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Gastrointestinal dysfunction (GDF) is one of the primary causes of morbidity and mortality in critically ill patients. Intensive care interventions, such as intravenous fluids and enteral feeding, can exacerbate GDF. There exists a paucity of high-quality literature on the interaction between these two modalities (intravenous fluids and enteral feeding) as a combined therapy on its impact on GDF.

Background and Aim: Chronic intestinal failure requiring home parenteral nutrition (HPN) is a disabling condition that is best facilitated by a multidisciplinary approach to care. Variation in care has been identified as a key barrier to achieving quality of care for patients on HPN and requires appropriate strategies to help standardize management. Method: The Australasian Society for Parenteral and Enteral Nutrition (AuSPEN) assembled a multidisciplinary working group of 15 clinicians to develop a quality framework to assist with the standardization of HPN care in Australia. Obstacles to quality care specific to Australia were identified by consensus. Drafts of the framework documents were based on the available literature and refined by two Delphi rounds with the clinician work group, followed by a further two involving HPN consumers. The Oxford Centre for Evidence‐Based Medicine Levels of Evidence was used to assess the strength of evidence underpinning each concept within the framework documents. Results: Quality indicators, standards of care, and position statements have been developed to progress the delivery of quality care to HPN patients. Conclusion: The quality framework proposed by AuSPEN is intended to provide a practical structure for clinical and organizational aspects of HPN service delivery to reduce variation in care and improve quality of care and represents the initial step towards development of a national model of care for HPN patients in Australia. While developed for implementation in Australia, the evidence‐based framework also has relevance to the international HPN community. [ABSTRACT FROM AUTHOR]

Gastrointestinal dysfunction/failure (GDF) is a common feature of critical illness. There is no consensus on the best way to measure severity of GDF. The aim of this systematic review was to evaluate and compare all gastrointestinal dysfunction scoring tools (GDSTs) to determine aspects that might be useful to construct a new gut scoring tool for intensive care patients. A comprehensive database search of MEDLINE and EMBASE on GDSTs in acute, surgical, and critically ill patients was conducted. Extraction of data was conducted for study characteristics, GDST domains, feasibility of the scoring process, clinical outcomes, and quality of life attributes; independent authors conducted the search, applied the selection criteria, and extracted the data. Methodological quality of studies was assessed. A GDST matrix was created using 14 scoring tools and was evaluated for validity. The 14 GDSTs identified were used in different clinical settings, including critical illness, acute intestinal failure, gastrointestinal disorders, and postoperative patients. There was marked variation between these GDSTs. There is a lack of emphasis in the use of objective laboratory parameters and gut-specific biomarkers to measure GDF in majority of the studies. The overall quality of evidence was poor, and most tools lacked formal validation. This review has highlighted the lack of an agreed and validated approach to scoring GDF in critical illness. The identified aspects of GDF relevant to critical illness should now be incorporated in a new scoring tool and prospectively tested in intensive care patients. [ABSTRACT FROM AUTHOR]

Abnormal glucose metabolism is present in almost 40% of patients after acute pancreatitis, but its pathophysiology has been poorly investigated. Pancreatic hormone derangements have been sparingly studied to date, and their relationship with abnormal glucose metabolism is largely unknown. The aim was to investigate the associations between pancreatic hormones and glucose metabolism after acute pancreatitis, including the effect of potential confounders. This was a cross-sectional study of 83 adult patients after acute pancreatitis. Fasting venous blood was collected from all patients and used for analysis of insulin, glucagon, pancreatic polypeptide, amylin, somatostatin, C-peptide, glucose, and hemoglobin A1c. Statistical analyses were conducted using the modified Poisson regression, multivariable linear regression, and Spearman's correlation. Age, sex, body mass index, recurrence of acute pancreatitis, duration from first attack, severity, and etiology were adjusted for. Increased insulin was significantly associated with abnormal glucose metabolism after acute pancreatitis, in both unadjusted (P = 0.038) and adjusted (P = 0.001) analyses. Patients with abnormal glucose metabolism also had significantly decreased pancreatic polypeptide (P = 0.001) and increased amylin (P = 0.047) in adjusted analyses. Somatostatin, C-peptide, and glucagon were not changed significantly in both unadjusted and adjusted analyses. Increased insulin resistance and reduced insulin clearance may be important components of hyperinsulinemic compensation in patients after acute pancreatitis. Increased amylin and reduced pancreatic polypeptide fasting levels characterize impaired glucose homeostasis. Clinical studies investigating islet-cell hormonal responses to mixed-nutrient meal testing and euglycemichyperinsulinemic clamps are now warranted for further insights into the role of pancreatic hormones in glucose metabolism derangements secondary to pancreatic diseases. [ABSTRACT FROM AUTHOR]

With the increasing prevalence of metabolic comorbidities, their impact on outcomes of patients with acute pancreatitis needs to be considered. Metabolic comorbidities, such as diabetes mellitus, obesity, and metabolic syndrome, have been shown to have a role to play in the course of disease. This scoping review aims to map published clinical studies that have investigated the impact of metabolic comorbidities on outcomes in patients with acute pancreatitis.