Chronic gastrointestinal ischaemia: shifting paradigms

Chronic gastrointestinal ischaemia (CGI) is generally considered to be a rare disease entity. The majority of patients with CGI are only diagnosed after a long period of slowly progressive abdominal symptoms, in some cases with impressive weight loss. These patients may have a broad range of clinical signs and quite often undergo repeated extensive evaluation of their symptoms with negative outcome. The classical triad of symptoms, also known as 'abdominal angina', is defined as the combination of postprandial pain, weight loss due to fear of pain after eating, and an abdominal bruit during physical examination. Recent studies have shed new lights on these long unchallenged concepts. These studies first showed that CGI is more prevalent than previously thought and can occur in patients with both single-and multi-vessel disease. Second, the disease presents with a much wider range in symptoms, and only a minority of patients present with the classical triad. Third, long-term positive outcomes can be achieved after endovascular or surgical revascularisation therapy in large proportion of patients. This knowledge results from a combination of clinical research by dedicated focus groups, the current widespread availability of new imaging techniques such as CT-angiography, the development of new functional tests for assessment of mucosal perfusion, and the evolution of endovascular stenting options. Clinicians diagnosing and treating patients with acute and chronic abdominal conditions have to be aware of these new developments. We therefore here review the new insights on CGI with a focus on epidemiology, pathophysiology, current diagnostics and treatment

Single vessel abdominal arterial disease

The long-standing discussion concerning the mere existence of single vessel abdominal artery disease can be closed: chronic gastrointestinal ischaemia (CGI) due to single vessel abdominal artery stenosis exists, can be treated Successfully and in a safe manner. The most common causes of single vessel CGI are the coeliac artery compression syndrome (CACS) in younger patients, and atherosclerotic disease in elderly patients. The clinical symptoms of single vessel CGI patients are postprandial and exercise-related pain, weight loss, and an abdominal bruit. The current diagnostic approach in patients suspected of single vessel CGI is gastrointestinal tonometry combined with radiological visualisation of the abdominal arteries to define possible arterial stenosis. Especially in single vessel abdominal artery stenosis, gastrointestinal tonometry plays a pivotal role in establishing the diagnosis CGI. First-choice treatment of single vessel CGI remains surgical revascularisation, especially in CACS. In elderly or selected patients endovascular stent placement therapy is an acceptable option. (C) 2008 Elsevier Ltd. All rights reserved

Low incidence of hyperamylasemia after proximal double-balloon enteroscopy: has the insertion technique improved?

Background and study aim: Reported complications of double-balloon enteroscopy (DBE) include post-enteroscopy pancreatitis. Hyperamylasemia after proximal DBE is reported frequently, but the relationship to development of pancreatitis remains unclear. Hyperamylasemia may be related to balloon inflation in the pancreatic head region. The aims of the study were to identify risk factors for hyperamylasemia and to determine the incidence of hyperamylasemia and pancreatitis when a modified cautious DBE insertion protocol was used. Patients and methods: In a prospective study, involving consecutive patients undergoing a proximal DBE, serum amylase activity was assessed immediately before and after the procedure. Results: 135 patients were included (men 78, women 57: mean age 49 years [range 17-88]). The mean total procedure time was 73 minutes (range 30-150 minutes), and mean number of passes during the proximal DBE was 14 (6-24). While patients (17%) developed hyperamylasemia after the DBE procedure, only one patient with hyperamylasemia had clinical symptoms indicating a mild acute pancreatitis (0.7%). Total procedure time and number of passes correlated significantly with the occurrence of hyperamylasemia. Conclusions: We found a low incidence of hyperamylasemia and pancreatitis post-DBE. Theoretically, this could result from the modified insertion technique, with local strain and friction of the small bowel as remaining causes of hyperamylasemia, a notion supported by the significant relation between hyperamylasemia and duration of DBE and total number of passes. We therefore advise use of the cautious insertion technique and, if possible, reduction of duration and of number of passes in every proximal DBE