209 Delayed Enteral Feeding Reduces Small Intestinal Nutrient Absorption and Impairs Clinical Outcomes in Critically Ill Patients

Abstract

BACKGROUND: Since the introduction of long-term total parenteral nutrition (TPN), morbidity due to inadequate replacement or toxicity of micronutrients has been well-described. More recently, recognition of hypermanganesemia and its associated complications has become a significant health concern. Manganese (Mn) is a trace element with affinity for the extrapyramidal system. It can be neurotoxic when in excess. The Mn content of commercially available trace element formulations far exceeds the American Society of Parenteral and Enteral Nutrition (ASPEN) clinical guidelines. Moreover, supplementation itself has been questioned as Mn deficiency in humans is anecdotal. Manganese poisoning presents clinically as Parkinsonian-like symptoms. Accumulation occurs in the basal ganglia as shown by symmetric, increased signal intensity on T1-weighted magnetic resonance images (MRI). AIMS: To prospectively survey the incidence of hypermagnesemia and radiographic evidence of Mn neurotoxicity in our long-term TPN population. METHODS: Sixteen (N=16) patients agreed to participate after informed consent. Each underwent baseline clinical, biochemical and MRI Brain evaluations. Descriptive statistics were attained. RESULTS: Eighty-one percent of patients (N=13/16) had significant Mn deposits in their basal ganglia on T1-weighted images. There was no difference in baseline clinical characteristics (presence of short gut syndrome or liver disease, length of TPN support, daily amount Mn provision, and whole blood Mn level) amongst those with MRI deposits versus those without. Ten (62.5%) had short bowel syndrome. The mean body mass index was 21.56 ± 0.69, with an average of 9.4 years of TPN support. The mean daily Mn supplementation was 7.28 ± 0.97 umol/day (400 ± 53 ug/day), which far exceeded the ASPEN 2002 recommendations of 1.09-1.82 umol/day (60-100 ug/day). The mean whole blood Mn level was 1.38 ± 0.29 times the upper limit of normal. Only two patients with positive MRI (15%) had a clinical diagnosis of Parkinson's disease. However, multiple neuropsychiatric complaints were reported, including depression (66%), lack of concentration (42%), memory disturbances (17%) and gait instability (8%). CONCLUSION: The Mn content of current commercially available trace element concentrates for TPN is likely excessive, as nearly all of our chronic TPN patients were hypermagnesemic and demonstrated significant basal ganglia deposits on MRI evaluation. Further research is necessary to better define the safe standards of Mn supplementation and to incur a paradigm shift in the current manufacturing of parenteral micronutrient formulations.