Safety of robotic assisted laparoscopic recurrent paraesophageal hernia repair: insights from a large single institution experience.

BACKGROUND: Laparoscopic repair of recurrent as opposed to primary paraesophageal hernias (PEHs) are historically associated with increased peri-operative complication rates, worsened outcomes, and increased conversion rates. The robotic platform may aid surgeons in these complex revision procedures. The aim of this study was to compare the outcomes of patients undergoing robotic assisted laparoscopic (RAL) repair of recurrent as opposed to primary PEHs. METHODS: Patients undergoing RAL primary and recurrent PEH repairs from 2009 to 2017 at a single institution were reviewed. Demographics, use of mesh, estimated blood loss, intra-operative complications, conversion rates, operative time, rates of esophageal/gastric injury, hospital length of stay, re-admission/re-operation rates, recurrence, dysphagia, gas bloat, and pre- and post-operative proton pump inhibitor (PPI) use were analyzed. Analysis was accomplished using Chi-square test/Fischer's exact test for categorical variables and the Mann-Whitney U test for continuous variables. RESULTS: There were 298 patients who underwent RAL PEH repairs (247 primary, 51 recurrent). They were followed for a median (interquartile range) of 120 (44, 470) days. There were no significant differences in baseline demographics between groups. Patients in the recurrent PEH group had longer operative times, increased use of mesh, and increased length of hospital stay. They were also less likely to undergo fundoplication. There were no significant differences in estimated blood loss, incidence of intra-operative complications, re-admission rates, incidence of post-operative dysphagia and gas bloat, and incidence of post-operative PPI use. There were no conversions to open operative intervention or gastric/esophageal injury/leaks. CONCLUSIONS: Although repair of recurrent PEHs are historically associated with worse outcomes, in this series, RAL recurrent PEH repairs have similar peri-operative and post-operative outcomes as compared to primary PEH repairs. Whether this is secondary to the potential advantages afforded by the robotic platform deserves further study.

Insulin Resistance in Critically Injured Adults: Contribution of Pneumonia, Diabetes, Nutrition, and Acuity.

PURPOSE: Changes in insulin resistance (IR) cause stress-induced hyperglycemia after trauma, but the numerous factors involved in IR have not been delineated clearly. We hypothesized that a statistical model could help determine the relative contribution of different clinical co-variates to IR in critically injured patients. PATIENTS AND METHODS: We retrospectively studied 726 critically injured patients managed with a computer-assisted glycemic protocol at an academic level I trauma center (639 ventilated controls without pneumonia (VWP) and 87 patients with ventilator-associated pneumonia (VAP). Linear regression using age, gender, body mass index (BMI), diabetes mellitus, pneumonia, and glycemic provision was used to estimate M, a marker of IR that incorporates both the serum blood glucose concentration (BG) and insulin dose. RESULTS: Increasing M (p<0.001) was associated with age (1.62%; 95% confidence interval [CI] 1.27%-1.97% per decade), male gender (9.78%; 95% CI 8.28%-12.6%), BMI (4.32% [95% CI 4.02%-4.62%] per 5 points), diabetes mellitus (21.2%; 95% CI 19.2%-23.2%), pneumonia (10.9%; 95% CI 9.31%-12.6%), and glycemic provision (27.3% [95% CI 6.6%-28.1%] per 100 g of glucose). Total parenteral nutrition was associated with a decrease in M of 10.3%; 95% CI 8.52%-12.1%; p<0.001. CONCLUSIONS: Clinical factors can be used to construct a model of IR. Prospective validation might enable early detection and treatment of infection or other conditions associated with increased IR.

Elevated serum creatine phosphokinase is associated with mortality and inotropic requirement in critically injured adults.

BACKGROUND: Hemeproteins such as free myoglobin can undergo autoxidation and catalyse lipid peroxidation, increasing oxidative stress. Creatine phosphokinase (CPK) elevation is a marker for free myoglobin after myocyte damage. Since oxidative injury is a key mechanism of injury-related organ dysfunction, we hypothesised that serum CPK levels correlate with mortality and need for inotropic medication and duration of inotropic support, i.e. shock, among critically injured patients. METHODS: We conducted a retrospective review of 17,847 patients admitted to a single Trauma Intensive Care Unit over 9 years. 2583 patients with serum CPK levels were included in the analysis. Patient data were collected continuously into an electronic ICU repository. Univariate analysis was accomplished using Spearman correlation and the Mann­Whitney U test. Propensity score adjustment models accounting for potential confounders were used to assess the independent effect of CPK level on mortality, need for inotropic support, and duration of inotropic support. RESULTS: Median CPK was significantly higher in patients who died (916 [IQR 332, 2472] vs. 711 [253, 1971], p = 0.004) and in those who required inotropic medications (950 [353, 2525] vs. 469 [188, 1220], p < 0.001). After adjusting for propensity score and potential confounders the odds of mortality increased by 1.10 (95% CI 1.02­1.19, p = 0.020) and the odds of inotropic medication use increased by 1.30 (95% CI 1.22­1.38, p < 0.001) per natural log unit increase in CPK. There was a significant association between CPK level and duration of inotropic support (Spearman's rho .237, p < 0.001) that remained significant in a propensity score-adjusted model. CONCLUSION: In critically injured patients, elevated serum CPK level is independently associated with mortality, need for inotropic medication, and duration of inotropic support. This study is the first to evaluate the relationship of CPK level and mortality in addition to surrogate measures of shock in a population of critically injured patients. If these associations are verified prospectively, there may be a role for treatment with hemeprotein reductants, such as paracetamol, to mitigate the effects of shock and end-organ dysfunction.

Insulin resistance increases before ventilator-associated pneumonia in euglycemic trauma patients.

BACKGROUND: Hyperglycemia caused by stress-induced insulin resistance is associated with both infection and mortality in critically injured patients. The onset of infection may increase stress-induced insulin resistance, leading to hyperglycemia. Hyperglycemia has been shown to precede the diagnosis of ventilator-associated pneumonia (VAP) in critically injured adults and has been suggested to have potential diagnostic importance. However, glycemic control (GC) protocols in critically ill patients limit the development of hyperglycemia despite increasing insulin resistance. Our computer-assisted GC protocol achieves excellent GC, limiting infection-related hyperglycemia while capturing prospectively all glucose values, insulin infusion rates, and the multiplier (M) used to calculate the insulin rate. We hypothesized that surrogate measures of insulin resistance, the insulin infusion rate and multiplier M, would increase prior to the clinical suspicion of VAP, even in euglycemic critically injured patients. METHODS: All critically injured patients (2,656) on the computerized glycemic control protocol were included in the analysis and categorized by those developing VAP and those without pneumonia on days 3-10 of their intensive care unit (ICU) stay. Median blood glucose concentration (BG), insulin infusion rate (IDR), and multiplier (M) [Insulin Drip Rate=M*(BG-60)] were determined for VAP patients (n=329) and non-infected ventilated (NIV) patients (n=2,327) on each day of mechanical ventilation. The day of VAP diagnosis according to U.S. Centers for Disease Control and Prevention (CDC) criteria was defined as day zero and VAP patients matched with NIV patients according to ventilator day from -10 to +10. Comparisons were conducted using the Mann-Whitney U test. RESULTS: Baseline characteristics between VAP and NIV groups did not differ. Measures of insulin resistance increased from the time of injury in both groups. Patients with VAP had significantly greater change in both measures of insulin resistance, IDR and M, in the 48 hours preceding the diagnosis of VAP. These changes occurred despite the fact that the computer-assisted GC protocol achieved lower glucose values in VAP patients for the majority of study days. CONCLUSIONS: Measures of insulin resistance increase in the two days prior to the clinical suspicion of VAP for critically injured patients on the GC protocol. These changes occur despite the protocol maintaining euglycemia. This data suggests that markers of insulin resistance may provide clinically useful information in the early diagnosis of VAP.