Dr. YK Amdekar lays out eight different scenarios under which oedema can present as a major symptom in children, and details the diagnostic and management approach for each of the underlying primary diseases.

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Oedema results from various factors such as increased hydrostatic pressure, reduced osmotic pressure, increased permeability of capillaries and lymphatic or venous obstruction. Fluid collects in interstitial spaces and serous cavities. Understanding pathogenesis helps in defining probable cause of oedema and allows for relevant timely intervention.

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Case-based discussions

Case 1

An 8-year-old child presented with acute onset of oedema of eyelids noticed one morning on waking up. The next day, he developed breathlessness. On direct questioning, he had oliguria and cola-coloured urine. Acute onset of periorbital oedema with oliguria and cola-coloured urine suggestive of haematuria is in favour of acute gloemerular nephritis- AGN. Breathlessness in this child may be due to hypertension a result of AGN.

Physical examination showed mild oedema in the feet and around the eyes, HR 140/min, RR 35/min, BP 150/100 mmHg. Systemic examination was normal. It is diagnostic of AGN. Investigations– urinalysis RBCs ++, granular casts +, proteins +, serum creatinine 1. mg%, ASO high titre.

Diagnosis- Acute Glomerular nephritis

In children >5 years of age, it is most likely due to post-streptococcal infection and if so, prognosis is very good. Improvement is quick with symptomatic treatment though microscopic haematuria may continue for a few weeks. To confirm improving situation, serum C3 level that is low at the peak of illness, starts rising. If C3 level continues to be low, it may indicate chronicity of the disease and needs referral to a specialist. If AGN presents in a younger child, it may be due to other infections and prognosis may not be so good.

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Case 2

A 4-year-old child presented with acute onset of oedema around the eyes. There were no other symptoms. On direct questioning, urine output was normal and urine was colourless. However, the child had itching. This suggests angiooedema– allergic process and not renal disease.

Physical examination showed oedema around both lower eyelids looking pink. There was no oedema anywhere else, Blood pressure was normal and so was heart and respiratory rate. Systemic examination was normal.

Diagnosis- Aangiooedema

There is no need for any investigation or any drug therapy. It settles down by itself. Antihistamines and steroids are not necessary unless the child presents with laryngeal oedema causing inspiratory obstruction.

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Case 3

A one-year-old infant presented with loose stools for two days followed by acute onset oedema of face and feet. He was born after full term and normal delivery with birth weight of 2.6 kg. He was on exclusive breastfeeding for the first 6 months and thereafter the mother started diluted cow milk and occasional watery mixture of rice and dal.

Diet history clearly suggests inadequate intake of calories and proteins for the last 6 months and hence oedema is likely to be due to nutritional deficiency- PEM. His subclinical deficiency must have been precipitated by an episode of loose stools and thus oedema developed acutely though he must have had low serum proteins even before the episode of loose stools.

Physical examination showed weight- 9 kg, length- 70 cm, head circumference- 45 cm, lethargic but irritable on disturbance, oedema feet ++, abdomen distended, liver 3F +, firm, liver span 7 cm, spleen not palpable, no ascites, and other systems normal.

Diagnosis- Protein energy malnutrition (PEM)

There is no need of investigation to prove the diagnosis, however, one may look for other deficiencies such as anaemia and also evidence of any occult infection such as tuberculosis or urinary tract infection. Treatment revolves around resuscitation in case of severe PEM, restoration of deficiencies, rehabilitation and prevention by proper counselling.

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Case 4

An 8-year-old child presented with oliguria and cola-coloured urine over the last 14 days. Physical examination showed minimal oedema in the feet and investigations suggested diagnosis of glomerulonephritis. While diagnosis of glomerulonephritis is acceptable, it seems to be different than classical post-streptococcal acute glomerulonephritis because of persistent symptoms over the last 14 days. Classical post-streptococcal disease should have gotten better by now. Hence, it was decided to follow this child clinically and also with repeat serum C3 level.

Physical examination showed persistent mild oedema in the feet, oliguria and hematuria. Also, his blood pressure revealed increasing though on 95th centile for age. It suggests development of hypertension. C3 level continued to be low even at the end of 6 weeks of persistent glomerulonephritis.

Diagnosis- Chronic glomerulonephritis

This child should be referred to a specialist for further management that may need renal biopsy to define probable cause and prognosticate the disease. This case illustrates value of serum C3 level in follow-up of acute glomerulonephritis and besides clinical abnormality, persistent low C3 level is a marker for need of referral.

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Case 5

A 2-year-old child presented with acute onset oedema noticed first around the eyelids that was followed 12 hours later with generalised oedema all over the body. There was no history of oliguria, high-coloured urine or any other symptoms. Sudden development of generalised oedema without any prior symptoms and oedema starting around the eyes suggests renal glomerular pathology. In view of absence of oliguria or high-coloured urine and massive oedema favour glomerular epithelial pathology such as nephrotic syndrome.

Physical examination showed a comfortable child, happy and active, blood pressure 90/50 mmHg with massive generalised oedema, abdominal distension with ascites but without hepatosplenomegaly. There were no other findings. These findings suggest severe hypoproteinemia that has led to massive generalised oedema and also ascites but without endothelial glomerular involvement as evident by absence of oliguria, high-coloured urine or hypertension.

Investigations showed urine protein +++, urine – creatinine protein ration of 3, serum proteins 4.2 Gm%, albumen 1 Gm%,, globulin 3.2 Gm%, serum cholesterol 320 mg and creatinine 0.5 mg. Massive proteinuria and albuminuria, hypercholesteremia and normal serum creatinine favour diagnosis of minimal lesion nephrotic syndrome.

Diagnosis- Minimal lesion nephrotic syndrome.

Minimal lesion indicates pathology restricted to epithelium of glomerulus. It typically presents for the first time between the age of 2 and 5 years and carries usually good prognosis despite relapse. If this child develops diarrhoea, there may also be oliguria due to dehydration and urine may also be high coloured.

Diarrhoea in such a child may be due to oedema of intestinal mucosa that leads to malabsorption but may also be due to infection. However, if such a child presents in later childhood (unusual age) or has oliguria and hypertension but with massive oedema, it may suggest primary glomerular epithelial disease (because of massive oedema) that has also involved glomerular endothelium (because of oliguria and hypertension). This is referred to as complicated nephrotic syndrome.

Management consists of oral prednisolone 2 mg/kg/day for 4 to 6 weeks followed by two-third total dose on alternate days for 4 weeks. Such a prolonged therapy during the first attack offers better chance of complete remission without further relapse. However, in case of relapse, similar therapy needs to be given but for a shorter period.

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Case 6

A 2-year-old child presented with history of fever and macular skin rash over three days. Considering it to be viral infection, symptomatic treatment was given and fever abated. However the very next day, the child started vomiting and had severe abdominal pain. This was followed by oedema in the feet and abdominal distension. On direct questioning, child had not passed urine over the previous 12 hours.

Initial symptoms do suggest viral infection but it did lead to unexpected symptoms of vomiting and abdominal pain. It indicates immune-mediated complication and not extended viral infection as original symptoms had totally disappeared. Sudden abdominal pain along with vomiting suggests probable vascular complication involving intestines that is immune mediated. As the child had not passed urine, it may denote shock and so abdominal pain is due to severe intestinal ischaemia. This suggests capillary leak syndrome.

Physical examination showed a child in shock with cold extremities, pale skin, marked tachycardia, low blood pressure, mild oedema of the feet, ascites and also mild pleural effusion. This is classical of capillary leak following probable dengue viral infection.

Diagnosis- Dengue fever

Investigations confirmed dengue fever. The child was treated aggressively for shock and recovered in the next two days. This case illustrates how primary infection may get better but lead to immune-mediated complications within a day or two of apparent cure of primary infection. Such a situation cannot be anticipated but every child should be observed for 2 to 3 days after apparent cure for such a possible complication. If diagnosed in time, the child can be saved.

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Case 7

An 8-year-old child presented with history of progressive abdominal distension over the previous 6 months and oedema of feet noticed over the previous two months. He had lost 3 kg weight and had poor appetite. This looks to be progressive disorder as is evident by loss of weight over few months. Abdominal distension could be due to organomegaly (commonly enlarged liver with or without spleen) or ascites. Further development of oedema in the feet in this case indicates chronic liver disease. In the absence of jaundice, it may be well compensated liver disease (means liver has not failed though poorly functioning).

Physical examination showed chronically sick-looking child, oedema feet +, abdominal distension, liver 3 cm +, firm, liver span 9 cm +, spleen 2 cm +, no ascites, no jaundice, other systems normal. Firm and enlarged liver with splenomegaly favours chronic liver disease with portal hypertension. Absence of ascites, bleeding or encephalopathy suggests well compensated chronic liver disease such as cirrhosis.

Diagnosis- Cirrhosis

Investigations – Hb 9 Gm%, serum proteins 5.2 Gm%, albumen 2.4 Gm%, globulin 2 Gm%, ALT (SGPT) 210 AST (SGOT) 160 serum bilirubin 0.9 mg. There was marked hypoalbuminemia with mild rise in liver enzymes with normal bilirubin (it is increased only when more than 5% of liver cells are damaged and so in chronic liver disease, increased bilirubin or jaundice suggests liver gradually failing. However, in acute hepatitis, increased bilirubin does not mean failing liver). Diagnosis of cirrhosis can be confirmed by liver biopsy. Management is palliative.

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Case 8

A 10-year-old child presented with history of breathlessness and oedema of the feet over the previous few days. On direct questioning, he used to feel breathless on exertion but had ignored the same. There was no past history of any major disease. This child seems to be having slowly progressive cardiac disease and now presenting with failure as was evident by breathlessness and oedema of the feet.

Physical examination showed sick child, HR 120/min, RR 27/min, BP 120/60 mm Hg, mild oedema of the feet, engorged neck veins with positive hepatojugular reflex, apex beat on 6th intercostal space outside midclavicular line, systolic murmur at mitral area conducted to axilla. These findings suggest mitral regurgitation with CCF. It is mostly due to rheumatic disease though there is no past history of throat infection or arthritis (throat infection may often be mild or even asymptomatic and so not reported).

Diagnosis– Rheumatic mitral regurgitation with CCF

Diagnosis can be confirmed by chest x-ray, ECG and 2D echocardiogram (showing active valvulitis) and aetiology indicated by high anti-streptolysin O titre. If this is active carditis, it is treated with steroids followed by aspirin and further long-acting penicillin to prevent relapses. Besides, symptomatic therapy for CCF is necessary.

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.