Anal incontinence after vaginal delivery or cesarean section.

INTRODUCTION: Uncertainties remain as to whether a cesarean section is protective for the short-term and long-term development of anal incontinence. Our aim was to explore whether women who had delivered only vaginally were at greater risk of anal incontinence than nulliparous women and women who had undergone cesarean sections only. MATERIAL AND METHODS: Background information, medical history, and data on anal incontinence (defined as fecal or flatus incontinence weekly or more) reported by women participating in a large population-based health survey in Norway (the Nord-Trøndelag Health Study 3) during the period October 2006 to June 2008 were collected and linked to data from the Medical Birth Registry of Norway. The prevalence of anal incontinence was calculated and multivariate logistic regression analyses were applied. RESULTS: The mean age of the 12 567 women was 49.9 years. The age and educational level of women who had cesarean sections only were similar to those who had a vaginal delivery and obstetric anal sphincter injuries (OASIS). Nulliparous women and those who had a vaginal delivery and no OASIS were older and had higher educational achievements than women who had delivered by cesarean section exclusively, and women with OASIS. One in four women with OASIS reported anal incontinence compared with one in six of the other women (P < .001). Age, educational level, diarrhea, constipation, birthweight, and OASIS increased the risk of anal incontinence in all women. Parity was associated with anal incontinence in parous women only. No differences were found for fecal urgency. CONCLUSIONS: Women with vaginal deliveries complicated by OASIS are at increased risk of anal incontinence. However, no increased risk of anal incontinence was found in nulliparous women or women who had cesarean sections only or vaginal deliveries not complicated by OASIS.

Cytomegalovirus infection and postoperative complications in patients with ulcerative colitis undergoing colectomy.

BACKGROUND: Ulcerative colitis (UC) can be complicated by reactivation of cytomegalovirus (CMV). CMV reactivation may change the course of UC and may require antiviral treatment. Some risk factors of CMV reactivation have previously been identified, whereas the association between CMV reactivation and postoperative complications has not been examined systematically. METHODS: Patients with UC operated with colectomy due to active UC were studied (n = 77). Patient and disease characteristics, as well as postoperative complications were recorded and CMV was detected by immunohistochemical examination of multiple sections from the colectomy specimen. RESULTS: CMV was found in nine (11.7%) colectomy specimens. CMV-positive patients received significantly higher doses of corticosteroids at colectomy than CMV-negative patients (61.1 ± 23 vs 32.5 ± 32 mg/day, p = 0.01). CMV-positive patients were also older, had a higher risk of severe complications, higher American Society of Anesthesiologists (ASA) score, longer preoperative stay, and a higher rate of acute surgery. Complications occurred in 30 (39%) patients after surgery, 8(10.4%) of whom were serious. Two CMV-positive patients (2.6%) died in-hospital after the colectomy. High ASA score was associated with the occurrence of serious complications. CONCLUSION: A relatively small proportion of patients with UC operated by colectomy were CMV positive. CMV positivity was associated with old age, high dose of corticosteroids at operation, high ASA score, acute surgery, and severe postoperative complications. Patients with such characteristics may be at risk of CMV infection and may require special management.

Prevalence of anal incontinence among Norwegian women: a cross-sectional study.

OBJECTIVE: Anal incontinence (AI) is a symptom associated with age, bowel symptoms and obstetric injuries. Primary aim of the study was to establish the prevalence of AI among women and secondarily to evaluate the impact on daily life and conditions associated with AI. DESIGN: A cross-sectional study. SETTING: Participants attended research stations located in different parts of Nord-Trøndelag county, Norway. Data were collected through interviews, questionnaires and clinical examinations. PARTICIPANTS: In total, 40 955 community-dwelling women aged 30 years and older were invited. A total of 25 037 women participated, giving a participation rate of 61.1%. PRIMARY AND SECONDARY OUTCOME MEASURES: Fecal incontinence and flatal incontinence was defined as involuntary loss of feces and flatus weekly or more, respectively. AI was defined as the involuntary loss of feces and/or flatus weekly or more. Urgency was defined as the inability to defer defecation for 15 min. Statistical methods included prevalence estimates and logistic regression analysis. RESULTS: Questions about AI were completed by 20 391 (82.4%) women. Among the 20 391 women, AI was reported by 19.1% (95% CI 18.6% to 19.7%) and fecal incontinence was reported by 3.0% (95% CI 2.8% to 3.2%). Urgency was experienced by 2586 women (12.7%, 95% CI 12.2 to 13.1). Impact on daily life was stated by 794 (26.0%, 95% CI 24.4 to 27.5) women with AI. In bivariate age-adjusted analysis of AI, OR and CI for urgency (OR 3.19, 95% CI 2.92 to 3.49) and diarrhoea (OR 3.81, 95% CI 3.32 to 4.38) revealed strongest associations with AI. CONCLUSIONS: AI affects one in five women older than 30 years. Strongest associated symptoms are urgency and diarrhoea. TRIAL REGISTRATION NUMBER: The study was approved by the Regional Committee for Medical and Health Research Ethics (No. 2009/1214) and followed the Declaration of Helsinki.

Primary sclerosing cholangitis and extraintestinal manifestations in patients with ulcerative colitis and ileal pouch-anal anastomosis.

OBJECTIVE: The aim of this study was to assess complications and functional outcomes in patients having ileal pouch-anal anastomosis for ulcerative colitis with or without primary sclerosing cholangitis or extraintestinal manifestations and to assess if primary sclerosing cholangitis is a risk factor for pouchitis. MATERIALS AND METHODS: From 1984 to 2007, 289 patients underwent proctocolectomy with ileal pouch-anal anastomosis for ulcerative colitis. Mean follow-up time was 12 years and data was recorded prospectively. Eleven patients had primary sclerosing cholangitis, six had pyoderma gangrenosum, and 12 had arthritis or ankylosing spondylitis. RESULTS: Early complications were similar for patients with or without extraintestinal manifestations. Functional outcomes were similar, but more incontinence among patients with sclerosing cholangitis was found. These patients had more frequent pouchitis, 5.25 vs. 2.72 average episodes of pouchitis (p = 0.048), and more chronic pouchitis, 4/11 vs. 17/260 (p < 0.001) compared to patients without adjunct disease. Neoplasm of the colon was more frequent in patients with primary sclerosing cholangitis, 4/11 vs. 4/260 in ulcerative colitis patients (p < 0.001). CONCLUSION: An association between primary sclerosing cholangitis and chronic/severe pouchitis was found, but not with other extraintestinal manifestations. Functional results were good and alike in patients with and without primary sclerosing cholangitis. Primary sclerosing cholangitis is a risk factor for chronic pouchitis and is associated with neoplasia.

Role of bradykinin in gastric vasodilation caused by hypertonic saline and acid back diffusion.

Protective vasodilation in response to tissue injury and acid back diffusion is associated with release of bradykinin in the rat stomach. We hypothesized that bradykinin might be involved in mechanisms behind such vasodilation via influence on mast cells and sensory neurons. Acid back diffusion after mucosal barrier disruption with hypertonic saline evoked degranulation of mast cells in the rat stomach wall. Acid back diffusion was also associated with increased luminal release of histamine and gastric blood flow in normal rats, but not in mast cell-deficient rats. Bradykinin (BK(2)) receptor blockade inhibited degranulation of submucosal mast cells in the stomach and attenuated gastric vasodilation both in response to acid back diffusion and after stimulation of sensory neurons with capsaicin. Gastric vasodilation caused by mucosal injury with hypertonic saline alone was associated with degranulation of mucosal mast cells. These events were unaffected by inhibition of prostaglandin synthesis, whereas bradykinin (BK(2)) receptor blockade was associated with abolished vasodilation and inhibition of mucosal mast cell degranulation. We conclude that bradykinin is involved in gastric vasodilation caused by hypertonic injury alone via influence on mast cells, and by acid back diffusion via influence on both sensory neurons and mast cells.

Histamine is involved in gastric vasodilation during acid back diffusion via activation of sensory neurons.

Protective vasodilation during acid back diffusion into the rat gastric mucosa depends on activation of sensory neurons and mast cell degranulation with histamine release. We hypothesized that these two mediator systems interact and that histamine partly exerts its effect via sensory nerves. Gastric blood flow (GBF) and luminal histamine were measured in chambered stomachs, and mast cell numbers were assessed by morphometry. Ablation of sensory neurons and depletion of mast cells were produced by pretreatment with capsaicin or dexamethasone, respectively. Mucosal exposure to 1.5 M NaCl and then to pH 1.0 saline in ablated and control rats caused increased luminal histamine and reduced numbers of mast cells. Enterochromaffin-like cell marker pancreastatin remained unchanged. Only control rats responded with an increase in GBF. Capsaicin stimulation (640 microM) of the undamaged mucosa induced identical increase in GBF and unchanged mast cell mass in normal and dexamethasone-treated rats. Increase in GBF after topical exposure to histamine (30 mM) in rats pretreated with capsaicin or a calcitonin gene-related peptide (CGRP)(1) antagonist human CGRP(8-37) or exposed to the calcium pore blocker ruthenium red was less than one-half of that in control rats. These data suggest that mast cell-derived histamine is involved in gastric vasodilatation during acid back diffusion partly via sensory neurons.