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Edema

Generalized edema—excessive accumulationof fluid in interstitial space—is usually obvious first inankles, lower legs, and eyelids.

Principal Causes of Edema

1. Disorderswith normal serum albumin
   1. Increased capillary permeability
      1. Skin disorders
      2. Allergic reaction
      3. Vasculitis
      4. Septicemia
      5. Vitamin E deficiency
      6. Hereditary angioedema
   2. Increased hydrostatic pressure
      1. Increasedblood volume
         1. Fluidoverload
         2. Cardiac failure
         3. Renal disease
      2. Increased venous pressure
         1. Constructivepericarditis
         2. Portal hypertension
         3. Venous thrombosis
         4. Tumor
      3. Increased lymph pressure
         1. Lymphedema
2. Disorders with decreased serum albumin(decreased oncotic pressure)
   1. Disorders with proteinuria
      1. Renaldisease
         1. Glomerulonephritis
         2. Nephrotic syndrome
   2. Disorders without proteinuria
      1. Acuteand chronic liver disease
         1. Hepatitis
         2. Cirrhosis
      2. Gastrointestinal disease
         1. Protein-losingenteropathy
            1. Cowmilk protein sensitivity
            2. Cystic fibrosis
            3. Celiac disease
            4. Inflammatory bowel disease
            5. Intestinal lymphangiectasia
      3. Protein-calorie malnutrition
      4. Congenital albumin deficiency
3. Hydrops fetalis: immune and nonimmune

Clinical Features and Diagnosis

Disorders with Normal Serum Albumin

Increased Capillary Permeability

Skin Disorders

Cellulitis,exfoliative dermatitis, and burns can cause increase in capillarypermeability and edema.

History and physical exam are diagnostic.

Allergic Reaction

Releaseof histamine and other vasoactive mediators can produce localizedor generalized edema.

Drugs, chemical exposure by inhalation,foods (especially milk, eggs, chocolate, nuts), and bee stings arecommon causes of allergic reactions.

Lips, eyelids, and face are frequentlyinvolved, and urticaria also may occur.

Wheezing, laryngospasm, and hypotensionmay be seen with anaphylactic reactions.

History and physical exam are usuallydiagnostic.

Vasculitis

Common causes of vasculitis causing edemainclude Kawasaki disease and collagen vascular disease.

Septicemia

Severe bacterial or rickettsial infectionscan cause increase in capillary permeability and edema.

Vitamin E Deficiency

Uncommonsince addition of vitamin E to infant formulas.

Preterm infants 4–6 wks ofage without normal intake of vitamin E may develop generalized edema,hemolytic anemia, and thrombocytosis.

Serum concentration of vitamin E islow.

Hereditary Angioedema

Deficiencyor functional defect of C1 inhibitor is responsible for this disorder,which is transmitted as autosomal-dominant trait. Gene locus hasbeen mapped to chromosome 11q11-q13.1.

In most common form (type I), serumlevels are 5–30% of normal and functional activityis diminished, whereas in type II, serum levels are normal or increased,but functional activity is decreased.

The 2 types are clinically indistinguishable.Episodic edema may involve face, trunk, and extremities. Most worrisomefeature is edema of larynx and upper airway. Episodes last severaldays, and interval between attacks can be days, months, or years.

Low serum C4 concentration is mostuseful screening test for this disease. Serum C3 concentration isnormal.

Diagnosis is confirmed by measurementof C1 inhibitor and assay of its activity.

Increased Hydrostatic Pressure

Increased Blood Volume

Administrationof excessive amounts of sodium or fluid can produce volume overloadand edema.

In cardiac failure, diminished renalblood flow leads to decrease in glomerular filtration rate (GFR)and edema.

Renal disease (e.g., glomerulonephritis)or any cause of renal failure also may lead to decrease in GFR andedema.

Increased Venous Pressure

Increasedvenous pressure from deep venous thrombosis, constrictive pericarditis, portalhypertension, or impaired venous drainage from tumor may produceedema.

Deep venous thrombosis in thigh orcalf produces pain and swelling of leg distal to thrombus. U/Sis usually diagnostic.

See Chap.30, Hepatomegaly, and Chap. 62, Splenomegaly,for discussion of constrictive pericarditis and portal hypertension.

Increased Lymph Pressure

Lymphedemais excessive accumulation of lymph in interstitial space and isprincipal cause of increased lymph pressure.

Can be congenital or acquired, sporadicor familial, and may appear at birth or in childhood or adolescence.

Abnormal development or dysfunctionof lymphatic vessels, lymph node obstruction, and venous stasisare common mechanisms producing lymphedema.

Common presentation is unilateral,painless edema of leg; however, pain may occur with massive edemaor cellulitis.

U/S and MRI are useful indetection of lymphatic malformations and obstructive lesions.

Disorders with Decreased Serum Albumin (Decreased OncoticPressure)

Disorders with Proteinuria

Any renaldisorder causing severe proteinuria may produce edema. Nephroticsyndrome and acute glomerulonephritis are common examples.

UA confirms presence of proteinuria.

See Chap.50, Proteinuria.

Disorders without Proteinuria

Acute and Chronic Liver Disease

Decreasein synthesis of albumin in liver produces hypoalbuminemia.

Serum albumin of <2.5 g/dLcauses decrease in plasma oncotic pressure and edema.

See Chap.30, Hepatomegaly, and Chap. 36, Jaundice, fordiscussion of causes of acute and chronic liver disease.

Gastrointestinal Disease

Loss ofserum albumin in GI tract leads to decreased plasma oncotic pressureand edema.

Causes of protein-losing enteropathyinclude cow milk protein sensitivity, cystic fibrosis, celiac disease,inflammatory bowel disease, and intestinal lymphangiectasia.

Screening test for protein loss instool is measurement of alpha₁-antitrypsinin spot stool sample.

See Chap.14, Diarrhea.

Protein-Calorie Malnutrition

Severe protein-caloriemalnutrition can produce edema because of decrease in serum albumin.

Growth failure, decreased muscle mass,diarrhea, hepatomegaly, anemia, pigment changes of hair and skin,fatigue, and apathy are other findings.

Edema resolves with adequate calorieand protein intake.

Congenital Albumin Deficiency

Severe edemaoccurs with congenital albumin deficiency, which is rare.

Very low or undetectable serum albuminconcentration in absence of other causes of hypoalbuminemia confirmsdiagnosis.

Hydrops Fetalis: Immune and Nonimmune

Hydrops fetalis is term used to describesevere generalized edema in fetus or newborn.Because of use of anti-D immune globulinfor Rh isoimmunization, most cases of hydrops are nonimmune type(Table 17.1 ).

Table 17.1. Principal Causes of Hydrops Fetalis

Immune

Rh isoimmunization

Nonimmune

Cardiovascular

Structural heart disease

Arrhythmias (supraventricular tachycardia)

Myocarditis

Cardiac tumors

Chromosomal

Turner syndrome

Trisomies 13, 18, and 21

Hematologic

Twin-to-twin transfusion

Chronic fetomaternal transfusion

Homozygous alpha-thalassemia

Intrauterine infection

Cytomegalovirus

Parvovirus B19

Herpes simplex virus

Rubella virus

Toxoplasmosis

Syphilis

Bacterial septicemia

Pulmonary

Diaphragmatic hernia with pulmonary hypoplasia

Cystic adenomatoid malformation of lung

Pulmonary lymphangiectasia

GI

Bowel atresia

Midgut volvulus

Urinary tract

Congenital nephrosis

Fetal urinary tract obstruction

Skeletal

Chondrodysplasias

Metabolic

Mucopolysaccharidoses

Gangliosidoses

Gaucher disease

Sialidosis

Neoplasm (fetal)

Neuroblastoma

Wilms tumor

Placental abnormalities

Umbilical vein thrombosis

Torsion of umbilical cord

Chorioangioma

Miscellaneous

Absent or decreased fetal movement syndromes

Noonan syndrome

Meckel syndrome

Amniotic band syndrome

Idiopathic

Diagnostic Approach

Age of onset is important in determiningcause of edema. Other distinguishing features are presence of hypoalbuminemia ± proteinuria.

Fetal and Neonatal Onset

Hydropsfetalis should be suspected in either second or third trimesterof pregnancy, when discrepancy exists between size of fetus andpresumed gestational age.

Polyhydramnios occurs in ≥50% ofcases, and this can be confirmed by U/S.

First step in diagnosis of fetal hydropsis to perform prenatal antibody screen to exclude any kind of isoimmunization.

Other tests include CBC and RBC indicesin both parents to screen for alpha-thalassemia; hemoglobin electrophoresis;Kleihauer-Betke test for fetomaternal transfusion; and maternalrapid plasma reagin, appropriate serology, and cultures for congenitalinfection.

U/S can detect multiple pregnancies(twin-twin transfusion), chondrodysplasias (limb length measurements),and many congenital anomalies.

Fetal movement studies also can bedone using real-time U/S.

Fetal echocardiography may detect cardiacstructural defects and fetal arrhythmias.

If these tests fail to reveal causeof fetal hydrops, amniocentesis can be performed. Several testsare commonly performed on amniotic fluid: fetal karyotype, culturesand polymerase chain reaction for infection, specific metabolictests for storage diseases, and alpha-fetoprotein (congenital nephrosis).

Fetal blood can be obtained by cordocentesisfor other tests: CBC, blood type, hemoglobin electrophoresis, serumalbumin, cultures and polymerase chain reaction, karyotype, andspecific tests for metabolic disorders.

After infant's birth, physicalexam as well as exam of umbilical cord and placenta narrow diagnosticpossibilities and suggest most appropriate investigations.

Several testsshould be considered depending on clinical circumstances: infant's bloodgroup and Rh type; CBC; hemoglobin electrophoresis; UA; chest, longbone, abdominal, and spine radiography; ECG; 2-D echocardiography;maternal and infant rapid plasma reagin; urine culture for cytomegalovirus;serology for toxoplasmosis; serum electrolytes, creatinine, glucose,and liver function tests; blood urea nitrogen; analysis of fluidfrom effusion or ascites for chyle, protein, or culture; chromosomalkaryotype; metabolic studies; and exam of placenta including histology.

Other investigations depend on resultsof these tests and suspected diagnosis.

Postneonatal Onset

UA screensfor proteinuria and renal disease.

In absence of significant proteinuriaor cardiac failure, serum albumin should be measured. Fluid overloadand allergic reactions are common causes of edema with normal serumalbumin. Decreased serum albumin without proteinuria suggests liverdisease, protein-losing enteropathy, or protein-caloric malnutrition.

Jaundice, hepatomegaly, and abnormalliver function tests are manifestations of liver disease.

Elevated fecal alpha₁-antitrypsinlevel indicates increased protein loss in stool and is seen withvarious causes of protein-losing enteropathy.

Protein-calorie malnutrition can beassessed by plotting weight and height on growth charts developedby CDC (2001).

U/S or MRI may help diagnosecauses of lymphedema.

References

1. CDC Growth Charts: United States. U.S.Department of Health and Human Services. Centers for Disease Controland Prevention. National Center for Health Statistics. Divisionof Data Services. Hyattsville, MD, 2001. World Wide Web URL: http://www.cdc.gov/growthcharts.
2. Ciarallo L. Edema. In: Fleisher GR, Ludwig S, eds.Textbook of pediatric emergency medicine, 4th ed. Philadelphia:Lippincott Williams & Wilkins, 2000:223–225.
3. Driscoll SG. Hydrops fetalis. N Engl J Med 1966;275:1432–1434.
4. Fisher DA. Obscure and unusual edema. Pediatrics 1966;37:506–528.
5. Hilliard RI, et al. Congenital abnormalities of thelymphatic system: a new clinical classification. Pediatrics 1990;86:988–994.
6. Holzgreve W, et al. Nonimmune hydrops fetalis: diagnosisand management. Semin Perinat 1985;9:52–67.
7. Kirks DR, ed. Practical pediatric imaging: diagnosticradiology of infants and children, 3rd ed. Philadelphia: Lippincott-Raven,1998.
8. McGillivray BC, Hall JG. Nonimmune hydrops fetalis.Pediatr Rev 1987;9:197–202.
9. Norman ME. Edema. In: Schwartz MW, ed. Pediatric primarycare: a problem-oriented approach, 2nd ed. Chicago: Year Book Medical,1990:213–216.
10. Online Mendelian Inheritance in Man (OMIM). McKusick-NathansInstitute for Genetic Medicine, Johns Hopkins University (Baltimore,MD) and National Center for Biotechnology Information, NationalLibrary of Medicine (Bethesda, MD), 2000. World Wide Web URL: http://www.ncbi.nlm.nih.gov/omim.
11. Poeshmann RP, et al. Differential diagnosis and causesof nonimmunological hydrops fetalis: a review. Obstet Gynecol Surv1991;46:223–231.
12. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.
13. Scriver CR, et al., eds. The metabolic and molecularbases of inherited disease, 8th ed. New York: McGraw-Hill, 2001.
14. Wolf RB, Moore TR. Amniotic fluid and nonimmune hydropsfetalis. In: Fanaroff AA, Martin RJ, eds. Neonatal-perinatal medicine:diseases of the fetus and infant, 7th ed. St. Louis: Mosby, 2002, 351–370.

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Book Source Details

• Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
• Author(s): Paul S. Bellet
• Year of Publication: 2006
• Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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More About This Book: Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics Authors: Paul S. Bellet Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 0-78172-899-1

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