2026 AuSPEN Consensus Statement: Nutrition Support for Children with Chronic Liver Disease

Full title: Nutrition support of children with chronic liver disease: A rapid review and consensus statements from the AuSPEN Paediatric Liver Group Issued by: AuSPEN (Australasian Society for Parenteral and Enteral Nutrition) Publication: June 2026, Digestive and Liver Disease Method: Rapid systematic review, 19 consensus statements developed by multidisciplinary paediatric liver nutrition working group; graded using NHMRC evidence levels; most recommendations are expert consensus due to limited high-quality paediatric CLD nutrition trials.

Core principle: Malnutrition and growth failure are highly prevalent in paediatric chronic liver disease (CLD), especially cholestatic liver disease. Early screening and multidisciplinary, individualised nutrition care are essential to preserve growth, improve quality of life and optimise liver transplant outcomes. Protein restriction is not routine for children with CLD.

1. Multidisciplinary team (MDT) requirement

✅ 100% consensus: Children with CLD require ongoing care by a specialist MDT including paediatric hepatologist/gastroenterologist, paediatric dietitian, nurse, social worker/psychologist, together with caregivers. Nutrition goals must be shared and agreed with families.

2. Nutrition screening and assessment

1. Screening timing: Nutrition risk screening at initial diagnosis, at every clinic review, during hospitalisation, and whenever liver function deteriorates.
2. Assessment tools: Growth Z-scores (weight-for-age, height-for-age, BMI, weight-for-height), mid-upper arm circumference (MUAC), serial growth velocity.

   Caution: Oedema and ascites can falsely raise weight, so MUAC and growth velocity are more reliable markers.

3. Full nutrition assessment for high-risk children: dietary intake history, stool fat loss, micronutrient testing, body composition, feeding behaviour, caregiver burden.
4. Malnutrition defined by reduced lean mass and impaired growth; not only low body weight.

3. Energy and macronutrient targets

Energy

• Increased energy requirement: 120–150% of age-appropriate estimated average requirement (EAR) for cholestatic CLD; may rise to 150–180% in severe disease.
• Small frequent meals, overnight enteral feeds are often needed to meet targets, given early satiety and fatigue.

Protein

✅ Strong consensus: Routine protein restriction is NOT recommended for children with CLD.

• Target: 2.0–3.0 g/kg/day for most children; up to 3.5–4.0 g/kg/day is safe for growing children.
• Only temporary protein reduction may be considered for acute, refractory hyperammonaemia / hepatic encephalopathy, and should be rapidly re-escalated once controlled. Long-term protein restriction causes sarcopenia and worsens outcomes.

Fat

• Cholestatic children have impaired bile salt-mediated fat absorption. Use MCT-rich formulas / feeds; MCT can be absorbed without micelle formation.
• Maintain a small amount of long-chain triglycerides (LCT) to prevent essential fatty acid deficiency.
• Limit long-chain fat only when severe steatorrhoea is refractory.

4. Micronutrients (key focus in cholestasis)

• Fat-soluble vitamins (A, D, E, K): routine monitoring and supplementation in cholestatic CLD, because of impaired absorption. Serum levels checked every 3–6 months.
• Zinc and selenium: monitor in children with poor intake, diarrhoea or advanced cirrhosis; deficiency contributes to poor growth and immune dysfunction.
• Sodium: restrict sodium only in ascites and oedema; avoid universal sodium restriction, which may reduce oral intake.

5. Enteral nutrition (EN) pathway

Gut function preserved → enteral nutrition preferred over parenteral nutrition.

1. Oral nutrition optimisation + high-energy oral nutritional supplements (ONS) first step, if oral intake insufficient.
2. Nasogastric (NG) or nasojejunal (NJ) tube feeding: indicated if oral intake cannot meet targets for ≥4–6 weeks, or growth failure persists. Overnight continuous feeds are often better tolerated.
3. Gastrostomy (PEG): careful risk assessment in portal hypertension, splenomegaly, ascites or varices, due to higher bleeding and peritoneal infection risk. PEG placement requires hepatology and interventional radiology/ surgery review.
4. Jejunal feeding may be used for recurrent vomiting, gastroparesis or risk of aspiration.

6. Parenteral nutrition (PN)

✅ PN only when intestinal absorption is inadequate, or EN is contraindicated.

• Indications: intractable diarrhoea, severe malabsorption, gastrointestinal complications, pre-transplant decompensated liver disease unresponsive to EN.
• Use minimal PN duration; continue trophic enteral feeds alongside PN whenever possible to preserve gut barrier.
• Monitor liver biochemistry closely to avoid PN-associated cholestasis.
• Avoid overfeeding; monitor triglycerides, copper and manganese.

7. Management of specific complications

Ascites and fluid overload

• Fluid and sodium restriction only for symptomatic ascites; monitor electrolytes.
• Energy-dense low-volume feeds to maximise nutrition while limiting fluid load.

Hepatic encephalopathy (HE)

• Acute HE: temporary protein reduction, treat precipitating factors (infection, bleeding, constipation).
• Resume full protein intake as soon as HE resolves. Chronic protein restriction is harmful.

Pre‑liver transplant nutrition

• Optimise nutrition status pre-transplant; malnutrition and sarcopenia increase surgical risk, infection risk and post-transplant mortality.
• Intensive enteral support is the mainstay of pre-transplant nutritional rehabilitation.

Post‑liver transplant nutrition

• Early enteral feeding after transplant when possible.
• Monitor for steroid-induced hyperglycaemia, obesity, dyslipidaemia, hypertension.
• Catch-up growth support in the first 1–2 years post-transplant.
• Monitor micronutrients, bone health (vitamin D, calcium).

8. Feeding behaviour and developmental issues

• Many children with CLD develop feeding aversion, prolonged tube dependency and oral motor dysfunction.
• Integrate feeding therapy, occupational therapy and family support; avoid prolonged nil-by-mouth periods where possible.

9. Consensus warnings and common pitfalls

❌ Pitfall 1: Restrict protein routinely in all children with cirrhosis to prevent encephalopathy ✅ Correction: Long-term protein restriction causes muscle wasting and poor growth. Protein is only reduced temporarily for acute refractory HE.

❌ Pitfall 2: All children with CLD need low-fat diets ✅ Correction: Cholestatic children need MCT-enriched fat; LCT is still required to prevent essential fatty acid deficiency.

❌ Pitfall 3: Weight is the best nutrition marker in CLD ✅ Correction: Ascites and oedema distort weight; use MUAC, height velocity and BMI Z-score.

❌ Pitfall 4: PEG can be safely placed in children with portal hypertension and varices ✅ Correction: High bleeding risk; MDT risk assessment is mandatory before gastrostomy.

❌ Pitfall 5: Once transplanted, nutrition problems resolve automatically ✅ Correction: Post-transplant metabolic complications, catch-up growth failure and bone disease require long-term nutrition follow-up.

10. Consensus summary

This 2026 AuSPEN consensus highlights that malnutrition and growth failure are modifiable, high-priority complications of paediatric CLD. Early nutrition screening, MDT-led individualised care, high-energy nutrition support and adequate protein intake are cornerstones. Enteral nutrition is first-line; PN is reserved for intestinal failure. Fat-soluble vitamin monitoring and replacement are essential for cholestatic children. Protein restriction is not routine and only temporary for acute hepatic encephalopathy. Pre-transplant nutritional optimisation improves transplant outcomes, while post-transplant care needs to address catch-up growth and metabolic side effects of immunosuppression.