The addition of a nurse practitioner to an inpatient surgical team results in improved use of resources.

BACKGROUND: Resident work hour restrictions and changes in reimbursement may lead to an adverse effect on the continuity of care of a patient after discharge. This study analyzes whether adding a nurse practitioner (NP) to a busy inpatient surgery service would improve patient care after discharge. METHODS: In 2007, a NP joined a team of 3 surgery attendings. She coordinated the discharge plan and communicated with patients after discharge. We reviewed the records of patients 1 year before (N = 415) and 1 year after (N = 411) the NP joined the team. The discharge courses of the patients were reviewed, and an unnecessary emergency room (ER) visit was defined as an ER visit that did not result in an inpatient admission. RESULTS: The 2 groups were statistically similar with regard to age, race, acuity of the operation, duration of hospital stay, and hospital readmissions. Telephone communication between nurses and discharged patients was 846 calls before the NP and 1,319 calls after the NP, representing an increase of 64% (P < .0001). Visiting nurse, physical therapy, or occupational therapy services were rendered to only 25% of patients before the NP compared to 39% after (P < .0001). There were more unnecessary ER visits before the NP (103/415; 25%) compared to after (54/411; 13%) (P = .001). CONCLUSION: Adding a NP to our inpatient surgery service led to an overall improvement in the use of resources and a 50% reduction in unnecessary ER visits. This study shows that the addition of a NP not only improves continuity of care on discharge but also has the potential to yield financial benefits for the hospital.

COX-2 inhibition results in alterations in nuclear factor (NF)-kappaB activation but not cytokine production in acute pancreatitis.

Acute pancreatitis is characterized by local inflammation and cytokine production, and release is thought to contribute to this process. Nuclear factor (NF)-kappaB activation and cytokine production are linked and inhibition of NF-kappaB has been shown to decrease the severity of pancreatitis. We have shown that inhibition of COX-2 ameliorates pancreatitis; however, the mechanism by which this effect occurs is unclear. Swiss Webster mice were injected intraperitoneally with either saline (control) or caerulein (CAE; 50 mg/kg) hourly for 8 hours; mice receiving CAE were further subdivided to receive saline or the cyclooxygenase-2 (COX-2) selective inhibitor (SC-58125; 10 mg, intraperitoneally) at the time of the first injection of CAE. Pancreata were harvested, histologic sections were scored, and protein was extracted to determine cytokine (interleukin [IL]-6, IL-1beta) levels and NF-kappaB subunits by ELISA and NF-kappaB activation by gel shift. In addition, serum was collected for measurement of cytokines. COX-2 inhibition resulted in decreased inflammation and a decrease in NF-kappaB activation. IL-6 and IL-1beta levels after COX-2 inhibition, however, remained elevated to levels equivalent to those of mice with histologic inflammation after CAE alone. COX-2 inhibition decreases inflammation as well as late-phase NF-kappaB activation but does not diminish levels of inflammatory cytokines, thus suggesting a two-phase activator of NF-kappaB. The attenuation of inflammation, despite unaltered cytokine levels, suggests that cytokines may not be critical for the inflammatory phase of pancreatitis.

Effect of aging on the adaptive and proliferative capacity of the small bowel.

Our society is aging at a rapid rate; the effects of aging on physiologic functions (e.g., small bowel adaptation) are poorly understood. The purpose of this study was to determine the ability of the aged small bowel mucosa to adapt after resection. Young (2-month-old) and aged (24-month-old) F344 rats underwent massive (70%) proximal small bowel resection (SBR) or sham operation; rats were killed at 9 or 16 days after surgery. The remnant small bowel and corresponding sham segments were harvested, weighed, and analyzed for DNA content and villus height. To determine whether the adaptive response after SBR could be enhanced, aged rats underwent SBR or sham operation and were treated with either neurotensin or saline solution (control). SBR resulted in adaptive hyperplasia in the remaining small bowel remnant in both young and aged rats at 9 and 16 days compared with sham animals. At 9 days, significant increases were noted in weight, villus height, and DNA content of the distal remnant in young and aged rats after SBR; the increases were similar in both young and aged rats. At 16 days, both young and aged rats displayed significant increases in remnant weight after SBR. Administration of neurotensin increased the weight of the remnant intestine in aged rats after SBR compared with saline treatment. Our findings demonstrate that aged small bowel mucosa exhibits a proliferative and adaptive capacity in response to SBR that was similar to that of the young animals. In addition, neurotensin administration enhanced the normal adaptive response of the small bowel in aged rats, providing further evidence that neurotensin may be therapeutically useful to augment mucosal regeneration in the early periods after massive SBR.

Cyclooxygenase-2 gene disruption attenuates the severity of acute pancreatitis and pancreatitis-associated lung injury.

BACKGROUND & AIMS: Cyclooxygenase (COX) catalyzes the rate-limiting step in prostaglandin production; the inducible isoform, COX-2, has been implicated in a variety of inflammatory processes. The role of COX in acute pancreatitis and pancreatitis-associated lung injury is not known. METHODS: Acute pancreatitis was induced in Swiss Webster mice or mice deficient in the COX-2 (Ptgs2) or the COX-1 (Ptgs1) genes. Pancreata and lungs were harvested, and histologic sections of these tissues were scored. COX-2 expression, myeloperoxidase activity (a measurement of neutrophil sequestration), and serum amylase levels were determined. RESULTS: Acute pancreatitis was associated with induction of COX-2 expression. Treatment with NS-398 (a COX-2 inhibitor) significantly decreased the severity of pancreatitis. Furthermore, Ptgs2-deficient mice showed minimal histologic evidence of pancreatitis, a marked attenuation in the severity of lung injury, and a significant reduction in myeloperoxidase activity. In contrast, Ptgs1-deficient mice had pancreatitis and pulmonary inflammation, which was as severe or, in some instances, more severe than in the wild-type mice. CONCLUSIONS: Inhibition of COX-2 by either pharmacologic inhibition or selective genetic deletion markedly attenuated the severity of acute pancreatitis. Our findings identify the COX-2 isoform as an important regulator of the severity of acute pancreatitis and pancreatitis-associated lung injury.