A critical evaluation of a percutaneous diagnostic and treatment strategy for chylothorax after thoracic surgery.

OBJECTIVE: Because chylothorax complicating thoracic surgery is difficult to diagnose and failure of nonoperative management necessitates further surgery, we critically evaluated an evolving percutaneous strategy for diagnosing and treating chylothorax. METHODS: After thoracic surgery, 37 patients with a clinical diagnosis of chylothorax were referred for lymphangiography for definitive diagnosis and percutaneous treatment. Successful localization of the cisterna chyli by lymphangiogram facilitated percutaneous cannulation of the thoracic duct and its embolization. In patients in whom cannulation was not possible, the thoracic duct was percutaneously disrupted. RESULTS: Diagnosis: Lymphangiography was successful in 36 of the 37 patients (97%). Contrast extravasation, confirming clinical diagnosis, was present in 21 of the 36 (58%). Management: Twenty-one of 36 patients underwent 22 lymphangiographically directed percutaneous interventions: 12 embolizations and 10 disruptions. Mortality was zero, with two manageable complications. Patients without percutaneous intervention were discharged a median of 7 days (range 4-58) after first lymphangiography, 8 days (range 2-19) after percutaneous embolization, and 19 days (range 6-48) after first disruption. Eight patients had nine subsequent reoperations for chylothorax, two with negative lymphangiograms; no embolization patient required reoperation. CONCLUSIONS: There is a discrepancy between the clinical diagnosis of chylothorax after thoracic surgery and the presumed gold standard of diagnosis, contrast extravasation at lymphangiogram. Percutaneous treatment by thoracic duct embolization or disruption is safe and may obviate reoperation, but embolization of the thoracic duct is preferable to its disruption.     

Major secondary surgery in blunt trauma patients and perioperative cytokine liberation: determination of the clinical relevance of biochemical markers.

BACKGROUND: The aim of this study is to assess the associations between the timing of secondary definitive fracture surgery on inflammatory changes and outcome in the patient with multiple injuries. The study population consists of a series of patients with multiple injuries who were managed using a strategy of primary temporary skeletal stabilization followed by delayed definitive fracture fixation. METHODS: In a prospective cohort study performed at a Level I trauma center, the patients' injuries and operative details as well as immune markers and clinical outcomes were studied. The patients were split into an early secondary surgery group (group ESS, surgery at days 2-4) and a late secondary surgery group (group LSS, surgery at days 5-8). During the posttraumatic course, inflammatory markers (interleukin [IL]-6, tumor necrosis factor-alpha) were determined on a daily basis. Perioperatively, these markers were additionally evaluated at 30 minutes, 7 hours, and 24 hours after initiation of surgery. RESULTS: Secondary surgery on days 2 to 4 was associated with a higher incidence of postoperative organ dysfunction (n = 33 [46.5%]) than secondary surgery on days 5 to 8 (n = 9 [15.7%], p = 0.01). A significant association between the combination of initial IL-6 values > 500 pg/dL plus surgery on days 2 to 4 and the development of multiple organ failure (r = 0.96, p < 0.001) occurred. A correlation between the initial IL-6 values > 500 pg/dL and surgery on days 5 to 8 (r = 0.57, p < 0.07) could not be found. IL-6 also demonstrated a predictive value for the development of multiple organ failure: IL-6 > 500 pg/dL in group ESS, r = 0.96, p < 0.001; IL-6 > 500 pg/dL in group LSS, r = 0.57, p < 0.07. CONCLUSION: According to our data, no distinct clinical advantage in carrying out secondary definitive fracture fixation early could be determined. In contrast, in patients who demonstrated initial IL-6 values above 500 pg/dL, it may be advantageous to delay the interval between primary temporary fracture stabilization and secondary definitive fracture fixation for more than 4 days. In patients with blunt multiple injuries undergoing primary temporary fixation of major fractures, the timing of secondary definitive surgery should be carefully selected, because it may act as a second hit phenomenon and cause a deterioration of the clinical status.     

Effect of lactate therapy upon cognitive deficits after traumatic brain injury in the rat

Summary Background. In previous studies, it has been shown that intravenous lactate therapy can improve brain neurochemistry, adenosine triphosphate (ATP) generation and outcome after traumatic brain injury (TBI) in rats. In this study, we examined: (1) four L-lactate concentrations to determine the optimal therapeutic dose post TBI in terms of cognitive function; (2) ATP production after TBI for the L-lactate concentration found to be the optimal dose; (3) the possible production of lactic acidosis with the highest L-lactate concentration tested. Methods. Thirty minutes following a fluid percussion injury (FPI) over the left cerebral hemisphere, the animals received an intravenous infusion of 10, 28, 100, or 280 mM L-lactate (n = 10 for each group) for 3 h at a rate of 0.65 ml/h. Shams and control injured animals received a saline infusion. At 11–15 days post injury, cognitive deficits were examined using the Morris Water Maze (MWM) test. Three groups of rats were used for ATP analysis: shams, injured + saline infusion, and injury + the optimal lactate dose as determined by the MWM (n = 4/group). Additionally, a group receiving 280 mM L-lactate (n = 5) and one receiving a saline infusion (n = 3) were monitored for arterial blood variables and blood pressures. Findings. In the MWM test, only the 100 mM L-lactate-treated injured animals showed a significant reduction in cognitive deficits when compared to saline-treated injured animals (p ≤ 0.05). In the ATP study, injured animals without treatment had a 53% reduction in ATP level in the ipsilateral cortex, while animals with 100 mM lactate treatment had a 28% reduction. (p ≤ 0.05). No lactic acidosis was induced by the intravenous infusion of 280 mM L-lactate. Conclusions. This study indicates that the intravenous infusion of 100 mM L-lactate provided the optimal concentration of the substrate to ameliorate cognitive impairment, probably via the regeneration of ATP following TBI in rats.     

Thoracoscopic resection of an apical extralobar pulmonary sequestration in an infant

Pulmonary sequestration is a form of bronchopulmonary-foregut malformation that is treated with surgical resection, either via a thoracotomy or the thoracoscopic approach. Apical extralobar pulmonary sequestrations are rare. We report a case of an apical pulmonary sequestration in an infant that was amenable to thoracoscopic resection. An 8-month-old girl, weighing 10.3 kg, with a left apical extralobar pulmonary sequestration underwent thoracoscopic resection. The pulmonary sequestration was identified and dissected free from surrounding tissue. The vascular peduncle was secured with an endo-GIA loaded with 2-mm vascular staples. The infant was discharged on postoperative day two without complications. In spite of the patient's small size and the apical nature of the sequestration, the operation was easily performed via a thoracoscopic approach. Thoracoscopic resection of an apical extrapulmonary sequestration in a small infant is feasible and may minimize the morbidity of this procedure.     

Plasmacytoid variant urothelial bladder cancer: Is it time to update the treatment paradigm?

ObjectivesPlasmacytoid variant (PCV) urothelial cancer (UC) of the bladder is rare, with poor clinical outcomes. We sought to identify factors that may better inform expectations of tumor behavior and improve management options in patients with PCV UC.Materials and methodsA retrospective analysis of the Indiana University Bladder Cancer Database between January 2008 and June 2013 was performed comparing 30 patients with PCV UC at cystectomy to 278 patients with nonvariant (NV) UC at cystectomy who underwent surgery for muscle-invasive disease. Multivariable logistic regression was used to assess precystectomy variables associated with non–organ-confined disease at cystectomy and Cox regression analysis to assess variables associated with mortality.ResultsPatients with PCV UC who were diagnosed with a higher stage at cystectomy (73% pT3-4 vs. 40%, P = 0.001) were more likely to have lymph node involvement (70% vs. 25%, P<0.001), and positive surgical margins were found in 40% of patients with PCV UC vs. 10% of patients with NV UC (P<0.001). Median overall survival and disease-specific survival were 19 and 22 months for PCV, respectively. Median overall survival and disease-specific survival had not been reached for NV at 68 months (P<0.001). Presence of PCV UC on transurethral resection of bladder tumor was associated with non–organ-confined disease (odds ratio = 4.02; 95% CI: 1.06–15.22; P = 0.040), and PCV at cystectomy was associated with increased adjusted risk of mortality (hazard ratio = 2.1; 95% CI: 1.2–3.8; P = 0.016).ConclusionsPCV is an aggressive UC variant, predicting non–organ-confined disease and poor survival. Differentiating between non–muscle- and muscle-invasive disease in patients with PCV UC seems less important than the aggressive nature of this disease. Instead, any evidence of PCV on transurethral resection of bladder tumor may warrant aggressive therapy.     

Activation of cAMP dependent protein kinase during surfactant release from type II pneumocytes

Release of surfactant from pulmonary type II epithelial cells was stimulated by the beta-adrenergic agonist terbutaline and the diterpene forskolin. Cytosolic cyclic adenosine monophosphate (cAMP) concentrations increased significantly following exposure to terbutaline or forskolin and reached maximal levels within 5 min after treatment. Terbutaline and forskolin had a synergistic effect on cytosolic cAMP levels when added simultaneously. cAMP-dependent protein kinase activity was identified in cytosolic preparations of type II pneumocytes by phosphorylation of the peptide substrate Kemptide (Leu-Arg-Arg-Ala-Ser-Leu-Gly) and binding of 3H-cAMP to the regulatory components of cAMP-dependent protein kinase. Type I and type II regulatory subunits of the cANP-dependent kinase were present in approximately equal concentrations in type II cell cytosol. Activation ratio of cAMP-dependent protein kinase in cultured type II cells increased significantly in the presence of terbutaline, forskolin, or terbutaline plus forskolin. Activation ratios increased from 0.45 +/- 0.03 for control cells to 0.96 +/- 0.06 for cells exposed to terbutaline (10 microM) plus forskolin (5 microM) for 20 min. Release of 3H-phosphatidylcholine was also stimulated by terbutaline and forskolin. Effects of terbutaline and forskolin on surfactant release were approximately additive. Our results demonstrated increased cytosolic cAMP levels, increased cAMP-dependent protein kinase activation ratios, and subsequent augmented surfactant release from isolated type II pneumocytes in response to terbutaline and forskolin. These data support a role for activation of cAMP-dependent protein kinase as a mediator of surfactant release and document the utility of forskolin for study of cAMP-mediated effects in isolated type II cells.