Nutrition in Clinical Practice

Nutrition support practitioners should be confident in their ability to recognize and treat various metabolic and respiratory disorders encountered in daily practice. A clinician’s comprehension of the underlying physiologic processes and/or exogenous causes that occur during acid-base disorders is essential when making therapeutic decisions regarding fluids, parenteral nutrition, and electrolyte management. This invited review will discuss basic metabolic and respiratory disorders while briefly addressing mixed acid-base disorders.

Phosphorus (P) and calcium (Ca) serve vital roles in the human body and are essential components of nutrition support therapy. Regulation of P and regulation of Ca in the body are closely interrelated, and P and Ca homeostasis can be affected by several factors, including disease states, clinical condition, severity of illness, and medications. Nutrition support clinicians must understand these factors to prevent and treat P and Ca disorders in patients receiving nutrition support therapy. This review provides an overview of P and Ca for the adult nutrition support clinician, with some emphasis on the hospitalized inpatient.

Selenium is a component of selenoproteins with antioxidant, anti-inflammatory, and immunomodulatory properties. Systemic inflammatory response syndrome (SIRS), multiorgan dysfunction (MOD), and multiorgan failure (MOF) are associated with an early reduction in plasma selenium and glutathione peroxidase activity (GPx), and both parameters correlate inversely with the severity of illness and outcomes. Several randomized clinical trials (RCTs) evaluated selenium therapy as monotherapy or in antioxidant cocktails in intensive care unit (ICU) patient populations, and more recently several meta-analyses suggested benefits with selenium therapy in the most seriously ill patients. However, the largest RCT on pharmaconutrition with glutamine and antioxidants, the REducing Deaths due to Oxidative Stress (REDOXS) Study, was unable to find any improvement in clinical outcomes with antioxidants provided by the enteral and parenteral route and suggested harm in patients with renal dysfunction. Subsequently, the MetaPlus study demonstrated increased mortality in medical patients when provided extra glutamine and selenium enterally. The treatment effect of selenium may be dependent on the dose, the route of administration, and whether administered with other nutrients and the patient population studied. Currently, there are few small studies evaluating the pharmacokinetic profile of intravenous (IV) selenium in SIRS, and therefore more data are necessary, particularly in patients with MOD, including those with renal dysfunction. According to current knowledge, high-dose pentahydrate sodium selenite could be given as an IV bolus injection (1000–2000 µg), which causes transient pro-oxidant, cytotoxic, and anti-inflammatory effects, and then followed by a continuous infusion of 1000–1600 µg/d for up to 10–14 days. Nonetheless, the optimum dose and efficacy still remain controversial and need to be definitively established.

Inadequate nutrient stores at birth are an inevitable consequence of being born prematurely. Preterm infants also have high nutrient requirements, which increase with earlier gestational ages. As a result, early nutrition intervention is required to prevent further deficits that, if not corrected, can affect growth and long-term outcomes. Preterm infants often require several weeks of parenteral nutrition (PN) support, which includes trace mineral supplementation. Trace minerals are considered essential nutrients, unable to be synthesized in the human body. Deficiencies of trace minerals have been reported, yet evidence-based guidelines for assessment and supplementation have not been clearly defined. Food and Drug Administration–approved parenteral trace mineral intake guidelines are more than 30 years old. In an effort to more clearly define trace mineral supplementation and monitoring guidelines for preterm infants, a review of literature was performed with the purpose to (1) summarize trace mineral roles in preterm infants, (2) describe clinical signs of deficiency and toxicity, and (3) present intake recommendations and considerations for preterm infants based on current available literature. Review of literature was completed using PubMed and Cochrane databases to find relevant studies specific to trace mineral requirements for preterm infants, trace mineral supplementation of PN, human milk fortifiers, and preterm infant formulas. Review of literature supports that trace mineral depletion can lead to clinical compromise in preterm infants; therefore, suggesting that every effort be made to ensure adequate provision of trace minerals is given to preterm infants. Practical considerations for the clinical nutrition management of preterm infants were also identified in this review.

Early enteral nutrition (EN) is consistently recommended as first-line nutrition therapy in critically ill patients since it favorably alters outcome, providing both nutrition and nonnutrition benefits. However, critically ill patients receiving mechanical ventilation are at risk for regurgitation, pulmonary aspiration, and eventually ventilator-associated pneumonia (VAP). EN may increase these risks when gastrointestinal (GI) dysfunction is present. Gastric residual volume (GRV) is considered a surrogate parameter of GI dysfunction during the progression of enteral feeding in the early phase of critical illness and beyond. By monitoring GRV, clinicians may detect patients with delayed gastric emptying earlier and intervene with strategies that minimize or prevent VAP as one of the major risks of EN. The value of periodic GRV measurements with regard to risk reduction of VAP incidence has frequently been questioned in the past years. Increasing the GRV threshold before interrupting gastric feeding results in marginal increases in EN delivery. More recently, a large randomized clinical trial revealed that abandoning GRV monitoring did not negatively affect clinical outcomes (including VAP) in mechanically ventilated patients. The results have revived the discussion on the role of GRV monitoring in critically ill, mechanically ventilated patients receiving early EN. This review summarizes the most recent clinical evidence on the use of GRV monitoring in critically ill patients. Based on the clinical evidence, it discusses the pros and cons and further addresses whether GRV is a dead marker or still alive for the nutrition management of critically ill patients.

Many new enteral nutrition (EN) formulas have been created over the past several decades with a variety of intended uses. Although each is intended to promote improved outcomes, research is often unclear and, in many cases, conflicting. It is important to note that EN products are considered medical foods by the U.S. Food and Drug Administration and therefore do not have to complete premarket review or approval and are not regulated to the same extent as pharmaceuticals. While standard EN formulas are designed to meet the basic macro- and micronutrient requirements of individuals who cannot meet nutrition needs orally, specialty EN products have been developed to exhibit pharmacologic properties, such as immune-enhancing formulas containing arginine, glutamine, nucleotides, and ω-3 fatty acids. With the vast number of products available, rising costs of healthcare, and the drive toward evidence-based practice, it is imperative that clinicians carefully consider research regarding use of specialty formulas, paying close attention to the quality, patient population, clinical end points, and cost to patient and/or facility.

Micronutrients are essential components of parenteral nutrition (PN). Problems related to deficiency and toxicity occur during routine practice, which could be related to the content of commercial sources, inadequate prescribed doses, and the high frequency of at-risk patients receiving PN. Shortages of commercial products result in increased risk of deficiency. Even though there are recommendations to conserve supplies for those at highest risk, practices that provide no micronutrients or doses less than desired are not safe. This article reviews the evidence describing patients at risk for micronutrient deficiency, the rationale for micronutrient product reformulation, and characteristics of deficiency observed during shortages of micronutrient products.

Background: Wernicke’s encephalopathy is a critical condition of neurological dysfunction resulting from a deficiency in thiamine. Chronic alcoholism is recognized as the most common cause of Wernicke’s encephalopathy, but other causes, including fasting/starvation and malnutrition, have been documented within the scientific literature. These causes may not be readily recognized by healthcare professionals and may lead to Wernicke’s encephalopathy being overlooked as a diagnosis when a nonalcoholic patient presents with classic signs and symptoms of the disorder. Materials and Methods: A narrative review of thiamine and its relationship to the development, diagnosis, and treatment of Wernicke’s encephalopathy is presented based on a review of evidence-based guidelines and published research. To heighten awareness of the development of Wernicke’s encephalopathy in fasted/starved and malnourished patients and to contribute to the scientific body of knowledge for the identification and management of Wernicke’s encephalopathy in these patients, the clinical course and treatment of an adult woman who developed Wernicke’s encephalopathy following a 40-day water-only fasting diet is outlined. Results: Clinical suspicion was required to identify the patient’s condition and initiate immediate intervention through parenteral thiamine administration. Oral thiamine supplementation of 100 to 800 mg per day for 6 months was required to aid recovery. Outcomes: The patient’s clinical course and response to treatment illustrate the necessity for clinical awareness and suspicion of Wernicke’s encephalopathy among healthcare professionals, timely and adequate parenteral thiamine administration, and oral thiamine supplementation at therapeutic doses to correct the nutrient deficiency, halt the progression of Wernicke’s encephalopathy, and promote recovery.

An 11-year-old male with autism became less responsive and was hospitalized with hepatomegaly and liver dysfunction, as well as severe lactic acidosis. His diet for several years was self-limited exclusively to a single “fast food”—a particular type of fried chicken—and was deficient in multiple micronutrients, including the B vitamins thiamine and pyridoxine. Lactic acidosis improved rapidly with thiamine; 2 weeks later, status epilepticus—with low serum pyridoxine—resolved rapidly with pyridoxine. Dietary B vitamin deficiencies complicated the care of this critically ill autistic child and should be considered in this setting.

Background: Thiamine plays a critical role in energy metabolism. Critically ill patients may have thiamine deficiency and increased mortality due to potentially irreversible consequences. The aim of this study was to show the impact of thiamine deficiency in a series of patients and the rapid response to thiamine replacement, showing the changes in clinical and metabolic conditions over time. Methods: We described 3 cases of hospitalized patients who had received parenteral nutrition (PN) without vitamin supplementation. All the patients were admitted to the ICU between 2010 and 2011 with a severe form of lactic acidosis, an unstable circulatory state, and a different neurological disorder (a lethargic state, a severe form of impaired near-coma consciousness, and Wernicke encephalopathy). Results: Intravenous (IV) administration of thiamine was associated with a rapid and marked restoration of acid-base balance, hemodynamic stability and the disappearance of neurological disturbances, and normalization of the clinical and biochemical conditions of all the patients within the following hours. Conclusions: The 3 cases demonstrated the rapidity of the reversal of severe thiamine deficiency, achieved by appropriate replacement in different hospitalized patients. The regression of clinical and biochemical disorders requires a prompt diagnosis and treatment based on the IV administration of thiamine and magnesium sulfate. In hospitalized patients at risk, thiamine deficiency is prevented by the integration of thiamine supplementation into PN and other forms of nutrition support.

Background: This study aimed to determine the prevalence of inadequate serum 25-hydroxyvitamin D (25(OH)D) levels in a pediatric Canadian cystic fibrosis (CF) population and to assess the effectiveness of a vitamin D supplementation protocol on improving vitamin D status. A secondary objective was to analyze factors that may be associated with inadequate 25(OH)D levels. Methods: Vitamin D supplementation, 25(OH)D levels, and factors hypothesized to be associated with 25(OH)D levels were collected through a retrospective chart review (2010 and 2011) of 96 patients (1–18 years) at one CF clinic in Canada. Adequacy of 25(OH)D was set at ≥75 nmol/L. Patients with inadequate 25(OH)D levels in 2010 were prescribed an additional 1000 IU/d for levels <60 nmol/L or 400 IU/d for levels 60–75 nmol/L. Results: Inadequate 25(OH)D levels were observed in 26% of patients in 2010 and 23% in 2011. After supplementation was increased for those with inadequate 25(OH)D levels in 2010 (n = 20), a significant increase in 25(OH)D levels was observed in 2011 (P = .03). Adequate status was achieved in 50% of these patients (n = 10). Age was significantly negatively associated with 25(OH)D levels in both years (P = .002). Percentage of forced expiratory volume in 1 second was significantly positively associated with 25(OH)D levels in 2011 (P = .03). Conclusion: While vitamin D supplementation was effective at increasing serum 25(OH)D, this protocol did not achieve optimal serum 25(OH)D levels in 25% of the population. Increasing age had the strongest association with 25(OH)D. Current supplementation protocols may require reevaluation based on emerging evidence and revised Cystic Fibrosis Foundation guidelines.

Background: Copper is a trace mineral essential for numerous physiological processes. The purpose of this article is to provide data on copper levels in pediatric patients receiving parenteral nutrition (PN) that are useful to guide supplementation in PN formulation. Method: This is a retrospective review of hospitalized pediatric patients receiving PN supplemented and not supplemented with copper. In total, 751 supplemented pediatric patients and 90 pediatric patients not supplemented had serum copper levels measured. We assessed patient demographics, days on PN before copper level was drawn, serum copper levels, conjugated bilirubin levels, and C-reactive protein (CRP). Results: The mean serum copper level was 80 mcg/dL at 20 days for supplemented patients and 64 mcg/dL at 14 days for the 90 nonsupplemented patients (P = .0002). In the supplemented patients, 50% of the levels were low and 45% were within the normal range. The remaining 5% of patients had high levels. In nonsupplemented patients, 71% were low and 29% within the normal range. There was no correlation between copper levels and conjugated bilirubin <2 mg/dL and >2 mg/dL (P = .3421). Copper levels correlated with CRP for CRP >4 mg/dL (P = .03). Conclusion: Pediatric patients receiving PN should be supplemented with copper to prevent deficiency. Serum copper levels should be assessed at 14 days. Assessment of copper status should not be determined by conjugated bilirubin levels. Serum copper levels may be elevated in patients with acute inflammation and may be falsely elevated when CRP is >4 mg/dL.

Objective: The purpose of this study was to determine the prevalence of low vitamin B₁₂ (VB12) in patients on admission to an amputation rehabilitation unit and identify specific populations at risk. Methods: A retrospective chart review was performed for 127 participants comprising patients with major lower limb amputations admitted to a regional amputation rehabilitation program between January 1, 2011 and December 31, 2012. Electronic medical records were reviewed for demographic data, amputation data, medication history, serum VB12 levels, and other related blood work. A literature-based cutoff of VB12 <260 pmol/L was used as the criterion for low VB12. Results: The prevalence of low VB12 was 59.8%. Patients aged ≥55 years were found to have an increased prevalence of low VB12 (P = .05). Serum VB12 levels were significantly lower among patients aged ≥55 years (P < .05) and among patients with a mean corpuscular volume >97 fL (P < .01). No other differences in prevalence were determined among different demographics, etiologies, or comorbidities. Conclusions: Patients with an amputation have a high prevalence of low VB12 levels compared with the general population. Low VB12 status may impact rehabilitation outcomes through anemia, cognitive decline, and neuropathy. No reliable indicators for which patients should be screened were found, and therefore, a universal approach to screening and treatment is needed.

Background: Temperature is known to affect bacterial growth, but current safety recommendations for enteral formula are based on studies conducted in thermoneutral environments, which are not representative of select burn intensive care units (ICUs) that are kept therapeutically hyperthermal. This project evaluated microbial growth in 3 enteral feeding systems: closed, open, and open with modular additives (modular tube feeding [MTF]) exposed to 2 different environments. Procedures: Product for each of the 3 systems was prepared and hung in both a thermoneutral (23.3°C) and a hyperthermal (32.5°C) ICU room. At baseline, 4 hours, and 8 hours, samples were plated and incubated overnight and the number of colony-forming units (CFUs) counted. Findings: In the thermoneutral and hyperthermal environments, there was no evidence of microbial growth in the open or closed feeding systems at any time point. The MTF exhibited baseline contamination with a median of 10 CFUs (95% CI, 8–16) and significant growth over time to 54 CFUs (95% CI, 20–230) by 8 hours in the thermoneutral setting. In the hyperthermal environment, the MTF showed baseline contamination of 390 CFUs (95% CI, 40–1600) and significant growth over time, with 30% of samples exhibiting contamination levels exceeding Food and Drug Administration standards by 4 hours and CFUs being too numerous to count by 8 hours. Conclusion: CFUs in enteral formula did not differ between open and closed feeding systems in either environment for up to 8 hours; however, the addition of modulars to open systems may result in an unacceptable risk of contamination in hyperthermal environments.

Background: The etiology of distal intestinal obstruction syndrome (DIOS) remains unclear. Food intake and pancreatic enzyme replacement therapy (PERT) are often blamed for its occurrence. This study evaluates the nutrition intake and PERT of patients with cystic fibrosis (CF) at a first episode of DIOS. Methods: All patients with CF perform annually a 3-day intake diary to evaluate their caloric, protein, fat, dietary fiber, liquid, and PERT intake. Patients diagnosed with a first episode of DIOS (n = 12) retrospectively completed an intake diary of the 3 days preceding the DIOS episode supervised by an expert dietitian. Results were compared with those of 1 year before and also with 36 CF controls matched for age, sex, genotype, and disease severity. All were pancreatic insufficient. Results: A first DIOS episode was diagnosed in 12 patients with CF. Only the absolute median fat intake (P = .015) and pancreatic enzyme intake (P = .035) were higher at the time of the DIOS attack in comparison to the preceding year. This could result from the difference in data collection or from the recommendations to increase fat intake and concomitant enzyme intake, since this trend was also found in the control group. The significant difference disappears when enzyme intake is expressed as units of lipase/g of fat. No other significant dietary differences were found. Conclusions: This study provides no indications for a potential role of nutrition factors or pancreatic enzymes in the first occurrence of DIOS.

The Academy of Nutrition and Dietetics (the Academy) and the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.), utilizing an evidence-informed, consensus-derived process, recommend that a standardized set of diagnostic indicators be used to identify and document pediatric malnutrition (undernutrition) in routine clinical practice. The recommended indicators include z scores for weight-for-height/length, body mass index-for-age, or length/height-for-age or mid–upper arm circumference when a single data point is available. When 2 or more data points are available, indicators may also include weight gain velocity (<2 years of age), weight loss (2–20 years of age), deceleration in weight for length/height z score, and inadequate nutrient intake. The purpose of this consensus statement is to identify a basic set of indicators that can be used to diagnose and document undernutrition in the pediatric population ages 1 month to 18 years. The indicators are intended for use in multiple settings (eg, acute, ambulatory care/outpatient, residential care). Several screening tools have been developed for use in hospitalized children. However, identifying criteria for use in screening for nutritional risk is not the purpose of this paper. Clinicians should use as many data points as available to identify and document the presence of malnutrition. The universal use of a single set of diagnostic parameters will expedite the recognition of pediatric undernutrition, lead to the development of more accurate estimates of its prevalence and incidence, direct interventions, and promote improved outcomes. A standardized diagnostic approach will also inform the prediction of the human and financial responsibilities and costs associated with the prevention and treatment of undernutrition in this vulnerable population and help to further ensure the provision of high-quality, cost-effective nutritional care.

Pappas S, Krzywda E, Mcdowell N. Nutrition and pancreaticoduodenectomy. Nutr Clin Pract. 2010;25:234-243. (Original DOI: 10.1177/0884533610368709)

In this article in the June 2010 issue of Nutrition in Clinical Practice, Figures 1–3 were reprinted from another source without permission credit lines. The following credit line has been added to each figure caption in the online article:

Reprinted from Evans D, ed. Questions and Answers Pancreatic Cancer. Houston, TX: M.D. Anderson: 2008:1, 6-7 with permission from M.D. Anderson.