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Approach to Oedema in
Children
Introduction &
Pathophysiology
What is edema?
● Edema can be defined as the presence of excess fluid in the
interstitial space of the body.
● Edema is divided into two types, localized edema and
generalized edema.
● The formation of edema is associated with renal sodium
retention.
Mechanism of generalised edema
● a reduced intravascular volume leading to sodium and water retention, that
is, an underfilling edema
● sodium and water retention secondary to expanded plasma and intracellular
tissue fluid volume accompanied by a lack of natriuresis, that is, an
"overfilling edema"
● The generalized edema occurs in the presence of parenchymal renal
damage (nephrotic syndrome, acute and chronic glomerulonephritis and renal
failure) or in the absence of structural renal disease (heart failure, liver
cirrhosis).
Underfilling theory
● The mechanism of "underfilling edema" is initiated with an increased glomerular
permeability to albumin, that is, albuminuria.
● The subsequent hypoalbuminemia leads to decreased plasma oncotic pressure
accompanied by movement of water from intravascular space to the interstitium.
● The intravascular contracted volume in turn stimulates the following neuroendocrinological
factors, resulting in sodium and water retention:
(1) an increased renin-angiotensin-aldosterone (RAA) activity;
(2) an increased sympathetic nervous system (SNS) activity;
(3) antidiuretic hormone (ADH) release
● These forces and perhaps as yet unidentified factors give rise to the consequential water
and sodium retention, which promotes the development of edema.
● The sodium and water retention leads to further decreased plasma oncotic pressure,
setting up a vicious cycle perpetuating the edema formation.
● The movement of water from intracellular space to interstitial space by itself also
contributes to the development of edema formation
Overfilling theory
In contrast, the mechanism of "overfilling edema" is expanded extracellular volume
that results from primary renal sodium retention, possibly secondary to the renal
damage, The RAA system, SNS system and ADH secretion are depressed in the
"overfilling edema”.
Causes of Edema
Generalized
- Increased capillary hydrostatic pressure
- Decreased capillary oncotic pressure
- Increased capillary permeability
Localised
- Increased capillary hydrostatic pressure
- Increased capillary permeability
Generalised edema causes
Increased capillary hydrostatic pressure
-Increased plasma volume from sodium and water retention
-Heart failure
-Renal disease- acute glomerulonephritis/renal failure
Causes- Decreased capillary oncotic pressure
(Hypoalbuminemia)
-Nephrotic syndrome
-Liver failure
-Protein losing enteropathy
-Protein malnutrition (kwashiorkor)
Causes -Increased capillary permeability- due to release of
cytokines/histamine/PG/complement
-Burn
-Sepsis
-Dengue
-Iatrogenic cause – intravenous fluid
Localized edema
Increased hydrostatic pressure
❖ Venous obstruction SVC/IVC obstruction
Thrombosis DVT
External compression- lymphnodes
❖ Cirrhosis
Fibrosis of the liver obstructing venous blood flow in the portal venous
system/lower limbs
Increased capillary permeability
● Angioedema
● Inflammation
-infection
- cellulitis
Clinical Evaluation
History
● Age
● Edema location – localised /generalised
● Duration of symptoms- acute onset/gradual /relapsing
● Associated complaints that suggest systemic disease or major organ dysfunction
➔ Liver/heart/bowel
➔ Kidney- change in color/frequency/frothy urine
● Additional concurrent illnesses . A streptococcal infection one to three weeks earlier may point to
post-streptococcal glomerulonephritis/recent skin infection
● Waxing and waning of the edema
● System review: headache/nocturnal cough
● Past medical and family history. A family history of recurrent angioedema, for example, may suggest
hereditary angioedema as a possible diagnosis./family hx of renal disease
● History of allergies and current medications. Allergies and adverse reaction to certain medications can
present as angioedema in childhood.
Physical examination
❖ General examination
-Anthropometry (height /weight)
-Vital signs, perfusion, bounding pulse, BP, RR,
-JVP
-Assessment of edema- generalised, pitting, extent
involvement of other areas – sacral, labial/scrotal
cervical lymphadenopathy
-Throat examination
-Skin – rash, signs of skin infection
❖ Systemic examination
Cardiovascular- raised JVP, murmur, gallop rhythm
Lungs - dullness on percussion. Bilateral crepitations
Abdomen- distension. Ascites
Genitalia- scrotal edema/skin excoriation
Fundoscopy- papilloedema
Investigation
Investigation
FBC, ESR, CRP
Urine analysis,Urine Dipstick, Renal profile, Cast: Proteinuria, Haematuria
Liver function test- serum albumin: normal in allergic
Serum lipid level: hypercholesterolemia in nephrotic syndrome
ASOT titre, anti DNAse B antibody, Culture
Complement level ( c3/c4)
CXR, U/S, ECG
Management
Supportive Treatment
● Focused on reversing the underlying cause
● General:
Medication: Diuretic (Frusemide) to increased urine output; no response to diuretic> Dialysis
Rest in bed
Dietary Modification: Sodium Restriction
Water Restriction: Avoid IV saline & enteral feedings in cardiac/renal disease; Promote fluid intake if
fever/diaphoresis
● Monitor
Vital signs: BP
Fluid Intake, Urine Output, Proteinuria
Daily Weight
Serum Electrolyte: Sodium & Albumin level

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Approach to Oedema in Children.pdf

  • 1. Approach to Oedema in Children
  • 3. What is edema? ● Edema can be defined as the presence of excess fluid in the interstitial space of the body. ● Edema is divided into two types, localized edema and generalized edema. ● The formation of edema is associated with renal sodium retention.
  • 4. Mechanism of generalised edema ● a reduced intravascular volume leading to sodium and water retention, that is, an underfilling edema ● sodium and water retention secondary to expanded plasma and intracellular tissue fluid volume accompanied by a lack of natriuresis, that is, an "overfilling edema" ● The generalized edema occurs in the presence of parenchymal renal damage (nephrotic syndrome, acute and chronic glomerulonephritis and renal failure) or in the absence of structural renal disease (heart failure, liver cirrhosis).
  • 5. Underfilling theory ● The mechanism of "underfilling edema" is initiated with an increased glomerular permeability to albumin, that is, albuminuria. ● The subsequent hypoalbuminemia leads to decreased plasma oncotic pressure accompanied by movement of water from intravascular space to the interstitium. ● The intravascular contracted volume in turn stimulates the following neuroendocrinological factors, resulting in sodium and water retention: (1) an increased renin-angiotensin-aldosterone (RAA) activity; (2) an increased sympathetic nervous system (SNS) activity; (3) antidiuretic hormone (ADH) release ● These forces and perhaps as yet unidentified factors give rise to the consequential water and sodium retention, which promotes the development of edema. ● The sodium and water retention leads to further decreased plasma oncotic pressure, setting up a vicious cycle perpetuating the edema formation. ● The movement of water from intracellular space to interstitial space by itself also contributes to the development of edema formation
  • 6. Overfilling theory In contrast, the mechanism of "overfilling edema" is expanded extracellular volume that results from primary renal sodium retention, possibly secondary to the renal damage, The RAA system, SNS system and ADH secretion are depressed in the "overfilling edema”.
  • 8. Generalized - Increased capillary hydrostatic pressure - Decreased capillary oncotic pressure - Increased capillary permeability
  • 9. Localised - Increased capillary hydrostatic pressure - Increased capillary permeability
  • 10. Generalised edema causes Increased capillary hydrostatic pressure -Increased plasma volume from sodium and water retention -Heart failure -Renal disease- acute glomerulonephritis/renal failure
  • 11. Causes- Decreased capillary oncotic pressure (Hypoalbuminemia) -Nephrotic syndrome -Liver failure -Protein losing enteropathy -Protein malnutrition (kwashiorkor)
  • 12. Causes -Increased capillary permeability- due to release of cytokines/histamine/PG/complement -Burn -Sepsis -Dengue -Iatrogenic cause – intravenous fluid
  • 13. Localized edema Increased hydrostatic pressure ❖ Venous obstruction SVC/IVC obstruction Thrombosis DVT External compression- lymphnodes ❖ Cirrhosis Fibrosis of the liver obstructing venous blood flow in the portal venous system/lower limbs
  • 14. Increased capillary permeability ● Angioedema ● Inflammation -infection - cellulitis
  • 16. History ● Age ● Edema location – localised /generalised ● Duration of symptoms- acute onset/gradual /relapsing ● Associated complaints that suggest systemic disease or major organ dysfunction ➔ Liver/heart/bowel ➔ Kidney- change in color/frequency/frothy urine ● Additional concurrent illnesses . A streptococcal infection one to three weeks earlier may point to post-streptococcal glomerulonephritis/recent skin infection ● Waxing and waning of the edema ● System review: headache/nocturnal cough ● Past medical and family history. A family history of recurrent angioedema, for example, may suggest hereditary angioedema as a possible diagnosis./family hx of renal disease ● History of allergies and current medications. Allergies and adverse reaction to certain medications can present as angioedema in childhood.
  • 17. Physical examination ❖ General examination -Anthropometry (height /weight) -Vital signs, perfusion, bounding pulse, BP, RR, -JVP -Assessment of edema- generalised, pitting, extent involvement of other areas – sacral, labial/scrotal cervical lymphadenopathy -Throat examination -Skin – rash, signs of skin infection
  • 18. ❖ Systemic examination Cardiovascular- raised JVP, murmur, gallop rhythm Lungs - dullness on percussion. Bilateral crepitations Abdomen- distension. Ascites Genitalia- scrotal edema/skin excoriation Fundoscopy- papilloedema
  • 20. Investigation FBC, ESR, CRP Urine analysis,Urine Dipstick, Renal profile, Cast: Proteinuria, Haematuria Liver function test- serum albumin: normal in allergic Serum lipid level: hypercholesterolemia in nephrotic syndrome ASOT titre, anti DNAse B antibody, Culture Complement level ( c3/c4) CXR, U/S, ECG
  • 22. Supportive Treatment ● Focused on reversing the underlying cause ● General: Medication: Diuretic (Frusemide) to increased urine output; no response to diuretic> Dialysis Rest in bed Dietary Modification: Sodium Restriction Water Restriction: Avoid IV saline & enteral feedings in cardiac/renal disease; Promote fluid intake if fever/diaphoresis ● Monitor Vital signs: BP Fluid Intake, Urine Output, Proteinuria Daily Weight Serum Electrolyte: Sodium & Albumin level