Treatment of Diaphragmatic Hernia Occurring After Transhiatal Esophagectomy.

BACKGROUND: Postesophagectomy diaphragmatic hernia (DH) is an uncommon problem but an important one to recognize and treat because of the risk of significant complications such as incarceration and strangulation. Diaphragmatic hernia appears to occur more frequently following transhiatal esophagectomy (THE) than after transthoracic procedures, likely because of the enlargement of the diaphragmatic hiatus required to perform THE. METHODS: After 199 consecutive esophagectomies were performed at Rutgers Robert Wood Johnson University Hospital between January 2000 and June 2013, ten patients were identified with DH; all underwent diaphragmatic hernia repair (DHR). All patients who underwent esophagectomy during this time period were cataloged in a prospectively maintained database that was then retrospectively reviewed. All DH were repaired using a novel biologic plug mesh technique. RESULTS: Ten esophagectomy patients developed DH; nine post-THE and one post-McKeown esophagectomy. One patient was excluded from analysis because of atypical presentation. Demographic data were similar between esophagectomy patients who developed DH and those who did not. Administration of neoadjuvant chemoradiation correlated with development of DH, but did not reach statistical significance. Complications directly related to DHR were few and mostly infectious, including empyema and pneumonia, and were more likely to occur in those who presented with acute obstruction. One patient presented with dysphagia post repair. CONCLUSIONS: 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.

Necrotizing soft tissue infections.

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.

Physiologic variability at the verge of systemic inflammation: multiscale entropy of heart rate variability is affected by very low doses of endotoxin.

INTRODUCTION: Human injury or infection induces systemic inflammation with characteristic neuroendocrine 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, investigate whether metrics of HRV exhibit a differing threshold dose from other inflammatory markers, and investigate the size of data sets required for meaningful use of multiscale 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 min for 6 h and then at 9, 12, and 24 h after LPS. Blood samples were drawn at specific time points for cytokine measurements. Heart rate variability analysis was performed using electrocardiogram epochs of 5 min. Multiscale entropy for HRV was calculated for all dose groups to scale factor 40. RESULTS: The lowest significant threshold dose was noted in core temperature at 0.25 ng/kg. Endogenous tumor necrosis factor α and interleukin 6 were significantly responsive at the next dosage level (0.5 ng/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 analysis of variance across scale factors, a significant decrease in MSE was seen at 1.0 and 2.0 ng/kg by 2 h after exposure to LPS. Although 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 using repeated-measures analysis of variance across scale factors, MSE can detect autonomic change after LPS challenge in a group of 25 subjects using electrocardiogram epochs of only 5 min 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, although 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.

Treatment of bronchomalacia in cystic fibrosis by silicone stent.

We report the case of a 15-year-old girl with cystic fibrosis and rapidly declining pulmonary function tests who was found to have collapse of the left main bronchus from bronchomalacia. She underwent successful deployment of an expandable silicone stent in the collapsed bronchus, after which her pulmonary function test results and her clinical picture markedly improved, obviating the need for immediate transplantation. A literature review yielded no prior reports of bronchomalacia in a cystic fibrosis patient being treated with a silicone stent. This case shows that a simple, effective treatment is possible for one cause of obstructive pulmonary function in cystic fibrosis.