The role of the gut in major surgical postoperative morbidity.
Gut mucosal hypoperfusion has been termed the motor of multiple organ failure. While a large proportion of high-risk surgery proceeds unremarkably, the insult to the inflammatory system during perioperative periods of regional hypoperfusion may manifest themselves over the subsequent few days, leading to microvascular thrombi, organ dysfunction, and failure. Several approaches have been made to prevent this, including systemic optimization of the cardiovascular system and specific targeting of the splanchnic circulation with monitoring techniques such as tonometry or metabolic markers of hepatic function to guide fluid and drug therapies. It is believed that in a proportion of patients such methods are not likely to suffice and gut mucosal hypoperfusion is probable. If these patients can be identified preoperatively, then recently developed techniques used prophylactically such as immunonutrition, passive and active immunization, specific antimediator agents, or nonspecific anti-inflammatory agents may help minimize the number of patients progressing to multiple organ dysfunction and failure. Techniques that may help us identify at-risk patients may include in-depth cardiovascular assessment, possibly with echocardiography or a noninvasive cardiac output monitor such as the suprasternal adaptation of the ODM esophageal Doppler. The measurement of baseline endotoxin immune status (EndoCAb) may select those patients in advance who are most at-risk from gut mucosal hypoperfusion, thus allowing a more rational use of tonometry. Conventional risk scoring systems used in conjunction with knowledge of the type of surgery to be undertaken and whether large fluid shifts are likely along with the less conventional techniques discussed above may enable perioperative therapy to be closer to optimal.
Chieveley-Williams
S
S
Department of Anaesthesia, Middlesex Hospital, London, England.
Hamilton-Davies
C
C
D006348:Cardiac Surgical Procedures; D019446:Endotoxemia / Q000209:etiology* / Q000503:physiopathology*; D004731:Endotoxins / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000503:physiopathology*; D008991:Monitoring, Physiologic; D009102:Multiple Organ Failure / Q000209:etiology* / Q000503:physiopathology*; D010477:Perfusion; D011183:Postoperative Complications / Q000209:etiology* / Q000503:physiopathology*
D004731:Endotoxins; D018836:Inflammation Mediators