Low BMI is NOT ‘normal’ for those with OA/TOF and is a sign of poor nutrition as a result of difficulties eating and/or malabsorption.
Food intake can be an ongoing problem post OA/TOF repair.
Multiple studies have shown that adults born with OA/TOF have lower BMIs, with one showing 24.3% had a BMI less than 18.5. (97) This can follow on from a childhood of poor nutrition, with growth stunting found in between 5% and 15% of adults. (94,95) Birketvedt et al. (94) found 71% of adolescents were eating less calories than the recommended calorie intake for their age and a third less than their basal metabolic rate. They posit two causes for this: dysphagia and severe postprandial fullness. Dysphagia leads to selective eating, avoiding foods like meat, bread and other foods which are difficult to swallow. Hyperalimentation (excessive drinking to expedite food down the oesophagus) and oesophageal stasis and gastroparesis lead to severe postprandial fullness with lower quantities of macronutrients consumed.
Malnutrition is related to surgical factors/type of OA – delayed primary anastomosis of long-gap OA, jejunostomy, gastric pull-up and pyloromyotomy all have a poorer prognosis for malnutrition. (96) However, poor growth and weight is commonest in early childhood, with catch up around age 8, so for many adults born with OA/TOF, any such issues will likely be historical. Nonetheless, none of the Adult TOFs in the study by Presse et al. were classified as ‘tall’, suggesting that whilst many TOFs reach a normal height, they may not reach their full height potential if they had not had OA/TOF. (96,97)
There is also low intake of micronutrients such as vitamin D, riboflavin, calcium and iron, as well as reduced intake of macronutrients, particularly carbohydrates. (94) Nutrition and weight are a particular issue for those with repaired long-gap OA/TOF. (31) Post gastric transposition, 47% of adults are anaemic, compared with 9% with primary repair, and 19% still need supplemental feeding.