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Oedematous children OSCE

Oedema = an increase in interstitial fluid volume and tissue swelling that can either be localized
(ascites/ pleural effusions) or generalized (severe = anasarca).

Causes

Increase hydrostatic acute nephritic syndrome, acute tubular necrosis, cardiac failure,
pressure cirrhosis (portal hypertension/ portal vein thrombosis)
Decrease plasma nephrotic syndrome, chronic liver failure, protein losing
oncotic pressure enteropathy, caloric malnutrition (kwashiorkor – bilateral pedal),
severe burns
Increased capillary insect bite, trauma, allergy, sepsis, angio-oedema
leakage
Impaired lymphatic lymphatic obstruction (tumour), congenital lymphoedema
flow
Impaired venous flow hepatic venous outflow obstruction, superior/inferior vena cava
obstruction

Clinical features

Nephrotic syndrome Nephritic syndrome


Periorbital oedema (worst on waking)

 lower limbs/ scrotum


 pleural effusion + ascites (cough shortness
of breath, tummy distension)
 generalised oedema

Foamy/ frothy urine Reddish-brown

Normal CVS/ BP (otherwise well) High BP  cardiomegaly + pulmonary


oedema
History of asthma, hayfever Most common causes UTI, Henoch, psgn

Frequent infections (peritonitis)

History for both:


1. joints pain? Skin rashes? Pallor? – HSP or SLE
2. infection recently – streptococcal sore throat – URTI (cold) or impetigo (3 days ago or 3
weeks ago)
3. difficulty passing urine, less frequent visit (PSGN)
4. diet? Malnourished? Kwashiorkor (persistent diarrhoea)
4. family history of renal problems

Nephritic
1. abdominal pain, diarrhoea, vomiting – HUS/ HSP
2. recent history of trauma
3. nose bleeds or abnormal bruising - HSP
4. beetroot

Typical Atypical (not steroid responsive)


1-10 Age <1 or >12
No Macroscopic haematuria
Normal Persistent hypertension + high creatinine
Normal Low C3
Family history

 If no atypical features then meaning it is minimal change  give steroids for 4 weeks
everyday, then alternate day for another 4 weeks, then tapered down in 4 months)
 If no response in 4 weeks OR any atypical features then meaning it is steroid resistant 
renal biopsy  diuretic, salt restriction, ACE inhibitors, NSAIDs,

Haematuria

 Most common = UTI


 Glomerular = brown urine accompanied by proteinuria
 Lower UT = red, not accompanied by proteinuria
 Calculi

Nephrotic vs Nephritic

Minimal change IgA


FSGS PSGN
MN Henoch
MPGN Anti-GBM
RPGN

Oedematous child, Nephrotic syndrome, Glomerulonephritis


Differentials:

Angioedema

Examination
General inspection – jaundice
Oedema exam
Normal pulse, blood pressure, capillary refill
Abdomen – Wilms tumour = haematuria/ liver enlargement

Investigation
1. Urine dipstick (protein 3+ or more, bloods 1+ in 20%, if got blood send to confirm via
microscopy) (24-hour urinary collection >3.5)
2. Urine – microscopy and culture, spot urine protein/creatinine ratio (will be >200
mg/mmol or ?3.5) in nephrotic syndrome, lipid cast or RBC cast
3. Blood pressure
4. U&Es – renal failure
5. LFTs (hypoalbuminaemia) + serum albumin (low albumin <30g/L) 37-50
6. Lipids profile (cholesterol/ triglyceride levels)
7. FBC (leukocytosis)

Observations and general measures


Nephrotic chart…. Weight chart, BP chart, Albumin Chart, Intake –output chart
Monitor of temperature, heart rate, BP, CRT, RR and O2 saturation, fluid balance and
urine output, daily weight.
Penicillin V 125mg BD( 1-5 years), 250mg BD (6-12 years ) [ recommended at diagnose
and during relapse, esp in presence of gross edema]
Fluid restriction – not recommended except in chronic edematous state.
Salt restricted diet is recommended ( No added salt)

Imaging

1. renal ultrasound (exclude calculi)

Special test
1. Throat swab + anti-streptolysin O titre (ASOT) and C3/C4 levels to investigate the
possibility of post-streptococcal disease + blood culture if febrile
2. antinuclear antibody (ANA) & ESR in SLE
3. hepatitis B antibodies if from an at-risk population, as this is a rare cause of nephrotic
syndrome
4. measles and Varicella zoster antibodies (these are important to know as children who
are on immunosuppressive therapy such as steroids are more vulnerable to these
conditions)

Complications
1. Thromboembolism – decrease in anti-thrombin III, protein C&S
2. infection – Urine losses of immunoglobulins & steroid treatment  peritonitis (strep
pneunomiae)
3. Hyperlipidaemia – cholesterol, LDL, triglycerides but decrease in HDL.
4. hypovolaemia – abdominal pain & vomiting – haematocrit >0.45

Nephritic
1. HF, ARF, Hypertensive encephalopathy,
2.

Systematic review
1. CVS
2. respi
3. abdo
4. neuro – fever, seizures, confusion, headache

Treatment
1. 60mg/m2 single morning dose for 4 weeks, followed by 40mg/m2 every alternate day
for 4 weeks, tapering reducing 25% over 4 weeks or stop.
2. Penicillin prophylaxis if increase risk of infection
3. Nephrotic chart – four hourly observations of blood pressure, weight once daily, input-
output chart and albumin chart
4. low salt diet.

Home urine albumin monitoring: the first morning urine specimen daily. High possibility of
relapse. The child is advised to consult the doctor: oedematous albuminuria ? 2+ for 3
consecutive days, or 3 out of 7 days.
Cautioned about contact live vaccine wait 6 weeks after stopped steroids

PSGN
1. 10 day course of oral penicillin
2. fluid restriction 1L and diet no salt
3. frusemide for hypertension  calcium channel blocker 

Complications can be caused by nephrotic syndrome itself due to the loss of normal proteins
from the blood. These include:
 An increased risk of developing infections. This is because you can lose antibodies in the
urine. (Antibodies are proteins that help to defend the body from infection.) Any signs
of infection (sore throat, high temperature (fever), etc) should be taken seriously and
reported promptly to a doctor.
 An increased risk of developing blood clots in the blood vessels (thrombosis). For
example, a deep vein thrombosis (DVT) in a leg. This can cause pain, swelling and other
complications. The reason for this is because there can be a change in the balance of
proteins in the blood that protect against blood clots forming.
 A high cholesterol level. If this persists long-term it is a risk factor for developing heart
disease.
 Increased risk of vitamin D deficiency which may lead to bone problems. This is due to
loss of vitamin D-binding protein from the bloodstream.
 Anaemia. This is due to loss of proteins that help to carry iron around in the
bloodstream. You need iron to make red blood cells and to prevent anaemia.

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