Parenteral nutrition is essential as a short-term measure or for long-term use in children with various gastrointestinal issues.¹ Here we report two cases with an untoward complication following the use of parenteral nutrition.

Case 1: 11yr old girl was transferred from district hospital with suspected fistulating small bowel Crohn’s disease evidenced on MRI scan. Due to poor oral intake, recurrent vomiting, even with nasal tube feeds, she was started on parenteral nutrition. A joint decision with the surgical team was to initiate medical treatment with infliximab. Five days into admission to the children’s hospital, she had blurred vision; difficulty with speech; wobbly gait; bilateral facial palsy; ptosis; intermittent confusion. She was investigated for possible metabolic, infective or autoimmune aetiology. MRI brain scan showed a high-intensity signal in the medial thalami, periaqueductal white matter, inferior colliculi, midbrain, pontine and medullary tegmentum. Fundoscopy showed chronic papilloedema. On retrospective review, although she had adequate weight for height, her recent nutritional intake was poor; she had been nil by mouth for one week in her local hospital before transfer and had lost 2kgs in weight. She was treated with intravenous thiamine for Wernicke’s encephalopathy. Her neurological signs recovered with treatment. She subsequently underwent a right hemicolectomy and recovered well post-surgery.

Case 2: 8m old boy with short gut secondary to volvulus and intestinal failure presented 15 days after first discharge on home PN with recurrent vomiting. He was admitted, had a normal upper gastrointestinal contrast study and less vomiting. He was discharged after a period of observation. Three days later, he re-presented with episodes of leaning to the right side, twitching of the right arm, and reduced movements of the right side with weak vocalisations. Blood gas showed high lactate and normal pH. Parenteral nutrition was stopped and he was started on intravenous fluids. Home parenteral nutrition prescription was reviewed which showed no water-soluble vitamin due to an error in transcribing from inpatient to home prescription. He was started on intravenous thiamine. He was also investigated with CSF analysis and MRI head, which were normal. His neurological signs gradually showed improvement.

Wernicke’s encephalopathy is an acute life-threatening neurological condition due to thiamine deficiency characterised by a triad of ataxia, ocular dysfunction and altered mental status. While it can be reversible it can also lead to permanent neurological impairment. It can be prevented by thiamine supplementation in children at risk of thiamine deficiency or in circumstances of increased thiamine requirement. Treatment for Wernicke’s encephalopathy should be with prompt administration of parenteral thiamine.² A thorough understanding of the patient‘s nutritional status and their recent nutritional intake before initiating nutritional rehabilitation with enteral or parenteral route can help to avoid this hazardous complication.

References

1. National Institute for Health and Care Excellence. Nutrition support for adults: oral nutrition support, enteral tube feeding and parenteral nutrition CG32 (Internet). London: NICE;2006(updated April 2017). Available from: https://www.nice.org.uk/guidance/cg32.

2. Vasan S, Kumar A. Wernicke Encephalopathy. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470344.