1. Prepared by : Madan Kumar Timalsena
1st year resident Dept of Pediatrics(KISTMCTH)
Moderator : Dr. Prabha Chhetri
2. Introduction
Edema is derived from the Greek words ‘etymon
oidema’ which mean to swell
Results from an accumulation of fluid in the
interstitial fluid compartment
Severe generalized edema is known as anasarca
Can be a manifestation of various underlying cause
either local or systemic
Can be pitting or non-pitting
3. Pathophysiology
Increased capillary hydrostatic pressure
more important in the production of localised
oedema
results from the release of chemical mediators,
such as histamine, leukotrienes and cytokines
Decreased plasma oncotic pressure
Increased capillary leakage
4. Obstruction of lymph channels
Renal salt and water retention
Deposition of connective tissue components in
subdermal region(myxedema)
5.
6. Causes of generalized edema
Nephrotic syndrome
Increased hydrostatic pressure due to renal sodium
retention
Decreased oncotic pressure due to hypoalbuminemia
Increased capillary permeability mediated by a still
unidentified factor
marked proteinuria, hypoalbuminemia, and
hyperlipidemia
7. Heart failure
Left ventricular (LV): pulmonary, but not peripheral
edema
Pure right ventricular (RV) failure: may result in
prominent edema in the lower extremities
Cardiomyopathies : simultaneous onset of pulmonary
and peripheral edema.
Tachycardia, tachypnea, rales or wheezes, gallop rhythm,
hepatomegaly
8. Acute glomerulonephritis
primarily due to renal sodium and water retention
Hypertension,hematuria and proteinuria, cola-colored
urine, and/or azotemia
Renal failure
acute or chronic renal failure can present with edema
due to renal retention of sodium and water
9. Cirrhosis
Ireversible hepatic parenchymal injury with fibrosis
Children with cirrhosis can develop portal hypertension
Increase in venous pressure below the diseased liver,
resulting in ascites and lower extremity edema
Relatively uncommon in children
can be caused by genetic disorders (alpha-1 antitrypsin
deficiency, cystic fibrosis, Wilson disease), infectious
etiologies (viral hepatitis), and structural problems of
the biliary tree (biliary atresia)
10. PEM
Insufficient albumin synthesis
considered in a child with generalized edema, skin rash
over the scalp and extremities, and hypopigmentation
of the hair
Protein losing enteropathy
severe protein loss through the gut
results in low plasma protein levels
hypertrophic gastritis (Ménétrier disease), milk protein
allergy, celiac disease, inflammatory bowel disease,
giardiasis
11. Lymphatic dysfunction/obstruction: Either a primary
defect of the lymphatics or a secondary (acquired)
defect
Angioedema
Swelling of the deep layers of the cutaneous or
submucosal tissues
Due to increased capillary permeability
Usually affects the face, lips, tongue, or larynx
12. Venous obstruction
Arises from extrinsic venous compression, thrombosis,
or congestion
Edema occurs distal to the site of obstruction
Increased capillary permeability in patients with burns
or sepsis
15. History (important points to
consider)
Edema location
Time course (age at onset and duration of
symptoms)
Associated complaints : shortness of breath
Additional concurrent illnesses or signs
Past medical and family history
Weight gain and tight-fitting clothes and shoes
History of allergies and current medications.
16. Physical examination
Child's growth parameters
Full evaluation of cardiovascular system, including
vital signs
Tachycardia, tachypnea, gallop, rales, or hepatomegaly
are seen in patients with heart failure
Tachypnea and rales alone may be indicative of
pulmonary edema
Increased blood pressure (BP) levels may reflect
hypervolemia from acute/chronic renal failure or
glomerulonephritis
17. Examination for the presence of a
pleural effusion
pulmonary edema
ascites
scrotal/labial edema
evidence of skin breakdown in regions of edema.
18. With regional edema
localization of the area of swelling to help deduce where
a region of venous or lymphatic obstruction is likely to
be present
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 evaluated for concurrent airway involvement
19. Symptoms constellation
Diaphoresis, dyspnea on exertion,
and/or a history of heart disease
heart failure
Acute onset,food allergies,airway
involvement,pruritis
Urticaria and angioedema
Jaundice, failure to thrive, steatorrhea,
or abdominal pain
Liver failure/disease or protein-losing
enteropathy
Progressive anasarca, significant
periorbital component, minimal
systemic complaints
Nephrotic syndrome
Cola-colored urine, generalized or facial
edema, hypertension
Acute glomerulonephritis
Edema, anorexia, and growth
impairment
Chronic kidney disease
Family history of angioedema Hereditary angioedema
Newborn girl,edema of the hands and
feet, webbed neck, nail dysplasia, high
palate, and short fourth metacarpal
Turner syndrome
20. Initial laboratory evaluation
Complete blood count (CBC)
Serum chemistry tests (serum creatinine, blood urea
nitrogen [BUN])
Albumin
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
21. Urinalysis including a dipstick for proteinuria
markedly positive dipstick for protein with
hypoalbuminemia and clinical edema is virtually
diagnostic of the nephrotic syndrome
Hematuria with red cell casts and dysmorphic red cells,
with or without heavy proteinuria, is virtually diagnostic
of glomerulonephritis, such as poststreptococcal
glomerulonephritis
22. Heavy proteinuria, few cells or casts : consistent with a
noninflammatory cause of nephrotic syndrome such as
minimal change disease (MCD) or focal segmental
glomerulosclerosis (FSGS).
Additional testing based on a suspected etiology and
results of the initial evaluation.
23. Kidney disease : suspected based on abnormal kidney
function tests (elevated serum creatinine and BUN) or
abnormal urinalysis
Suspected glomerulonephritis
Complement testing can classify glomerulonephritis as either
hypocomplementemic or normocomplementemic
Serologic testing may identify specific disorders and includes
antistreptococcal antibodies (poststreptococcal
glomerulonephritis)
antinuclear antibodies (ANA), anti-double-stranded DNA
antibodies (lupus nephritis)
24. antiglomerular basement membrane (GBM) antibodies (anti-
GBM [Goodpasture]) disease
antineutrophil cytoplasmic autoantibodies (ANCA
vasculitides)
Renal biopsy may be considered in children with
suspected glomerulonephritis
Significant renal dysfunction
Normocomplementemia
Heavy proteinuria without an underlying diagnosis
To stage the histologic severity to guide approach to
treatment for suspected lupus nephritis
25. Suspected nephrotic syndrome: C3, C4, ANA, and
anti-double stranded DNA
Renal imaging is used to determine if there is an
underlying congenital or acquired structural
abnormality of the kidney. The most commonly used
modality is renal ultrasonography.
26. Chronic liver disease or protein-losing enteropathy:
suspected in the child with hypoalbuminemia, but no
proteinuria
liver function tests
total serum protein levels
prothrombin times
stool level of alpha-1 antitrypsin is the best screening
test for protein-losing enteropathy
27. Congestive cardiac failure : suspected based on the
pattern of general edema with findings(tachycardia,
tachypnea, gallop, rales, or hepatomegaly)
chest radiography
Electrocardiogram
Echocardiography
Brain natriuretic peptide
28. Venous thrombosis : Suspected based on the pattern
of edema localized swelling with associated
discoloration of the extremity
Duplex ultrasonography establishes the diagnosis
29. Supportive care(specific treatment based on cause)
Sodium and fluid restriction:
Sodium restriction is usually appropriate in the setting
of generalized edema, which includes patients with
renal failure, acute glomerulonephritis, heart failure,
hepatic ascites, and nephrotic syndrome
2 to 3 mEq of sodium/kg per da
Fluid restriction can be considered
Must be done cautiously in patients with reduced
effective circulating blood volume
30. Diuretics
Used in case of edema and an associated expanded
intravascular volume (eg. Heart failure and kidney
failure)
Risk of both precipitating acute kidney injury and
decreasing perfusion to peripheral tissues
Creatinine and BUN levels should be monitered
Should be avoided or used cautiously in children with
intravascular depletion
31. Intravenous albumin infusion
Nephrotic syndrome
Protein-losing enteropathy
Protein malnutrition
Cirrhosis and severe ascites
25 percent albumin at a dose of 0.5 g/kg infused over four
hours with intravenous furosemide at a dose of 1 mg/kg
Respiratory status should be monitored
