Effect of Early Enteral Nutrition on Intestinal Permeability, Intestinal Protein Loss, and Outcome in Dogs with Severe Parvoviral Enteritis

Mohr, Albert J.; Leisewitz, Andrew L.; Jacobson, Linda S.; Steiner, Jörg M.; Ruaux, Craig G.; Williams, David A.

A randomized, controlled clinical trial investigated the effect of early enteral nutrition (EN) on intestinal permeability, intestinal protein loss, and outcome in parvoviral enteritis. Dogs were randomized into 2 groups: 15 dogs received no food until vomiting had ceased for 12 hours (mean 50 hours after admission; NPO group), and 15 dogs received early EN by nasoesophageal tube from 12 hours after admission (EEN group). All other treatments were identical. Intestinal permeability was assessed by 6‐hour urinary lactulose (L) and rhamnose (R) recoveries (%L, %R) and L/R recovery ratios. Intestinal protein loss was quantified by fecal α(1)‐proteinase inhibitor concentrations (α(1)‐PI). Median time to normalization of demeanor, appetite, vomiting, and diarrhea was 1 day shorter for the EEN group for each variable. Body weight increased insignificantly from admission in the NPO group (day 3: 2.5±2.8% day 6: 4.3±2.3% mean ± SE), whereas the EEN group exhibited significant weight gain (day 3: 8.1±2.7% day 6: 9.7 ± 2.1%). Mean urinary %L was increased, %R reduced, and L/R recovery ratios increased compared to reference values throughout the study for both groups. Percent lactulose recovery decreased in the EEN group (admission: 22.6±8.0% day 6: 17.9 ± 2.3%) and increased in the NPO group (admission: 11.0±2.6% day 6: 22.5 ± 4.6%, P= .035). Fecal α(1)‐PI was above reference values in both groups and declined progressively. No significant differences occurred for %R, L/R ratios, or α(1)‐PI between groups. Thirteen NPO dogs and all EEN dogs survived (P= .48). The EEN group showed earlier clinical improvement and significant weight gain. The significantly decreased %L in the EEN versus NPO group might reflect improved gut barrier function, which could limit bacterial or endotoxin translocation.