Optimizing perioperative Crohn's disease management: role of coordinated medical and surgical care.

AIM: To investigate rates of re-establishing gastroenterology care, colonoscopy, and/or initiating medical therapy after Crohn's disease (CD) surgery at a tertiary care referral center. METHODS: CD patients having small bowel or ileocolonic resections with a primary anastomosis between 2009-2012 were identified from a tertiary academic referral center. CD-specific features, medications, and surgical outcomes were abstracted from the medical record. The primary outcome measure was compliance rates with medical follow-up within 4 wk of hospital discharge and surveillance colonoscopy within 12 mo of surgery. RESULTS: Eighty-eight patients met study inclusion criteria with 92% (n=81) of patients returning for surgical follow-up compared to only 41% (n=36) of patients with documented gastroenterology follow-up within four-weeks of hospital discharge, P<0.05. Factors associated with more timely postoperative medical follow-up included younger age, longer length of hospitalization, postoperative biologic use and academic center patients. In the study cohort, 75.0% of patients resumed medical therapy within 12 mo, whereas only 53.4% of patients underwent a colonoscopy within 12 mo of surgery. CONCLUSION: Our study highlights the need for coordinated CD multidisciplinary clinics and structured handoffs among providers to improve of quality of care in the postoperative setting.

Implementation of surgical quality improvement: auditing tool for surgical site infection prevention practices.

BACKGROUND: Surgical site infections are a potentially preventable patient harm. Emerging evidence suggests that the implementation of evidence-based process measures for infection reduction is highly variable. OBJECTIVE: The purpose of this work was to develop an auditing tool to assess compliance with infection-related process measures and establish a system for identifying and addressing defects in measure implementation. DESIGN: This was a retrospective cohort study using electronic medical records. SETTING: We used the auditing tool to assess compliance with 10 process measures in a sample of colorectal surgery patients with and without postoperative infections at an academic medical center (January 2012 to March 2013). PATIENTS: We investigated 59 patients with surgical site infections and 49 patients without surgical site infections. MAIN OUTCOME MEASURES: First, overall compliance rates for the 10 process measures were compared between patients with infection vs patients without infection to assess if compliance was lower among patients with surgical site infections. Then, because of the burden of data collection, the tool was used exclusively to evaluate quarterly compliance rates among patients with infection. The results were reviewed, and the key factors contributing to noncompliance were identified and addressed. RESULTS: Ninety percent of process measures had lower compliance rates among patients with infection. Detailed review of infection cases identified many defects that improved following the implementation of system-level changes: correct cefotetan redosing (education of anesthesia personnel), temperature at surgical incision >36.0°C (flags used to identify patients for preoperative warming), and the use of preoperative mechanical bowel preparation with oral antibiotics (laxative solutions and antibiotics distributed in clinic before surgery). Quarterly compliance improved for 80% of process measures by the end of the study period. LIMITATIONS: This study was conducted on a small surgical cohort within a select subspecialty. CONCLUSIONS: The infection auditing tool is a useful strategy for identifying defects and guiding quality improvement interventions. This is an iterative process requiring dedicated resources and continuous patient and frontline provider engagement.

Measuring briefing and checklist compliance in surgery: a tool for quality improvement.

Operating room briefings improve patient outcomes; however, implementation and methods to measure are lacking. A briefing audit tool was developed with 4 domains: briefing logistics, briefing basics, specific briefing content, and briefing participation. The tool evaluated preoperative briefings across surgical services at an academic medical center. Sixty-three preoperative briefings were observed. Introduction by name and role occurred in 15% of cases. There was a wide variation in discussion of the critical goals of the surgical procedure among services D (100%), A (26%), B (19%), and C (0%). Participation in the briefing was variable among stakeholders and between services. Verbal contributions were variable across all roles ranging from 65% (surgeons) to 11% (trainees and surgical technologist). Preoperative briefing compliance is variable. Deficiencies varied between service lines, possibly highlighting the need for service-specific customization of the briefing tool in surgery. This tool is a practical method for the study of briefing implementation.

Hospital readmission by method of data collection.

BACKGROUND: Hospital readmissions are increasingly used to pay hospitals differently. We hypothesized that readmission rates, readmissions related to index admission, and potentially unnecessary readmissions vary by data collection method for surgical patients. STUDY DESIGN: Using 3 different data collection methods, we compared 30-day unplanned readmission rates and potentially unnecessary readmissions among colorectal surgery patients at a single institution between July 2009 and November 2011. We compared the NSQIP clinical reviewer method, the University HealthSystem Consortium (UHC) administrative billing data method, and physician medical record review. RESULTS: Seven hundred and thirty-five colorectal surgery patients were identified with readmission rates as follows: NSQIP 14.6% (107 of 735) vs UHC 17.6% (129 of 735). The NSQIP method identified 9 readmissions not found in billing records because the readmission occurred at another hospital (n = 7) or due to a discrepancy in definition (n = 2). The UHC method identified 31 readmissions not identified by NSQIP because of a broader readmission definition (n = 20) or were missed by reviewers (n = 11). The NSQIP method identified 72% of readmissions as related to index admission and physician chart review identified 83%. The UHC method identified 51% of readmissions as related to index admission and physician chart review identified 86%. Sixty-six of 129 UHC readmissions (51%) were deemed potentially preventable; based on physician chart review, 112 of 129 readmissions (87%) were deemed clinically necessary at the time of presentation. Most readmissions were due to surgical site infections (46 of 129 [36%]) and dehydration (30 of 129 [23%]). With improved patient-care efforts, 41 of 129 (31.8%) complications might not have required readmission. CONCLUSIONS: Readmission rates and unnecessary readmissions vary depending on data collection methodology. Reimbursements based on readmission should use standardized and fair methods to minimize perverse incentives that penalize hospitals for appropriate care of high-risk surgical patients.

Implementation of a surgical comprehensive unit-based safety program to reduce surgical site infections.

BACKGROUND: Surgical site infections (SSI) are a common and costly problem, prolonging hospitalization and increasing readmission. Adherence to well-known infection control process measures has not been associated with substantial reductions in SSI. To date, the global burden of preventable SSI continues to result in patient harm and increased health care costs on a broad scale. STUDY DESIGN: We designed a study to evaluate the association between implementation of a surgery-based comprehensive unit-based safety program (CUSP) and postoperative SSI rates. One year of pre- and post-CUSP intervention SSI rates were collected using the high-risk pilot module of the American College of Surgeons National Surgical Quality Improvement Program (July 2009 to July 2011). The CUSP group met monthly and consisted of a multidisciplinary team of front-line providers (eg, surgeons, nurses, operating room technicians, and anesthesiologists) who were directly involved in the care of colorectal surgery patients. Surgical Care Improvement Project process measure compliance was monitored using standard methods from the Centers for Medicare and Medicaid Services. RESULTS: In the 12 months before implementation of the CUSP and interventions, the mean SSI rate was 27.3% (76 of 278 patients). After commencement of interventions, the rate was 18.2% (59 of 324 patients) for the subsequent 12 months--a 33.3% decrease (95% CI, 9-58%; p < 0.05). The interventions included standardization of skin preparation; administration of preoperative chlorhexidine showers; selective elimination of mechanical bowel preparation; warming of patients in the preanesthesia area; adoption of enhanced sterile techniques for skin and fascial closure; addressing previously unrecognized lapses in antibiotic prophylaxis. There was no difference in surgical process measure compliance as measured by the Surgical Care Improvement Project during the same time period. CONCLUSIONS: Formation of small groups of front-line providers to address patient harm using local wisdom and existing evidence can improve patient safety. We demonstrate a surgery-based CUSP intervention that might have markedly decreased SSI in a high-risk population.

Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats.

Findings from our laboratory and others have demonstrated that the hormone insulin has chronic effects within the CNS to regulate energy homeostasis and to decrease brain reward function. In this study, we compared the acute action of insulin to decrease intake of a palatable food in two different behavioral tasks-progressive ratios sucrose self-administration and micro opioid-stimulated sucrose feeding-when administered into several insulin-receptive sites of the CNS. We tested insulin efficacy within the medial hypothalamic arcuate (ARC) and paraventricular (PVN) nuclei, the nucleus accumbens, and the ventral tegmental area. Administration of insulin at a dose that has no chronic effect on body weight (5 mU) into the ARC significantly suppressed sucrose self-administration (75+/-5% of paired control). However, although the mu opioid DAMGO, [D-Ala2,N-MePhe4,Gly5-ol]-enkephalin acetate salt, stimulated sucrose intake at all four CNS sites, the ventral tegmental area was the only sensitive site for a direct effect of insulin to antagonize acute (60 min) micro opioid-stimulated sucrose feeding: sucrose intake was 53+/-8% of DAMGO-induced feeding, when insulin was coadministered with DAMGO. These findings demonstrate that free feeding of sucrose, and motivated work for sucrose, can be modulated within unique sites of the CNS reward circuitry. Further, they support the interpretation that adiposity signals, such as insulin, can decrease different aspects of ingestion of a palatable food, such as sucrose, in an anatomically specific manner.

Deconstructing the vanilla milkshake: the dominant effect of sucrose on self-administration of nutrient-flavor mixtures.

Rats and humans avidly consume flavored foods that contain sucrose and fat, presumably due to their rewarding qualities. In this study, we hypothesized that the complex mixture of corn oil, sucrose, and flavor is more reinforcing than any of these components alone. We observed a concentration-dependent increase in reinforcers of sucrose solutions received (0%, 3%, 6.25%, and 12.5%) in both fixed ratio and progressive ratio procedures, but with equicaloric corn oil solutions (0%, 1.4%, 2.8%, and 5.6%) this finding was replicated only in the fixed ratio procedure. Likewise, addition of 1.4% oil to 3% or 12.5% sucrose increased fixed ratio, but not progressive ratio, reinforcers received relative to those of sucrose alone. Finally, addition of 3% vanilla flavoring did not change self-administration of 3% sucrose or 3% sucrose+1.4% oil solutions. These data suggest that, calorie-for-calorie, sucrose is the dominant reinforcing component of novel foods that contain a mixture of fat, sucrose, and flavor.

Intraventricular insulin and leptin decrease sucrose self-administration in rats.

Data from our laboratory and others have demonstrated an effect of the candidate adiposity signals insulin and leptin to decrease brain reward function, as assessed by lateral hypothalamic self-stimulation and food-conditioned place preference. In this study, we evaluated the effect of centrally administrated insulin or leptin to acutely decrease motivated performance for 5% sucrose, i.e., progressive ratio (PR) sucrose self-administration. Consistent with findings using other behavioral assays, both insulin and leptin significantly decreased the number of bar presses (62+/-7 and 76+/-8% of paired controls respectively), and the number of sucrose rewards obtained (87+/-4 and 91+/-4% of paired controls respectively), relative to within-subjects' control day performance on PR sucrose self-administration, whereas acute intraventricular cerebrospinal fluid had no effect. Rats fed a higher fat diet for 5 weeks were resistant to the effects of the intraventricular insulin or leptin, suggesting a central resistance to their action. Thus the findings of this study extend and support previous observations which suggest that neuroendocrine signals which regulate energy homeostasis in the CNS may also play a role in modulating reward circuitry, and specifically, food reward.

Inactivation of the DMH selectively inhibits the ACTH and corticosterone responses to hypoglycemia.

We have previously reported that repeated bouts of insulin-induced hypoglycemia (IIH) in the rat result in blunted activation of the paraventricular, arcuate, and dorsomedial hypothalamic (DMH) nuclei. Because DMH activation has been implicated in the sympathoadrenal and hypothalamic-pituitary-adrenal (HPA) responses to stressors, we hypothesized that its blunted activation may play a role in the impaired counterregulatory response that is also observed with repeated bouts of IIH. In the present study, we evaluated the role of normal DMH activation in the counterregulatory response to a single bout of IIH. Local infusion of lidocaine (n = 8) to inactivate the DMH during a 2-h bout of IIH resulted in a significant overall decrease of the ACTH response and a delay of onset of the corticosterone response compared with vehicle-infused controls (n = 9). We observed suppression of the ACTH response at time (t) = 90 and 120 min (50 +/- 12 and 63 +/- 6%, respectively, of control levels) and early suppression of the corticosterone response at t = 30 min (59 +/- 13% of the control level). The epinephrine, norepinephrine, and glucagon responses were not altered by DMH inactivation. Our finding suggests that DMH inactivation may play a specific role in decreasing the HPA axis response after repeated bouts of IIH.

Expression of simian immunodeficiency virus (SIV) nef in astrocytes during acute and terminal infection and requirement of nef for optimal replication of neurovirulent SIV in vitro.

As the most numerous cells in the brain, astrocytes play a critical role in maintaining central nervous system homeostasis, and therefore, infection of astrocytes by human immunodeficiency virus (HIV) or simian immunodeficiency virus (SIV) in vivo could have important consequences for the development of HIV encephalitis. In this study, we establish that astrocytes are infected in macaques during acute SIV infection (10 days postinoculation) and during terminal infection when there is evidence of SIV-induced encephalitis. Additionally, with primary adult rhesus macaque astrocytes in vitro, we demonstrate that the macrophage-tropic, neurovirulent viruses SIV/17E-Br and SIV/17E-Fr replicate efficiently in astrocytes, while the lymphocyte-tropic, nonneurovirulent virus SIV(mac)239 open-nef does not establish productive infection. Furthermore, aminoxypentane-RANTES abolishes virus replication, suggesting that these SIV strains utilize the chemokine receptor CCR5 for entry into astrocytes. Importantly, we show that SIV Nef is required for optimal replication in primary rhesus macaque astrocytes and that normalizing input virus by particle number rather than by infectivity reveals a disparity between the ability of a Nef-deficient virus and a virus encoding a nonmyristoylated form of Nef to replicate in these central nervous system cells. Since the myristoylated form of Nef has been implicated in functions such as CD4 and major histocompatibility complex I downregulation, kinase association, and enhancement of virion infectivity, these data suggest that an as yet unidentified function of Nef may exist to facilitate SIV replication in astrocytes that may have important implications for in vivo pathogenesis.

Inactivation of the PVN during hypoglycemia partially simulates hypoglycemia-associated autonomic failure.

The anatomic connections of the paraventricular nucleus of the hypothalamus (PVN) are such that it is ideally situated to modulate and/or control autonomic responses to a variety of stressors, including hypoglycemia. In our experimental model of hypoglycemia-associated autonomic failure (HAAF), a syndrome in which the counterregulatory response to hypoglycemia is partially compromised via unknown mechanisms, activation of the PVN is blunted (15). We hypothesized that this blunted PVN activation during HAAF may be sufficient to cause the impaired counterregulatory response. To test this hypothesis, we anesthetized the PVN with lidocaine during insulin-induced hypoglycemia in rats and measured counterregulatory hormone levels. PVN inactivation decreased indexes of the sympathoadrenal response (plasma epinephrine and norepinephrine) and the hypothalamic-pituitary axis response (ACTH). Inactivation decreased the peak epinephrine response to hypoglycemia by almost half (-42 +/- 6% from control; P = 0.04) and the peak norepinephrine response by 34 +/- 5% (P = 0.01). The peak plasma ACTH levels attained were suppressed by 35 +/- 6% (P = 0.02). Adrenal corticosterone and pancreatic glucagon responses were not impaired. This pattern of neuroendocrine response is unlike that previously seen with our HAAF model. Control infusions of lidocaine >or=1 mm anterior or posterior to the PVN did not simulate this neuroendocrine pattern. Thus it appears that decreased PVN activation, as occurs with HAAF, may be involved in specific components of HAAF (i.e., blunting the sympathoadrenal and hypothalamic-pituitary-adrenocortical axis response), but not in others (i.e., blunting the glucagon response).