Although the patient exhibited a A-1210477 mouse transient improvement during the immediate postoperative period, she eventually died 24h later from multiple organ failure. Histology showed transmural colonic necrosis without evidence of a thromboembolic

process or vasculitis. Therefore, the aetiology was felt to be a low flow state within the intestinal circulation most likely secondary to the cardiac arrest. Discussion The colon presents weak points on blood supply and poor autoregulation of blood flow that constitute the main predisposing factors for splachnic vasoconstriction and non-occlusive ischaemia [1]. Following experiments on flow characteristics within the mesenteric circulation when subjected to changing haemodynamics, Nikas D et al. found that the colon has the greatest sensitivity to hypotension [14]. An experimental model has also been used involving cardiogenic shock produced by pericardial tamponade [15]. This was associated with marked reductions in the intestinal blood flow. More recently Toung et al.[16], in another experimental model, involved variable degrees of hypovolaemic shock produced by graded levels of haemorrhage, from 12.5 to 50% of the calculated blood volume. This was associated with disproportional mesenteric ischaemia

due to mesenteric vasoconstriction. They concluded that like cardiogenic shock, haemorrhagic shock generates selective mesenteric ischaemia by producing a VX-689 manufacturer disproportionate mesenteric

vasospasm that, which is mediated primarily by the https://www.selleckchem.com/products/ca-4948.html renin-angiotensin axis. Both haemorrhagic and cardiogenic shocks can result in decreased perfusion pressure, prompting selective vasoconstriction of the mesenteric arterioles to maintain perfusion pressure of the vital organs, at the selective expense of the mesenteric organs. The response to any of these conditions can, variably Sitaxentan and unpredictably, cause haemorrhagic gastric stress erosions, non-occlusive mesenteric ischaemia of the small bowel, ischaemic colitis, ischaemic hepatitis, acalculous cholecystitis, and ischaemic pancreatitis. Injury to the mesenteric organs can also initiate the systemic inflammatory response syndrome and, consequently, multiple organ failure [17, 18]. Post-traumatic shock-associated colonic ischaemia has been previously reported in young, healthy patients and has involved primarily the right colon in most instances [1–5]. Only a few cases of extensive non-occlusive colonic necrosis have been reported [6–10] (Table 1). In all cases this entity has been attributed to decreased colonic perfusion but other factors could also have been involved, such as inadequate collateral circulation and increased plasma viscosity [8].