edema,swelling,child,children

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)

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

13.  Other causes:
 Trauma
 Cellulitis/abscess
 Vasoocclusive crisis
 SIADH
 Pre-menstural syndrome
 Vasculitis

14. Edema
(localized?)
Yes
(Congenital?
)
Yes
Lymphatic
anomaly
No
(fever?)
Yes
Abscess
,cellulitis,
urticaria
No
(Recurrent?,Se
vere?
Family
history?)
Yes
Angiodema
No
(Enviromental
exposure?)
Yes
Sunburn,
frostbite,
insect
bites
No
Trauma
,thrombo
phlebitis
No
(Evidence of cardiac
disease?)
Yes
CHF,Peric
ardial
effusion
No
(Abnormal
urinalysis?)
Yes
Renal
disease
No
Abnormal
(electrolytes,LFT,
Hypoalbuminemia
?)
Yes
Hepatic
disease,GI
cause,SIA
DH
No
Vasculitis,
allergic
reaction,
pre-
enstural
syndrome
Approach to
edema in children:

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

32. Thank you!

33. References
 https://www.uptodate.com/contents/evaluation-and-
management-of-edema-in-children
 https://www.uptodate.com/contents/pathophysiology-
and-etiology-of-edema-in-children
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707228/
 https://www.sciencedirect.com/science/article/abs/pii/S08
89852918304869
 https://epomedicine.com/clinical-medicine/approach-to-
a-child-with-edema/
 C Leung AK, M Robson Alexander K C Leung WL, M
Robson WL, of Paediatricts P, C Leung AK. Article Oedema
in childhood