# Haemolytic Uraemic Syndrome in Children

> Haemolytic uraemic syndrome for NEET-PG Paediatrics: triad, STEC and Shigella links, why antibiotics are avoided, dialysis and anaemia management.

- Canonical URL: https://prepelephant.com/topics/neet-pg/paediatrics/haemolytic-uraemic-syndrome-in-children
- Exam / course: NEET-PG · Subject: Paediatrics
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Haemolytic Uraemic Syndrome in Children", PrepElephant, https://prepelephant.com/topics/neet-pg/paediatrics/haemolytic-uraemic-syndrome-in-children

## Direct answer

Pallor, oliguria and a preceding week of bloody diarrhoea in a toddler — with fragmented red cells and thrombocytopenia on the smear and a rising creatinine — is the triad of haemolytic uraemic syndrome: microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury from endothelial injury, most often triggered by Shiga toxin-producing organisms after dysentery. In Indian outbreaks the classical trigger is Shigella dysenteriae type 1; globally Escherichia coli O157:H7 dominates. Management is meticulous supportive care — fluids, controlled transfusion, nutrition, dialysis when indicated — with two prohibitions: antibiotics and antimotility agents in bloody diarrhoea (both increase toxin exposure), and no routine steroids or plasma exchange in typical disease.

## What you must remember

- **The triad:** microangiopathic haemolytic anaemia (haemoglobin often 5-8 g/dL with schistocytes and helmet cells, negative direct antiglobulin test), thrombocytopenia (typically 20,000-100,000/cumm, disproportionately mild relative to the anaemia), and acute kidney injury with oligoanuria.
- **Typical (diarrhoea-associated) HUS:** Shiga toxin from E. coli O157:H7 or Shigella dysenteriae type 1; children under five, summer outbreaks, prodrome of watery then bloody diarrhoea with abdominal pain; the Indian experience is Shigella-driven, with institutional and slum outbreaks.
- **Why antibiotics are withheld:** antimicrobial lysis of bacteria releases Shiga toxin and antimotility drugs retain it in the gut — both increase the risk and severity of HUS.
- **Atypical HUS:** complement-mediated (factor H and related mutations) or pneumococcal (neuraminidase exposes the T antigen — Coombs positive, unlike typical HUS) and drug or cobalamin C disease; no diarrhoea, relapsing, responds to eculizumab.
- **Supportive care package:** strict input-output with daily weight, correct hyperkalaemia and acidosis, treat hypertension (nifedipine acutely), transfuse packed cells slowly for symptomatic anaemia, avoid platelet transfusion unless bleeding, maintain nutrition.
- **Dialysis indications:** uraemia (encephalopathy or pericarditis), refractory hyperkalaemia, severe acidosis, fluid overload with hypertension or pulmonary oedema, and prolonged anuria — peritoneal dialysis is the usual Indian modality in small children.
- **Complications and course:** most children survive the acute phase with supportive care; mortality and chronic kidney disease concentrate in those with anuria over a week, hypertension and central nervous system involvement (seizures, stroke); long-term follow-up of blood pressure, proteinuria and renal function is mandatory for years.
- **Infection-control reality:** the index child sheds organisms; hand hygiene, exclusion from daycare during diarrhoea, safe water and food (avoid raw milk, undercooked meat) are the prevention stack — no vaccine exists.

## How to work through it

A three-year-old, one week after bloody diarrhoea treated with "an antibiotic and a red suspension", is pale, puffy and anuric for a day. Assess volume and hypertension; send haemoglobin with smear (schistocytes), platelets, creatinine, electrolytes and lactate dehydrogenase. Fluid management is the tightrope — a child who is oligoanuric gets restriction to insensible losses plus output, not boluses, unless clearly hypovolaemic; hyperkalaemia gets calcium, salbutamol or glucose-insulin and a dialysis plan. Transfuse slowly for symptomatic anaemia, treat hypertension, and start peritoneal dialysis when uraemia, fluid overload or hyperkalaemia demand it. Counsel on the weeks-long course, dialysis as a bridge, and yearly renal follow-up.

The contrast case is the afebrile six-year-old with the same smear but no diarrhoea, a positive direct antiglobulin test and pneumococcal pneumonia: pneumococcal, complement-mediated territory — avoid plasma (it delivers complement), consider eculizumab, and think of the hereditary forms in any child with recurrent HUS or a family history.

## How the exam frames it

Three testable rules lead. One, the triad plus the smear: fragmented cells with a negative Coombs test (typical HUS) versus positive in pneumococcal atypical HUS — a discriminating detail that separates the well-prepared. Two, the prohibitions: no antibiotics, no antimotility agents in bloody diarrhoea — the Indian vignette usually hides them in the treatment history and rewards the candidate who spots the harm. Three, the system: thrombotic thrombocytopenic purpura is the adult, brain-dominant relative with severe ADAMTS13 deficiency, while childhood typical HUS is kidney-dominant with only mildly low platelets. Programme-level Indian facts include Shigella outbreaks in crowded settings and rational drug use in dysentery.

## Frequently asked questions

### What is the diagnostic triad of haemolytic uraemic syndrome?

Microangiopathic haemolytic anaemia with fragmented red cells, thrombocytopenia, and acute kidney injury — classically following bloody diarrhoea from Shiga toxin-producing organisms.

### Why are antibiotics avoided in diarrhoea-associated HUS?

Antibiotics lyse Shiga toxin-producing bacteria, releasing more toxin, and antimotility agents prolong gut exposure — both are associated with increased risk and severity of HUS.

### Which organisms cause typical HUS in India?

Shigella dysenteriae type 1 in outbreaks, alongside Shiga toxin-producing Escherichia coli such as O157:H7 from contaminated food and water.

### When is dialysis indicated in HUS?

Refractory hyperkalaemia, severe metabolic acidosis, fluid overload with hypertension or pulmonary oedema, symptomatic uraemia, and prolonged anuria — peritoneal dialysis is standard in small children.

### How does atypical HUS differ and what is its specific therapy?

It occurs without diarrhoea, is complement- or pneumococcal (Coombs-positive)-mediated, tends to relapse, and is treated with eculizumab — with plasma therapy avoided in pneumococcal disease.