Publications by authors named "Kenneth A Kudsk"

Background: Our pharmacy department performed a medication-use evaluation using administrative data to assess prescription of parenteral nutrition (PN). They found that 31.6% (185 of 586) of nutrition support team (NST) patients received ≤5 days of PN, whereas 120 received ≤3 days.

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Background: Nutrients, such as glutamine (GLN), have been shown to effect levels of a family of protective proteins termed heat shock proteins (HSPs) in experimental and clinical critical illness. HSPs are believed to serve as extracellular inflammatory messengers and intracellular cytoprotective molecules. Extracellular HSP70 (eHSP70) has been termed a chaperokine due to ability to modulate the immune response.

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Background: Critically ill patients with acute kidney injury may require parenteral nutrition (PN) and continuous renal replacement therapy (CRRT). Introduction of a phosphate-free premixed renal replacement fluid without system-wide education in May 2011 resulted in increased incidence of hypophosphatemia, necessitating change in practice. Changes included (1) maximizing phosphate in PN, (2) modifying the CRRT order set, and (3) developing a CRRT competency evaluation for nutrition support team members.

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Background: Critically ill patients with acute kidney injury may require parenteral nutrition (PN) and continuous renal replacement therapy (CRRT). Introduction of a phosphate-free premixed renal replacement fluid without system-wide education in May 2011 resulted in increased incidence of hypophosphatemia, necessitating change in practice. Changes included (1) maximizing phosphate in PN, (2) modifying the CRRT order set, and (3) developing a CRRT competency evaluation for nutrition support team members.

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Objective: To determine whether glutamine (GLN)-supplemented parenteral nutrition (PN) improves clinical outcomes in surgical intensive care unit (SICU) patients.

Summary Background Data: GLN requirements may increase with critical illness. GLN-supplemented PN may improve clinical outcomes in SICU patients.

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Stimulation of digestive organs by enteric peptides is lost during total parental nutrition (PN). Here we examine the role of the enteric peptide bombesin (BBS) in stimulation of the exocrine and endocrine pancreas during PN. BBS protects against exocrine pancreas atrophy and dysfunction caused by PN.

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Background: Loss of protein mass and lower fat-free mass index (FFMI) are associated with longer length of stay, postsurgical complications, and other poor outcomes in hospitalized patients. Normative data for FFMI of U.S.

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Hirschsprung's disease (HSCR) is characterized by aganglionosis from failure of neural crest cell (NCC) migration to the distal hindgut. Up to 40% of HSCR patients suffer Hirschsprung's-associated enterocolitis (HAEC), with an incidence that is unchanged from the pre-operative to the post-operative state. Recent reports indicate that signaling pathways involved in NCC migration may also be involved in the development of secondary lymphoid organs.

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Introduction: Parenteral nutrition (PN) increases the risk of infection in critically ill patients and is associated with defects in gastrointestinal innate immunity. Goblet cells produce mucosal defense compounds, including mucin (principally MUC2), trefoil factor 3 (TFF3), and resistin-like molecule β (RELMβ). Bombesin (BBS), a gastrin-releasing peptide analogue, experimentally reverses PN-induced defects in Paneth cell innate immunity.

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Background: Drug shortages pose prescribing problems to clinicians. During fiscal year (FY) 2014, an acute shortage of intravenous potassium phosphate (K-Phos IV), a common supplement in parenteral nutrition (PN), prompted the use of premixed instead of individualized PN to conserve K-Phos IV. Here we quantify the K-Phos IV conserved by using premixed PN and the associated cost differences.

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Circadian clocks and metabolism are inextricably intertwined, where central and hepatic circadian clocks coordinate metabolic events in response to light-dark and sleep-wake cycles. We reveal an additional key element involved in maintaining host circadian rhythms, the gut microbiome. Despite persistence of light-dark signals, germ-free mice fed low or high-fat diets exhibit markedly impaired central and hepatic circadian clock gene expression and do not gain weight compared to conventionally raised counterparts.

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Objective: To define gut-associated lymphoid tissue (GALT) phenotype changes with parenteral nutrition (PN) and PN with bombesin (BBS).

Background: PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers gut and RT immunoglobulin A (IgA) levels, and destroys established RT antiviral and antibacterial immunity. BBS, an enteric nervous system neuropeptide, reverses PN-induced IgA and RT immune defects.

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Background: Outbred mice exhibit increased airway and intestinal immunoglobulin A (IgA) following injury when fed normal chow, consistent with humans. Parenteral nutrition (PN) eliminates IgA increases at both sites. Inbred mice are needed for detailed immunological studies; however, specific strains have not been evaluated for this purpose.

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Background: Lack of enteral stimulation during parenteral nutrition (PN) impairs mucosal immunity. Bombesin (BBS), a gastrin-releasing peptide analogue, reverses PN-induced defects in acquired immunity. Paneth cells produce antimicrobial peptides (AMPs) of innate immunity for release after cholinergic stimulation.

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Background/purpose: Hirschsprung's disease (HSCR), characterized by the absence of ganglia in the distal colon, results in functional obstruction. Despite surgical resection of the aganglionic segment, around 40% of patients suffer recurrent life threatening Hirschsprung's-associated enterocolitis (HAEC). The aim of this study was to investigate whether gut microbiota and intestinal immunity changes contribute to the HAEC risk in an HSCR model.

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Background: Patients receiving parenteral nutrition (PN) are at increased risk of infectious complications compared with enteral feeding, which is in part explained by impaired mucosal immune function during PN. Adding glutamine (GLN) to PN has improved outcome in some clinical patient groups. Although GLN improves acquired mucosal immunity, its effect on innate mucosal immunity (defensins, mucus, lysozymes) has not been investigated.

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The intestinal mucosal immune system is challenged with bacteria, viruses, and parasites, in addition to food and environmental antigens, that require dynamic immune responsiveness for homeostasis. One central signaling pathway is JAK-STAT, which regulates the adaptive and innate immune arms of mucosal immunity as well as epithelial repair and regeneration. Adaptive immunity includes lymphocyte mediated secretion of specific antibodies, while innate immune respones include secretion of non-antigen specific compounds.

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Background: Parenteral nutrition (PN) is available as individualized prescriptions frequently prepared with an automated compounding device or as commercially prepared premixed solutions. Our institution exclusively used individualized PN until an amino acid shortage forced a temporary switch to premixed solutions. In general, premixed solutions contain lower electrolyte levels than individualized formulations prescribed for patients with normal organ function.

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Background: The parotid and submandibular salivary glands are gut-associated lymphoid tissues (GALTs) that secrete immune compounds into the oral cavity. Parenteral nutrition (PN) without enteral stimulation decreases GALT function, including intestinal lymphocyte counts and secretory immunoglobulin A (sIgA) levels. Since the neuropeptide bombesin (BBS), a gastrin-releasing peptide analogue, stimulates intestinal function and restores GALT parameters, we hypothesized that PN + BBS would stimulate parotid and salivary gland IgA levels, T lymphocytes, and IgA plasma cell counts compared with PN alone.

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The search to improve outcomes in critically ill patients through nutrition support has steadily progressed over the past 4 decades. One current approach to this problem is the addition of specific nutrients as primary therapy to improve host defenses and improve the outcome of critically ill patients. The field is referred to as "pharmaconutrition," with the hope of focusing investigations on each nutrient to understand its pharmacological effects on immune and clinical outcomes.

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Defining malnutrition and nutrition risk has been a topic of many papers and discussions throughout the modern literature. Multiple definitions have been proposed, ranging from simple body weight measurements to a more all-encompassing concept looking at disease-specific inflammatory states. Biochemical markers, elements of a history examination, physical examination findings, calculations, and technical tests have all been proposed to help further characterize and delineate those who might be at risk for malnutrition, translating to an increased risk of adverse outcomes after major surgery.

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Introduction: Parenteral nutrition (PN) increases the risk of infection in patients with contraindication to enteral feeding. Paneth cells produce and secrete antimicrobial products that protect the mucosa from pathogens. Their loss is associated with increased host-pathogen interactions, mucosal inflammation, and altered microbiome composition.

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Introduction: Parenteral nutrition (PN) is a necessary therapy used to feed patients with gastrointestinal dysfunction. Unfortunately, PN results in intestinal atrophy and changes to host immune function. PN may also induce additional effects on gut motility that we hypothesized would result from changes in the enteric nervous system.

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