Necrotising soft tissue infection (NSTI) presents unique challenges in diagnosis and management. The key to a successful outcome is a high index of suspicion in appropriate clinical settings. Type II NSTI tends to occur on an extremity in younger, healthier patients with a history of known trauma, and to be monomicrobial. Type I NSTI tends to occur on the trunk of older, less healthy patients without an obvious history of trauma, and tends to be polymicrobial. Other, rarer types exist as well. The pathophysiology of both types involves superantigen acticivty, as well as a number of microbial byproducts which collectively decrease the viscosity of pus, facilitating its spread along deep tissue planes and ultimately causing diffuse deep thrombosis and aggressive systemic sepsis. The most important physical finding is tenderness to palpation beyond the area of redness, and the lack of crepitus should not be seen as a reassuring sign. Suspected cases should undergo early surgical exploration for diagnosis, which may be performed at bedside through a small incision. Most imaging techniques are not sufficiently specific to warrant a delay in surgical exploration. The Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) shows promise as a tool for excluding suspected cases. Successful outcomes in cases of NSTI require early and aggressive serial debridement and a multidisciplinary critical care approach.

Diaphragmatic hernia development post esophagectomy is an uncommon complication, but can have devastating results when there is bowel compromise. Repair by plugging the diaphragmatic hiatus with a biologic mesh is a safe and effective method for closing the defect and results in few complications.

Introduction Human injury or infection induces systemic inflammation with characteristic neuro-endocrine responses. Fluctuations in autonomic function during inflammation are reflected by beat-to-beat variation in heart rate, termed heart rate variability (HRV). In the present study, we determine threshold doses of endotoxin needed to induce observable changes in markers of systemic inflammation, we investigate whether metrics of HRV exhibit a differing threshold dose from other inflammatory markers, and we investigate the size of data sets required for meaningful use of multi-scale entropy (MSE) analysis of HRV. Methods Healthy human volunteers (n=25) were randomized to receive placebo (normal saline) or endotoxin/lipopolysaccharide (LPS): 0.1, 0.25, 0.5, 1.0, or 2.0 ng/kg administered intravenously. Vital signs were recorded every 30 minutes for 6 hours and then at 9, 12, and 24 hours after LPS. Blood samples were drawn at specific time points for cytokine measurements. HRV analysis was performed using EKG epochs of 5 minutes. MSE for HRV was calculated for all dose groups to scale factor 40. Results The lowest significant threshold dose was noted in core temperature at 0.25ng/kg. Endogenous TNF-α and IL-6 were significantly responsive at the next dosage level (0.5ng/kg) along with elevations in circulating leukocytes and heart rate. Responses were exaggerated at higher doses (1 and 2 ng/kg). Time domain and frequency domain HRV metrics similarly suggested a threshold dose, differing from placebo at 1.0 and 2.0 ng/kg, below which no clear pattern in response was evident. By applying repeated-measures ANOVA across scale factors, a significant decrease in MSE was seen at 1.0 and 2.0 ng/kg by 2 hours post exposure to LPS. While not statistically significant below 1.0 ng/kg, MSE unexpectedly decreased across all groups in an orderly dose-response pattern not seen in the other outcomes. Conclusions By usingrANOVA across scale factors, MSE can detect autonomic change after LPS challenge in a group of 25 subjects using EKG epochs of only 5 minutes and entropy analysis to scale factor of only 40, potentially facilitating MSE’s wider use as a research tool or bedside monitor. Traditional markers of inflammation generally exhibit threshold dose behavior. In contrast, MSE’s apparent continuous dose-response pattern, while not statistically verifiable in this study, suggests a potential subclinical harbinger of infectious or other insult. The possible derangement of autonomic complexity prior to or independent of the cytokine surge cannot be ruled out. Future investigation should focus on confirmation of overt inflammation following observed decreases in MSE in a clinical setting.

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