Urinalysis

The results of these initial tests, the clinical history and physical examination should provide information on the underlying general cause and help to select subsequent tests.

●Subsequent evaluation – Subsequent testing, including laboratory studies and imaging, is based on the suspected etiology/category (eg, kidney, heart, and liver disease) informed by results from the initial evaluation. (See 'Subsequent testing' above.)

●Management – The most effective therapeutic intervention is to treat the underlying cause. (See 'Treatment of underlying disease' above.)

General supportive measures can be used as adjunctive therapy or when specific intervention is not available (see 'General supportive care' above):

•General measures – General measures include sodium and fluid restriction. We suggest that a daily dietary sodium intake be restricted to 2 to 3 mEq of sodium per kg weight of the patient (maximum intake 90 mEq [2000 mg] per day) (Grade 2C). (See 'Sodium and fluid restriction' above.)

•Diuretics – The use of diuretics varies based on the clinical setting. They should be avoided or used cautiously in children with reduced intravascular volume. (See 'Diuretics' above.)

However, diuretic therapy is commonly used to treat edema in the setting of expanded intravascular volume (eg, heart failure, nephrotic syndrome, acute or chronic kidney failure). Loop diuretics (eg, furosemide) are the most commonly used agents. Care should be taken to avoid over diuresis, which can further impair kidney function. If there is concern regarding the volume status and the child’s ability to tolerate diuresis, it can be given concomitantly with a 25 percent albumin infusion. (See 'Diuretics' above and 'Intravenous albumin infusion' above.)

Guidance regarding diuretic therapy in these conditions is discussed in greater detail separately:

-Heart failure (see "Heart failure in children: Management", section on 'Diuretics')

-Nephrotic syndrome (see "Symptomatic management of nephrotic syndrome in children", section on 'Diuretics')

-Acute kidney failure (see "Prevention and management of acute kidney injury (acute renal failure) in children", section on 'Furosemide')

-Ascites due to liver failure (see "Acute liver failure in children: Management, complications, and outcomes", section on 'Ascites')