Effect of early enteral nutrition on intestinal permeability, protein-losing enteropathy and outcome in canine parvoviral enteritis

Abstract

Canine parvovirus (CPV) infection is characterized by a disruption of gut barrier function, which allows the systemic entry of bacteria and endotoxin, and the development of the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). Despite the lack of prospective data, conventional wisdom has dictated that “gut rest” with initial nil per os (NPO) remains the nutritional treatment of choice for CPV enteritis. However, early enteral nutrition (EEN) has been shown to be superior to starvation in human critical illnesses associated with gut barrier dysfunction. Documented benefits of EEN include improved intestinal permeability, reduced incidences of bacteremia, endotoxemia, SIRS and MODS, decreased catabolism, and improved clinical outcome. A prospective, randomized, controlled clinical trial was conducted to evaluate the effect of EEN on intestinal permeability, protein-losing enteropathy, and clinical outcome in naturally occurring severe CPV enteritis in 30 puppies. Parvoviral infection was confirmed by fecal electron microscopy, and dogs were hospitalized for 6 days. Dogs were randomly assigned to 2 groups. Fifteen dogs received nil per os until vomiting had ceased for 12 hours, after which a low fat diet was fed (initial NPO group; control). Fifteen dogs were fed immediately (Pedigree® Canine Concentration Instant Diet) by nasoesophageal tube (EEN group). All other treatments were identical. Disease severity was semi-quantified by a clinical scoring system. Intestinal permeability was assessed using urinary lactulose and rhamnose recoveries (%L and %R) and L/R ratios. Fecal <FONT FACE=”SYMBOL”>a</FONT>1-proteinase inhibitor concentrations (<FONT FACE=”SYMBOL”>a</FONT>1-PI) quantified protein-losing enteropathy. Enteral tube feeding was not associated with any significant complications. The median time taken to normalization of habitus and appetite, and the resolution of vomiting and diarrhea, was consistently 1 day shorter for the EEN group for each parameter. Body weight remained stable in the NPO group, while EEN was associated with significant weight gain (8.4% by day 6). This supports reduced catabolism with EEN. Compared with reference values, urinary %Ls were elevated, %Rs reduced, and L/R ratios increased throughout the study for both groups. %L behaved significantly differently between groups (p=0.035), with a progressive decrease in the EEN group vs. a progressive increase in NPO. This may indicate earlier repair of intestinal epithelial necrosis, or improved tight junction structure and/or function due to EEN. Such an improvement in gut barrier function might potentially limit endotoxin and/or bacterial translocation. The decreased %R in both groups is consistent with villus atrophy. There were no significant differences in %R or L/R ratios between the two groups over time. Fecal <FONT FACE=”SYMBOL”>a</FONT>1-PI concentrations were increased throughout the study in both groups. There were no significant differences between the declines over time for fecal <FONT FACE=”SYMBOL”>a</FONT>1-PI concentrations between groups. Thirteen of 15 NPO dogs (87%) and all of the EEN dogs (100%) survived (non-significant; p = 0.48). This study demonstrates that EEN may be effectively instituted in CPV enteritis, and supports the use of EEN in gut barrier dysfunction.