Developing patient education to enhance recovery after colorectal surgery through action research: a qualitative study.

OBJECTIVES: To understand the role of preoperative education for patients undergoing colorectal surgery by involving patients, carers and staff in: (1) identifying its perceived value and deficits for enhanced recovery; (2) modifying current education practices to address educational deficits; and (3) evaluating these changes for preparing patients to enhance their recovery. DESIGN: Qualitative study of three cycles of action research using mixed methods within a 24-month naturalistic enquiry to identify, implement and evaluate changes through observations, questionnaires, semistructured longitudinal interviews, focus groups and documentation review. SETTING: A UK 1200-bed National Health Service (NHS) hospital providing colorectal surgery in a small city in a rural county. PARTICIPANTS: Ninety-sevenpatients having colorectal surgery, 19 carers and 22 clinical staff. RESULTS: Themes identified were: (1) knowledge and engagement; (2) situated understanding and confidence building; and (3) partnership and proactive involvement in enhancing recovery. All patients articulated needs to prepare mentally and physically to plan for colorectal surgery and rehabilitation. Patients and carers wanted to counter uncertainty about medical procedures: likely bodily changes, recovery timescales and future. They therefore sought as much personalised, relevant information as possible about their disease, planned surgery and recovery. Staff implemented preoperative education to more specifically inform and respond multimodally to individual needs. CONCLUSIONS: Patients wanted to be proactively involved in managing their recovery to re-engage with their everyday lives. Preoperative education supported this through developing patients' situated understanding of hospital and bodily processes related to colorectal surgery. Situated understanding was achieved through educational product to give knowledge and processes promoting engagement. Multimodal, comprehensive and timely preoperative education on the whole patient pathway facilitates active engagement. Situated understanding increased patients' confidence to work in partnership with healthcare professionals and proactively self-manage recovery.

Cystogram use and outcomes in colorectal surgery involving bladder repair: a clinical audit.

BACKGROUND: The role of routine cystograms after bladder repair during colorectal surgery is unclear so we aimed to evaluate this in our department. METHODS: We conducted a retrospective audit of colorectal surgical patients who had an operation and subsequent cystogram between 2006 and 2011 at the Norfolk and Norwich University Hospital. Data on patient characteristics, operative procedures and findings, and cystogram results were collected from electronic discharge summaries, operative notes and radiological records. RESULTS: A total of 59 operations were included and 92% had documented bladder involvement. The most common indications for surgery were diverticular disease (49%) and neoplastic disease (39%). Operations evaluated included high anterior resection, anterior resection, Hartmann's procedures and sigmoid colectomy. Although all patients had at least one post-operative cystogram, only 46% of cases had instructions documented in the operative note for a cystogram to be arranged. Out of the 59 operations, 4 (7%) had cystograms that showed a leak. Repeat cystography in these cases showed no leak or smaller leak and no additional procedures were required. Two of the leaks occurred in cases that had extensive bladder involvement or bladder wall sepsis, and two occurred in cases where the operative findings revealed less major bladder pathology. CONCLUSIONS: Our results suggest that majority of cystograms are negative. More studies are needed to evaluate if selective use of cystogram should be performed to reduce unnecessary the risks associated with radiation exposure and contrast exposure.

Canonical Wnt signals combined with suppressed TGFß/BMP pathways promote renewal of the native human colonic epithelium.

BACKGROUND: A defining characteristic of the human intestinal epithelium is that it is the most rapidly renewing tissue in the body. However, the processes underlying tissue renewal and the mechanisms that govern their coordination have proved difficult to study in the human gut. OBJECTIVE: To investigate the regulation of stem cell-driven tissue renewal by canonical Wnt and TGFß/bone morphogenetic protein (BMP) pathways in the native human colonic epithelium. DESIGN: Intact human colonic crypts were isolated from mucosal tissue samples and placed into 3D culture conditions optimised for steady-state tissue renewal. High affinity mRNA in situ hybridisation and immunohistochemistry were complemented by functional genomic and bioimaging techniques. The effects of signalling pathway modulators on the status of intestinal stem cell biology, crypt cell proliferation, migration, differentiation and shedding were determined. RESULTS: Native human colonic crypts exhibited distinct activation profiles for canonical Wnt, TGFß and BMP pathways. A population of intestinal LGR5/OLFM4-positive stem/progenitor cells were interspersed between goblet-like cells within the crypt-base. Exogenous and crypt cell-autonomous canonical Wnt signals supported homeostatic intestinal stem/progenitor cell proliferation and were antagonised by TGFß or BMP pathway activation. Reduced Wnt stimulation impeded crypt cell proliferation, but crypt cell migration and shedding from the crypt surface were unaffected and resulted in diminished crypts. CONCLUSIONS: Steady-state tissue renewal in the native human colonic epithelium is dependent on canonical Wnt signals combined with suppressed TGFß/BMP pathways. Stem/progenitor cell proliferation is uncoupled from crypt cell migration and shedding, and is required to constantly replenish the crypt cell population.

Should the macroscopically normal appendix be removed during laparoscopy for acute right iliac fossa pain when no other explanatory pathology is found?

BACKGROUND: Acute appendicitis remains the most common surgical emergency and although diagnosis should be made on clinical grounds, sometimes this can be difficult. Laparoscopy has gained increasing favour as a method of both investigating right iliac fossa pain and treating the finding of appendicitis. The aim of this study was to determine the accuracy of intraoperative diagnosis of appendicitis. PATIENTS AND METHODS: Records of all patients who underwent laparoscopy for possible appendicitis at the Norfolk and Norwich University Hospital over a 1-year period were reviewed. Notes of those patients who underwent an open appendicectomy were also reviewed for comparison. Intraoperative findings were recorded, as were the subsequent pathologic findings. RESULTS: Over the 1-year period from September 2005 to September 2006, 355 operations for suspected appendicitis were performed. In 277 (78%) cases, these were performed laparoscopically. Seventy-three out of 78 open appendectomies were confirmed as appendicitis. Only 1 of these was not macroscopically evident to the surgeon. The appendix was removed in 259 of the 277 laparoscopic procedures. Correct intraoperative diagnosis was made in 217 (84%) of removed appendices, 12 (29%) of the appendices thought to be macroscopically normal and removed were found to be appendicitis after histologic examination. Eighteen patients undergoing the laparoscopic procedure had their appendix left in situ due to normal appearance; none had represented at 6 months postsurgery. CONCLUSIONS: Laparoscopy may aid in the diagnosis of acute right iliac fossa pain. However, intraoperative diagnosis is not easy with almost one-third of apparently normal appendices being inflamed histologically. We would therefore advocate the removal of a normal looking appendix in the absence of other explanatory pathology.

The SPINK1 N34S variant is associated with acute pancreatitis.

OBJECTIVE: Acute pancreatitis (AP) is a disease whose pathogenesis remains largely obscure. Genetic research has focussed attention upon the role of the pancreatic protease/protease inhibitor system. The aim of this study was to investigate the prevalence of genetic variants of the trypsin inhibitor, SPINK1, in acute pancreatitis. METHODS: We genotyped 468 patients with AP and 1117 healthy controls for SPINK1 alterations by single-strand conformation polymorphism analysis and by melting curve analysis using fluorescence resonance energy transfer probes. RESULTS: The c.101A>G (p.N34S) variant was detected in 24/936 alleles of patients and in 18/2234 alleles of healthy controls (odds ratio=3.240; 95% confidence interval: 1.766-5.945; P<0.001). In the UK patients, the mean age of patients with N34S was 11.9 years younger compared with N34S negative patients (P=0.023), but this was not apparent in the German patients. Allele frequencies for the c.163C>T (p.P55S) variant did not differ between patients and controls. CONCLUSION: The SPINK1 N34S variant is associated with acute pancreatitis. This supports the importance of premature protease activation in the pathogenesis of AP and suggests that mutated SPINK1 may predispose certain individuals to develop this disease.

The value of routine histopathological examination of appendicectomy specimens.

BACKGROUND: Appendicectomy specimens removed from patients with suspected acute appendicitis often appear macroscopically normal but histopathological analysis of these cases may reveal a more sinister underlying pathology. We evaluated histopathological reports of 1225 appendicectomy specimens at the Norfolk and Norwich University Hospital (NNUH) over the past three years. METHODS: Histopathology reports for all appendices analysed at the NNUH between March 2003 and March 2006 were reviewed by examination of the case notes. The analysis focussed on the confirmation of acute appendicitis, incidental unexpected incidental findings other than inflammation, whether these abnormalities were suspected on gross examination at the time of surgery, and the effect on patient management and prognosis. RESULTS: The histopathology reports disclosed a variety of abnormal incidental lesions. Of the 1225 specimens, 46 (3.75%) revealed abnormal diagnoses other than inflammatory changes. Twenty-four (1.96%) of these were clinically significant and affected further patient management. Only two of these (0.16%) were suspected on macroscopic examination intra-operatively. CONCLUSION: Twenty-four of the 1225 specimens (1.96%) had an impact on patient management or outcome and were not suspected on macroscopic examination at the time of surgery. These would have been missed had the specimens not been examined microscopically. The intra-operative diagnosis of the surgeon is therefore unreliable in detecting abnormalities of the appendix. This study supports the sending of all appendicectomy specimens for routine histopathological examination.

Tumour necrosis factor microsatellite haplotypes are associated with chronic pancreatitis.

CONTEXT: Alcohol is the major aetiological agent for both chronic pancreatitis and alcoholic liver disease. However, as only a minority of alcoholics develop either chronic pancreatitis or alcoholic liver disease, there are clearly genetic or environmental cofactors that determine individual susceptibility to these diseases. OBJECTIVE: To determine whether polymorphisms of the TNF gene may account for individual susceptibility to develop chronic pancreatitis or alcoholic liver disease. DESIGN: A controlled study. PATIENTS: We analyzed 73 patients with chronic pancreatitis, 103 healthy controls, 39 patients with alcoholic liver disease and 29 alcoholics without liver or pancreatic disease. RESULTS: The intermediate/low TNF secreting haplotype a6b5c1d3e3 was over-represented in chronic pancreatitis compared to healthy controls (OR=2.08; 95% CI: 1.07-4.06); P=0.019) and in alcoholic chronic pancreatitis compared to healthy controls (OR=2.08; 95% CI: 1.01-4.29; P=0.029). The high TNF secreting haplotypes, a2b3c1d1e3 and a2b5c2d4e3 were under-represented in chronic pancreatitis compared to healthy controls (OR=0.48; 95% CI: 0.22-1.04; P= 0.043) and in alcoholic chronic pancreatitis compared to alcoholic controls (OR=0.20; 95% CI: 0.05-0.77; P=0.014), respectively. CONCLUSION: A reduced capacity to produce TNF may be responsible for the induction of chronic pancreatitis.