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To the Editor: Wilkie’s syndrome or superior mesenteric artery syndrome (SMAS) is a rare form of intestinal obstruction, caused by compression of the third part of duodenum between the aorta and superior mesenteric artery due to the loss of fat padding in acute malnutrition.

A 16-y-old boy, weighing 50 kg weight (25th − 50th centile, BMI 19.4) presented after a road traffic accident with severe traumatic brain injury (sTBI) and was managed conservatively. Nasogastric feeds were initiated within 5 d at 30 kcal/kg/d, 15% protein given as 300 ml aliquots every 2nd hour, which he tolerated well. Over 2 wk, his feeds were increased to 45 kcal/kg/d, 20% protein. Despite being on feeds and being quadriplegic, he developed SMAS on the 58th day of admission while in rehabilitation.

SMAS’s link in children is notable as our patient had all the features noted by Phillips PA: Age 12–18 y, lean for height, time from injury to SMAS 38–72 d, sTBI, spastic quadriparesis, hip flexion deformity and > 10 kg weight loss [1].

Features such as hip flexion contracture may reduce aorto-mesenteric angle and explain susceptibility to SMAS but what remains unexplained is the significant weight loss despite adequate nasogastric feeds.

Current guidelines recommend basal calorie replacement by days 5–7 post injury, aiming for 100–140% of resting metabolic expenditure [2, 3]. Requirements, however, may be 140-200% of expected values due to a hypermetabolic state [4]. Furthermore, it is likely that children with sTBI who are in an active pubertal growth spurt and those with spastic quadriparesis where there is constant increased tone of muscles can have a far higher calorie requirement than what is anticipated.

More research using indirect calorimetry in this vulnerable population is required to define nutritional guidelines during rehabilitation. SMAS in children with sTBI is a complication that can be prevented and increased awareness will improve recovery and reduce morbidity.