All-Cause 30-Day Mortality After Surgical Treatment for Head and Neck Squamous Cell Carcinoma in the United States.

OBJECTIVES: Thirty-day (30-day) mortality, a common posttreatment quality metric, is yet to be described following surgery for head and neck squamous cell carcinoma (HNSCC). This study aimed to measure 30-day postoperative mortality in HNSCC and describe clinical/nonclinical factors associated with 30-day mortality. METHODS: In this retrospective cohort study, the National Cancer Database (2004 to 2013) was queried for eligible cases of HNSCC (n=91,858). Adult patients were included who were treated surgically with curative intent for the primary HNSCC, not missing first treatment, survival, and follow-up information. The outcome of interest was all-cause mortality within 30 days of definitive surgery. Clinical and nonclinical factors associated with all-cause 30-day postoperative mortality were estimated using a fully adjusted, multivariable logistic regression, which accounted for time-varying nature of adjuvant therapy. RESULTS: A total of 775 patients died within 30 days of definitive surgery for HNSCC (30-day mortality rate of 0.84%). Thirty-day mortality rate was however up to 2.33% (95% confidence interval [CI], 1.91%-2.75%) depending on comorbidity. In the fully adjusted model, increasing severity of comorbidity was associated with greater odds of 30-day mortality (Charlson-Deyo comorbidity scores of 1: adjusted odds ratio [aOR], 1.43; 95% CI, 1.21-1.69, and of 2+ aOR, 2.55; 95% CI, 2.07-3.14). Odds of 30-day mortality were greater among Medicaid patients (aOR, 1.77; 95% CI, 1.30-2.41), and in patients in neighborhoods with little education (≥ 29% missing high school diploma: aOR, 1.35; 95% CI, 1.02-1.78). CONCLUSIONS: Patients with higher 30-day mortality were those with a greater burden of comorbidities, with little education, and covered by Medicaid.

Role of the Gut⁻Liver Axis in Driving Parenteral Nutrition-Associated Injury.

For decades, parenteral nutrition (PN) has been a successful method for intravenous delivery of nutrition and remains an essential therapy for individuals with intolerance of enteral feedings or impaired gut function. Although the benefits of PN are evident, its use does not come without a significant risk of complications. For instance, parenteral nutrition-associated liver disease (PNALD)-a well-described cholestatic liver injury-and atrophic changes in the gut have both been described in patients receiving PN. Although several mechanisms for these changes have been postulated, data have revealed that the introduction of enteral nutrition may mitigate this injury. This observation has led to the hypothesis that gut-derived signals, originating in response to the presence of luminal contents, may contribute to a decrease in damage to the liver and gut. This review seeks to present the current knowledge regarding the modulation of what is known as the "gut⁻liver axis" and the gut-derived signals which play a role in PN-associated injury.

No Gut No Gain! Enteral Bile Acid Treatment Preserves Gut Growth but Not Parenteral Nutrition-Associated Liver Injury in a Novel Extensive Short Bowel Animal Model.

BACKGROUND: Parenteral nutrition (PN) provides nutrition intravenously; however, this life-saving therapy is associated with significant liver disease. Recent evidence indicates improvement in PN-associated injury in animals with intact gut treated with enteral bile acid (BA), chenodeoxycholic acid (CDCA), and a gut farnesoid X receptor (FXR) agonist, which drives the gut-liver cross talk (GLCT). We hypothesized that similar improvement could be translated in animals with short bowel syndrome (SBS). METHODS: Using piglets, we developed a novel 90% gut-resected SBS model. Fifteen SBS piglets receiving PN were given CDCA or control (vehicle control) for 2 weeks. Tissue and serum were analyzed posteuthanasia. RESULTS: CDCA increased gut FXR (quantitative polymerase chain reaction; P = .008), but not downstream FXR targets. No difference in gut fibroblast growth factor 19 (FGF19; P = .28) or hepatic FXR (P = .75), FGF19 (P = .86), FGFR4 (P = .53), or Cholesterol 7 α-hydroxylase (P = .61) was noted. PN resulted in cholestasis; however, no improvement was noted with CDCA. Hepatic fibrosis or immunostaining for Ki67, CD3, or Cytokeratin 7 was not different with CDCA. PN resulted in gut atrophy. CDCA preserved (P = .04 vs control) gut mass and villous/crypt ratio. The median (interquartile range) for gut mass for control was 0.28 (0.17-0.34) and for CDCA was 0.33 (0.26-0.46). CONCLUSIONS: We note that, unlike in animals with intact gut, in an SBS animal model there is inadequate CDCA-induced activation of gut-derived signaling to cause liver improvement. Thus, it appears that activation of GLCT is critically dependent on the presence of adequate gut. This is clinically relevant because it suggests that BA therapy may not be as effective for patients with SBS.