Epidural analgesia in the era of enhanced recovery: time to rethink its use?

BACKGROUND: Previous assessments of the impact of epidural analgesia (EA) on outcomes after colorectal surgery were related to the period before widespread implementation of the enhanced recovery after surgery (ERAS) protocols. This study evaluates the impact of EA on postoperative recovery after colectomy using recent multicenter data. METHODS: Patients who underwent elective colectomy from the American College of Surgeons (ACS) National Surgical Quality Improvement Program (NSQIP) data (2014-2015) were identified. Demographics, comorbidities, diagnosis, procedure type and approach, and postoperative complications associated with EA were assessed. Impact of EA on postoperative ileus, length of stay (LOS), and prolonged LOS (defined as LOS > 75 percentile) was evaluated for all, open, and laparoscopic cases using univariable and multivariable analyses. RESULTS: Of 9045 elective colectomy procedures, 3081 (34.1%) received EA. Epidural analgesia was associated with greater rates of postoperative ileus (15.9% vs. 10.8%, p < 0.0001), superficial (5.5% vs. 4%, p = 0.001) and deep (1.8% vs. 0.6%, p < 0.0001) wound infections, pulmonary embolism (0.8% vs. 0.4%, p = 0.004), deep vein thrombosis (1.3% vs. 0.7%, p = 0.01), sepsis/septic shock (4.6% vs. 3.1%, p < 0.0001), unplanned reintubation (1.5% vs. 0.8%, p = 0.003), cardiac complications (1.2% vs. 0.7%, p = 0.03), and transfusion (9.1% vs. 5.9%, p < 0.0001). Postoperative length of stay (LOS) [mean (SD), days: 6.7(6.2) vs. 5(4.5) days, p < 0.0001] was greater for EA. On multivariable analysis, EA had no impact on postoperative ileus for all and laparoscopic cases. However, EA increased the likelihood for ileus (OR 1.34, 95% CI 1.02-1.78) after open colectomy alone. Similarly, EA did not influence prolonged LOS for all and laparoscopic cases but was independently associated with prolonged LOS after open colectomy (OR 1.4, 95% CI 1.1-1.8). CONCLUSION: Epidural analgesia was not associated with improved recovery after elective colectomy in the era of ERAS.

Improving Telestroke Treatment Times in an Expanding Network of Hospitals.

BACKGROUND: Like all medical innovations, telestroke must demonstrate successful outcomes to achieve sustained growth and acceptance. Asserting that telemedicine is faster, employs the latest technology, or promotes a better use of limited resources is laudable but insufficient. An analysis of stroke treatment within a telemedicine network in 2013 showed that tissue-type plasminogen activator (tPA) could be safely and reliably administered within a practice-based model of telestroke care. Since then, hospital volume and tPA administration within this network have tripled. We hypothesize that a practice-based model of telestroke can maintain positive outcomes in the face of rapid growth. METHODS: Data on tPA treatment times and outcomes after thrombolysis were gathered for 165 patients treated with alteplase between November 2012 and November 2014. Comparisons were made to a previous published study of 54 patients seen between October 2010 and October 2012 in the same network. Primary outcome measures were average door-to-needle (DTN) time for TPA administration and average call-to-needle (CTN) time. RESULTS: Significant reductions were observed in median DTN (93 versus 75 minutes, P < .01) and median CTN (56 versus 41 minutes, P < .01). Quality outcome measures such as post-tPA symptomatic hemorrhage (2 [4%] versus 9 [5%], P = .23), length of stay (4 versus 4 days, P = .45), mortality (8 [15%] versus 16 [10%]; P = .32), and percentage of stroke patients treated remained stable. CONCLUSIONS: This study shows that a practice-based telemedicine system can produce meaningful improvement in markers of telestroke efficiency in the face of rapid growth of a telestroke network.

Expanding access to intravenous tissue-type plasminogen activator treatment with a practice-based telestroke system.

Emergency stroke treatment would benefit from the increased use of thrombolysis via academic or practice-based telemedicine systems. However, a comparative analysis of these systems has not been undertaken. Data on stroke severity and outcomes after thrombolysis were gathered on patients treated by a practice-based system and compared to published data from academic systems. Patient demographics and outcome measures were not significantly different for patients treated by practice-based or academic providers with the exceptions of lower age and shorter duration of stay in the practice-based treatment group. This study shows that emergency stroke care provided by academic and practice-based telemedicine systems can achieve similar outcomes.

Pelvic sepsis after IPAA adversely affects function of the pouch and quality of life.

BACKGROUND: Pelvic sepsis after IPAA predisposes to pouch failure. There are limited data on long-term pouch function for patients with pelvic sepsis. OBJECTIVE: The aim of this study was to investigate functional outcomes and quality of life for patients undergoing IPAA who develop pelvic sepsis and preserve their pouch long-term. DESIGN: This study is based on retrospective analysis of prospectively accrued data. SETTINGS: This study was conducted at a single-center institution. PATIENTS: All patients undergoing IPAA from 1983 to 2007 were included. MAIN OUTCOME MEASURES: The primary outcomes measured were functional outcomes (urgency, incontinence, bowel movements) and quality-of-life (restrictions, energy, happiness) parameters. RESULTS: Two hundred (6.2%) of 3234 patients developed pelvic septic complications within 3 months of IPAA. In the comparison of complications at the time of IPAA for the 2 groups, patients with pelvic sepsis had higher rates of postoperative hemorrhage (13.5% vs 3.7%, p < 0.001), anastomotic leak (35% vs 3.7%, p < 0.001), wound infection (14% vs 7.4%, p < 0.001), and fistula formation (37% vs 7.1%, p < 0.001). The overall median follow-up was 7 years. Pelvic sepsis was associated with greater pouch failure (19.5% vs 4%, p < 0.001). For patients with follow-up (pelvic sepsis = 144, nonpelvic sepsis = 2677) with a retained pouch, for whom we compared functional outcomes and quality of life, incontinence was worse (never/rare: 69.5% vs 77.8%, p = 0.03). Urgency scores were lower in pelvic sepsis but not statistically significant. The overall Cleveland Global Quality of Life score (and components) in the sepsis group were significantly worse than in the nonsepsis group (0.74 vs 0.79, p < 0.001). Patients who developed sepsis were also less likely to recommend IPAA to others than patients who did not develop pelvic sepsis. LIMITATIONS: This study was limited by the retrospective analysis and the use of questionnaires. CONCLUSIONS: Pelvic sepsis after IPAA leads to worse functional outcomes and quality of life even when it does not lead to pouch failure. This finding argues for careful attention to preoperative and intraoperative planning and strategies aimed at reducing this complication after IPAA.

Palliative stenting for late malignant gastric outlet obstruction.

Malignant gastric outlet obstruction (MGO) is a late complication of pancreatobiliary and gastric cancers. Although surgical gastrojejunostomy provides good palliation, many of these patients may be nonoperative candidates or underwent previous extensive resection such as a Whipple procedure. Recently, endoscopically placed self-expanding metallic stents (SEMS) have been used to palliate MGO. The aim of this study was to evaluate the efficacy of SEMS for palliation of late MGO. Medical records of patients with endoscopic placement of SEMS for palliation of MGO were reviewed. Results showed that 30 patients with MGO had SEMS placed for late gastroduodenal (n = 20) or jejunal (n = 10) obstruction. Twenty-one patients (70%) had previous surgery. Return to oral feeding was observed in 90% of patients who presented with recurrent obstruction after prior bypass surgery and in 88% of nonoperative patients in whom SEMS were placed as the primary therapy for obstruction. No major complications were observed, and median survival after SEMS was 4.1 months (0.1 to 10.5 months). SEMS also did not interfere with biliary drainage. In conclusion, endoscopically placed SEMS are safe and provide good palliation for late malignant gastroduodenal and jejunal strictures and are an excellent complement to recurrent obstruction after surgical gastrojejunostomy.

Impaired intestinal cell proliferation and cell death in leptin-deficient obese mice.

BACKGROUND: After massive small-bowel resection and loss of absorptive capacity, residual intestine has compensatory ability to adapt by cellular hyperplasia and increased absorptive function. Growth factors have been shown to enhance intestinal adaptation, but the mechanisms involved are not well defined. Leptin has been shown to function as a trophic factor in the intestine and enhances carbohydrate absorption after small-bowel resection. Therefore, we hypothesized that leptin deficiency may impair the adaptive response by modulating cellular proliferation or cell death after small-bowel resection. METHODS: Twelve-week-old male lean control (C57BL/6J, n = 28) and leptin-deficient (Lep(ob), n = 24) obese mice underwent sham laparotomy, intestinal transection, or 50% proximal small-bowel resection. Mice were killed at 48 hours postresection, and remnant intestine was harvested. Phenotypic analysis to assess adaptation included characterization of cell proliferation (percentage BrdU incorporation), apoptosis (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nickend labeling assay), and morphometric response (villus height, crypt depth). RESULTS: The percentage S-bromodeoxyuridine (BrdU) incorporation and apoptotic indices of obese transected mice were significantly lower than lean transected mice (7.3 vs 21.9% and 0.70 vs 1.53% respectively, p < .05). In resected animals, the percentage BrdU incorporation and apoptotic indices of obese resected mice were significantly lower than for lean resected (6.1 vs 22.0% and 0.93 vs 1.80% respectively, p < .05). No differences between groups, regardless of surgery, were identified in villus height or crypt depth. CONCLUSIONS: Therefore, we conclude that leptin deficiency impairs both cell proliferation and cell death in the early adaptive period after either small-bowel transection or resection.

Gallbladder myocytes are short and cholecystokinin-resistant in obese diabetic mice.

BACKGROUND: Obesity is associated with diabetes and gallstone formation. Obese leptin-deficient (Lepob) and leptin-resistant (Lepdb) mice are hyperglycemic and have enlarged gallbladders with diminished response in vitro to cholecystokinin (CCK) and acetylcholine (ACh). Whether this phenomenon is secondary to hyperosmolar myocytes and/or decreased neuromuscular transmission remains unclear. We hypothesize that myocytes from Lepob and Lepdb obese mice would not respond normally to neurotransmitters. METHODS: Cholecystectomy was performed on 39 lean, 19 Lepob, and 20 Lepdb 12-week-old female mice. The gallbladder was divided and enzymatically digested. Half of each gallbladder's myocytes had contraction induced by CCK (10(-8) mol/L, n = 38) or ACh (10(-5) mol/L, n = 40). RESULTS: Body weights, gallbladder volumes, and serum glucoses were greater for Lep(ob) and Lepdb mice compared to controls (P < .001). Resting myocyte lengths from Lepob and Lepdb mice were 93% and 91% of the length of controls (P < .001). In response to CCK, lean myocytes shortened 6% (P < .01), while myocytes from obese mice demonstrated no shortening. None of the myocytes demonstrated significant shortening with ACh. CONCLUSIONS: These data suggest that gallbladder myocytes from obese mice are (1) foreshortened and (2) have a diminished response to cholecystokinin. We conclude that altered leptin and/or increased glucose may foreshorten myocytes and decrease response to cholecystokinin.

Cystic pancreatic neoplasms: enucleate or resect?

Asymptomatic cystic pancreatic neoplasms are being detected by abdominal imaging with increasing frequency. Enucleation of small cystic neoplasms can be performed without recurrence but has been associated with a higher incidence of pancreatic fistula. Thus the procedure has been modified to include intraoperative ultrasound imaging and closure of the pancreatic defect. This analysis was performed to determine whether these modifications have improved operative outcome. Thirty patients with mucinous cystic neoplasms (n=16), serous cystadenomas (n=10), and cystic islet cell tumors (n=4) were studied. Enucleation was performed in 11 patients (7 with mucinous cystic neoplasms, 2 with serous cystadenomas and 2 with islet cell tumors), whereas 19 underwent resection of cystic tumors (pancreatoduodenectomy in 8 and distal pancreatectomy in 11). The mean groups did not differ with regard to age (57 years), gender (73% female), presentation (63% incidental), or site (43% head, neck, or uncinate). Patients undergoing enucleation had smaller tumors (2.2 vs. 4.7 cm, P<0.01) that were less likely to be in the tail (9% vs. 42%). Operative time was significantly shorter in the enucleation group (199 vs. 298 minutes, P<0.01). Blood loss also was significantly reduced in the enucleation group (114 vs. 450 ml, P<0.001). Pancreatic fistula rates (27% vs. 26%) and length of hospital stay (12.6 vs. 15.7 days) were similar in the two groups. Enucleation of benign cystic pancreatic neoplasms reduces operative time and blood loss without increasing postoperative complications or length of stay. Therefore enucleation should be the standard operation for small benign cystic neoplasms in the uncinate, head, neck, and body of the pancreas.

Nonobese diabetic mice have diminished gallbladder motility and shortened crystal observation time.

Diabetes and obesity are strongly associated and are risk factors for cholesterol gallstone disease. Leptin-deficient and leptin-resistant diabetic obese mice have enlarged, hypomotile gallbladders. In addition, bile from gallbladders of leptin-deficient mice has enhanced cholesterol crystal formation, whereas bile from gallbladders of leptin-resistant mice has delayed crystal observation time. To determine the effect of diabetes alone, we hypothesized that leptin-normal, nonobese diabetic (NOD) mice would have reduced biliary motility and rapid crystal formation. Twenty control and 9 prediabetic and 11 diabetic NOD, 12- to 26-week-old mice underwent glucose measurement and cholecystectomy for muscle bath stimulation with neurotransmitters. An additional group of 200 control and 78 NOD 12-week-old mice underwent microscopic bile examination for cholesterol crystal formation. Compared with control mice, prediabetic NOD mice had similar glucose levels and gallbladder volumes. Diabetic NOD mice had higher sugar levels and larger gallbladder volumes (P < 0.001) than control mice. Prediabetic NOD gallbladders had less contractility (P < 0.01) than control gallbladders, and contractility worsened (P < 0.01) in diabetic NOD mice. NOD mice formed cholesterol crystals earlier than did control mice (P < 0.05). Nonobese diabetic NOD mice have (1) decreased gallbladder contraction to neurotransmitters, which worsens with development of diabetes, and (2) rapid crystal formation. We conclude that diabetes alone alters gallbladder motility and cholesterol crystal formation.

Small pancreatic and periampullary neuroendocrine tumors: resect or enucleate?

OBJECTIVE: The aim of this study was to compare the outcomes of enucleation versus resection in patients with small pancreatic, ampullary, and duodenal neuroendocrine tumors (NETs). METHODS: Multi-institutional retrospective review identified all patients with pancreatic and peri-pancreatic NETs who underwent surgery from January 1990 to October 2008. Patients with tumors < or =3 cm and without nodal or metastatic disease were included. RESULTS: Of the 271 patients identified, 122 (45%) met the inclusion criteria and had either an enucleation (n = 37) and/or a resection (n = 87). Enucleated tumors were more likely to be in the pancreatic head (P = 0.003) or functioning (P < 0.0001) and, when applicable, less likely to result in splenectomy (P = 0.0003). The rate of pancreatic fistula formation was higher after enucleation (P < 0.01), but the fistula severity tended to be worse following resection (P = 0.07). The enucleation and resection patients had similar operative times, blood loss, overall morbidity, mortality, hospital stay, and 5-year survival. However, for pancreatic head tumors, enucleation resulted in decreased blood loss, operative time, and length of stay compared to pancreaticoduodenectomy (P < 0.05). CONCLUSION: These data suggest that most outcomes of enucleation and resection for small pancreatic and peri-pancreatic NETs are comparable. However, enucleation has better outcomes than pancreaticoduodenectomy for head lesions and the advantage of preserving splenic function for tail lesions.

Leptin regulates gallbladder genes related to gallstone pathogenesis in leptin-deficient mice.

BACKGROUND: Little is known about the genetic factors that cause alterations in gallbladder motility, cholesterol crystal nucleation, biliary lipids, and, ultimately, cholesterol gallstones. Obese, leptin-deficient (Lep(ob)) mice have large gallbladder volumes with decreased contraction in vitro and are predisposed to cholesterol crystal formation. Leptin administration to these mice causes weight loss and restores gallbladder function. We hypothesize that administration of leptin to Lep(ob) mice would cause weight loss, decrease gallbladder volume, and change gallbladder genes related to gallbladder motility, nucleating factors, and lipid metabolism. STUDY DESIGN: Twenty-four 8-week-old Lep(ob) mice were fed a nonlithogenic diet for 4 weeks. Twelve mice received daily IP saline injections, and 12 received 5 mug/g recombinant leptin. Gallbladder mRNA was pooled and analyzed on murine genome microarray chips. Selected genes were confirmed by real-time polymerase chain reaction (PCR) in a second group of mice treated by the same protocol. RESULTS: Leptin-deficient mice given leptin had significant weight loss and reductions in gallbladder volume. These mice had upregulation of the leptin receptor (p = 0.007; PCR = 1.1-fold increase) but downregulation of leptin (p = 0.003; PCR = 13.5-fold decrease). Leptin upregulated the cholecystokinin A receptor (p < 0.001; PCR = 3.1-fold increase), acetylcholine beta2 receptor (p = 0.005), and the Ca+-calmodulin-dependent protein kinase (p = 0.002) genes. Leptin also altered immunoglobulin heavy chain 4 (p = 0.005; PCR = 17.7-fold increase), mucin 3 (p = 0.006), and carboxylesterase (p = 0.016; PCR = 2.5-fold decrease) genes. Leptin downregulated 3-hydroxy 3-methylglutaryl coenzyme A reductase (p = 0.006; PCR = 2.5-fold decrease) and LDL receptor (p = 0.003). CONCLUSIONS: Leptin modulates obesity and regulates gallbladder genes related to cholesterol gallstone pathogenesis.

Leptin regulates gallbladder genes related to absorption and secretion.

Dysregulation of gallbladder ion and water absorption and/or secretion has been linked to cholesterol crystal and gallstone formation. We have recently demonstrated that obese, leptin-deficient (Lep(ob)) mice have enlarged gallbladder volumes and decreased gallbladder contractility and that leptin administration to these mice normalizes gallbladder function. However, the effect of leptin on gallbladder absorption/secretion is not known. Therefore, we sought to determine whether leptin would alter the expression of genes involved in water and ion transport across the gallbladder epithelium. Affymetrix oligonucleotide microarrays representing 39,000 transcripts were used to compare gallbladder gene-expression profiles from 12-wk-old control saline-treated Lep(ob) and from leptin-treated Lep(ob) female mice. Leptin administration to Lep(ob) mice decreased gallbladder volume, bile sodium concentration, and pH. Leptin repletion upregulated the expression of aquaporin 1 water channel by 1.3-fold and downregulated aquaporin 4 by 2.3-fold. A number of genes involved in sodium transport were also influenced by leptin replacement. Epithelial sodium channel-alpha and sodium hydrogen exchangers 1 and 3 were moderately downregulated by 2.0-, 1.6-, and 1.3-fold, respectively. Carbonic anhydrase-IV, which plays a role in the acidification of bile, was upregulated 3.7-fold. In addition, a number of inflammatory cytokines that are known to influence gallbladder epithelial cell absorption and secretion were upregulated. Thus leptin, an adipocyte-derived cytokine involved with satiety and energy balance, influences gallbladder bile volume, sodium, and pH as well as multiple inflammatory cytokine genes and genes related to water, sodium, chloride, and bicarbonate transport.

Ciliary neurotrophic factor restores gallbladder contractility in leptin-resistant obese diabetic mice.

BACKGROUND: Obesity and diabetes are major risk factors for cholesterol gallstones, and the majority of obese people are leptin-resistant. Our previous work has shown that both leptin-deficient (Lepob) and leptin-resistant (Lepdb) obese diabetic mice have decreased in vitro gallbladder motility. Leptin administration to leptin-deficient (Lepob) animals restores gallbladder motility and reverses obesity and hyperinsulinemia. However, additional leptin in leptin-resistant obesity would not be expected to improve obesity-related parameters. Recent studies demonstrate that ciliary neurotrophic factor (CNTF) reduces weight and hyperinsulinemia in leptin-resistant obesity. Our hypothesis is that CNFT would cause weight loss, lower blood sugars, and restore gallbladder contractility in leptin-resistant (Lepdb) mice. MATERIALS AND METHODS: 20 C57b/6J and 20 Lepdb 8-week-old female mice were injected daily with either intraperitoneal saline or 0.3 microg/g CNTFAx15 for 17 days. Gallbladders were mounted in muscle baths and stimulated with acetylcholine, neuropeptide Y, and cholecystokinin. Gallbladder volume, serum glucose, insulin, liver weight, liver fat, and gallbladder responses were measured. Data were analyzed by ANOVA. RESULTS: Saline treated obese mice had greater body weight and obesity parameters, but decreased gallbladder contractility to neurotransmitters compared to saline treated lean mice. CNTF administration to obese mice decreased body weight and obesity parameters, and restored gallbladder contractility. CNTF treated lean animals had weight loss and decreased gallbladder contraction to acetylcholine and cholecystokinin compared to saline treated lean animals. CONCLUSIONS: Ciliary neurotrophic factor (CNTF) causes 1) weight loss, 2) improvement of diabetes, and 3) alterations in gallbladder motility that is improved in obese mice but decreased in lean mice. We conclude that CNTF may improve gallbladder contractility in leptin-resistant obesity with diabetes.

Altered small intestinal absorptive enzyme activities in leptin-deficient obese mice: influence of bowel resection.

BACKGROUND: Residual bowel increases absorption after massive small bowel resection. Leptin affects intestinal adaptation, carbohydrate, peptide, and lipid handling. Sucrase, peptidase, and acyl coenzyme A:monoacylglycerol acyltransferase (MGAT) are involved in carbohydrate, protein, and lipid absorption. We hypothesized that leptin-deficient obese mice would have altered absorptive enzymes compared with controls before and after small bowel resection. METHODS: Sucrase, peptidase (aminopeptidase N [ApN], dipeptidyl peptidase IV [DPPIV]), and MGAT activities were determined from lean control (C57BL/6J, n = 16) and leptin-deficient (Lep(ob), n = 16) mice small bowel before and after 50% resection. RESULTS: Ileal sucrase activity was greater in obese mice before and after resection. Jejunal ApN and DPPIV activities were lower for obese mice before resection; ileal ApN activity was unaltered after resection for both strains. Resection increased DPPIV activity in both strains. Jejunal MGAT in obese mice decreased postresection. In both strains, ileal MGAT activity decreased after resection, and obese mice had greater activity in remnant ileum. CONCLUSIONS: After small bowel resection, leptin-deficient mice have increased sucrase activity and diminished ileal ApN, DPPIV, and MGAT activity compared with controls. Therefore, we conclude that leptin deficiency alters intestinal enzyme activity in unresected animals and after small bowel resection. Altered handling of carbohydrate, protein, and lipid may contribute to obesity and diabetes in leptin-deficient mice.

Interictal and postictal circadian and ultradian luteinizing hormone secretion in men with temporal lobe epilepsy.

PURPOSE: Hypothalamic regulation of the reproductive axis in temporal lobe epilepsy (TLE), represented by the ultradian pulsatile secretion of luteinizing hormone (LH), has been shown to be altered interictally and postictally. Our objective is to determine if epilepsy or seizures disrupt normal circadian fluctuations of LH as well as circadian organization of ultradian bursts of LH. METHODS: We characterized LH secretion in 10 men with TLE during two 24-h blocks: an interictal epoch and a postictal epoch initiated by a seizure. Serum LH was measured every 10 min and characterized by circadian and ultradian patterns with cosinor and deconvolution analysis. RESULTS: Mean peak serum concentrations of LH occurred at approximately 0400 in controls, were significantly delayed approximately 5 h interictally, and were randomly distributed postictally. Burst amplitudes differed significantly by phase among controls, with the largest amplitudes between 0101 and 0700 and the smallest between 1301 and 1900. No phase differences were present in interictal or postictal epochs. Burst frequency weakly but significantly was slowest between 0101 and 0700 in controls, but did not differ significantly by phase in either interictal or postictal epochs. Postictal LH burst frequencies, but not amplitudes, were significantly decreased immediately postictally. CONCLUSION: The pulsatile secretion of LH in TLE is abnormal both in the circadian as well as the ultradian domain. Interictal effects consist mainly in loss of circadian fluctuations in LH burst amplitude, whereas postictal effects consist of altered burst timing. Altered daily patterns of neuroendocrine signals may underlie other disorders of homeostasis in TLE.

Predicting quality of life six months after traumatic injury.

BACKGROUND: Many factors are known to impact quality of life (QoL) after injury, but predictors of diminished QoL and the time course of recovery remain incompletely understood. This study examines predictors and correlates of QoL measured by the Short Form-36 (SF-36) one and six months postinjury. METHODS: Adults with nonneurologic blunt injury were prospectively enrolled. Demographic, injury, and socioeconomic data were collected. Patients were assessed with functional and psychologic measures. In all, 196 patients had 1-month data and 123 had 6-month data available. Scores were compared at each time point and also to population norms using t-tests. Multiple regression techniques were used to identify associations between the physical and mental component scores (PCS & MCS) of the SF-36 and patient characteristics. RESULTS: PCS scores improved significantly (32.8 +/- 0.9 versus 41.3 +/- 1.0, p < 0.05) whereas MCS scores (47.5 +/- 1.1 versus 47.2 +/- 1.1, p = NS) did not. Both remained significantly below population norms. Functional Independence Measure (FIM) at one month was predictive of PCS at 6 months. Posttraumatic stress disorder (PTSD) was predictive of lower MCS, and depression was associated with poor MCS. Injury Severity Score was not associated with PCS or MCS. CONCLUSIONS: Overall physical and mental QoL measured by the SF-36 remains significantly below population norms 6 months after traumatic injury. It is possible to identify patients at risk for diminished QoL early during recovery by screening for functional status, PTSD, social support, and depression. Interventions to address these areas should be further studied with respect to their impact on long-term QoL.

Correlation of SF-12 and SF-36 in a trauma population.

BACKGROUND: The SF-36 is a commonly used general measure of health-related quality of life (QoL). The SF-12 is a related tool with less response burden, but its performance in a general trauma population is unknown. HYPOTHESIS: The SF-12 would provide similar QoL information to the SF-36 in blunt trauma patients. METHODS: Adults with nonneurological blunt injury were prospectively enrolled. Demographic, injury, and socioeconomic data were collected. Patients were assessed with functional and psychologic questionnaires 1 and 6 months after injury. Physical (PCS) and mental (MCS) component scores of the SF-36 and SF-12 were compared using Pearson's correlation coefficient. Linear regression identified factors associated with the SF-12 and SF-36 PCS and MCS. Responsiveness to change was assessed using the standardized response mean. RESULTS: Correlation of the PCS was 0.924 and MCS was 0.925 (both P < 0.001). QoL remained below population norms at 6 months. PCS was moderately responsive to change and was equivalent using either the SF-12 or the SF-36. MCS was not responsive to change using either tool. At both time points, at least 25% of patients with normal SF-12 PCS or MCS had SF-36 subscale scores significantly below the normal population. CONCLUSIONS: The SF-12 can be used to assess QoL in trauma patients. The lack of responsiveness to change of the MCS suggests other methods may be necessary to fully evaluate mental QoL. Summary scores may not be sufficient to fully assess QoL in this population. Combining the SF-12 with measures to assess psychosocial variables should be further investigated.

Chemoembolization in patients at high risk: results and complications.

PURPOSE: Transarterial chemoembolization (TACE) has become a standard treatment option for unresectable hepatocellular carcinoma (HCC) and is often used to palliate hepatic metastases. Many patients who are candidates for TACE present with poor hepatic reserve, advanced tumor stage with major portal vein (PV) invasion or thrombosis, and/or biliary dilation. These factors have been associated with a poor prognosis and increased complications after chemoembolization. Accordingly, these patients are classified as being at high risk and may not be considered for therapy. The aim of this study is to evaluate the results of TACE in these patients. MATERIALS AND METHODS: Over a period of 5 years, 141 patients underwent 355 TACE procedures. Thirty-six patients (26%) were in the high-risk group as a result of major PV thrombosis, increased serum bilirubin level (>2 mg/dL), and/or intrahepatic biliary dilation. HCC was the underlying tumor in 60% of patients. Thirty-seven percent of patients had Child-Pugh class B/C disease. Patients in the high-risk group received more selective embolization with fewer particles and fewer procedures (2.0 vs 2.7; P < .04). RESULTS: Patients in the high-risk group were more likely to have HCC (83% vs 51%; P < .01) and were also more likely to have advanced disease according to Child-Pugh classification versus patients in the low-risk group (49% vs 20%; P < .01). The overall complication rate was 4.3%, with no significant difference in complication rate between groups (3.2% vs 8.2%; P = .12). The overall 30-day mortality rate was 2.3%, and no significant difference in 30-day mortality rate was observed between the high- and low-risk groups (5.5% vs 1.4%; P = .11). A trend toward increased survival in the low-risk group did not reach statistical significance. CONCLUSIONS: These data suggest that patients with advanced disease and decreased hepatic reserve who are treated with TACE exhibit no significant increase in morbidity or mortality and no significant decrease in survival. With variations in technique, TACE can be performed safely in patients with the relative risk factors that may classify them in high-risk groups.

Leptin increases small intestinal response to cholecystokinin in leptin-deficient obese mice.

INTRODUCTION: Leptin receptors are present in the jejunum, ileum, and vagal neurons. Leptin increases duodenal secretion of cholecystokinin (CCK) and acts with CCK on vagal mechanoreceptors in the regulation of small intestinal motility. We have demonstrated that leptin-deficient (Lepob) obese mice have increased jejunal and normal ileal responses to CCK. Therefore, we hypothesized that leptin administration alters small intestinal motility observed in leptin-deficient obese mice. MATERIALS AND METHODS: Twelve-week-old female leptin-deficient (Lepob) obese mice received either saline (n=12) or 5 microg/g leptin ip (n=12) injections daily. After 4 weeks, jejunal and ileal segments were harvested, mounted in an organ bath, and reacted with acetylcholine (ACh, 10(-5)M) and CCK (10(-8,-7,-6)M). Data were expressed as N/cm2 and compared by ANOVA and Student's t test. RESULTS: The average body weights in the leptin-treated group were significantly decreased compared to those of the saline-treated group (34 versus 49 g, P <0.01). Jejunal responses to ACh within each group were significantly decreased (P <0.05) when compared to ileal responses. No significant differences in responses to ACh were observed between groups. Jejunal responses to 10(-7,-6)M CCK in the leptin-treated group were significantly greater than those in the saline-treated group. Ileal responses in the leptin group were similarly increased at all CCK concentrations. CONCLUSIONS: These data suggest that daily leptin administration for 4 weeks in leptin-deficient (Lepob) obese mice increases jejunal and ileal responses to CCK and does not alter responses to ACh. Therefore, we conclude that regulation of small intestinal motility may be influenced by synergistic action of cholecystokinin and leptin.