These cases illustrate that patients with ileostomies can develop sudden acute electrolyte and acid-base disorders, usually in association with an increase in ileostomy output. The specific disorder that develops appears to depend on the nature of the ileostomy losses, but in all cases was sustained by the acute decrease in glomerular filtration rate that occurred in association with extra cellular fluid volume depletion. The 2 patients with metabolic alkalosis are of particular interest in this regard. The association of metabolic alkalosis with high-volume ileostomy drainage has been reported previously in only 2 patients. One was an infant with cystic fibrosis who rapidly developed severe metabolic alkalosis after placement of an ileostomy. The investigators noted a link between metabolic alkalosis and cystic fibrosis, but did not speculate on the cause in their patient. In that patient and the 2 patients reported here, ileal drainage was characterized by abnormally high chloride concentrations and high volume losses, likely accounting for the nature of the acid-base disorder . In 1 prior report in an adult, metabolic alkalosis(serum bicarbonate level. 32 mmol/L.) also developed rapidly after ileostomy placement, with recorded ileostomy volumes of 1.5-2L/d.

We presume the alkalosis in all these patients was caused by the selective loss of chloride in their ileostomy drainage. Selective chloride depletion is the most common cause of metabolic alkalosis. 12 The cause of the excessively high chloride concentrations in the ileal drainage in these patients is unclear. The patient with cysticfibrosis makes it unlikely that increased secretion of chloride into the gut lumen is responsible because this patient lacks cystic fibrosis transmembrane

regulator (CFTR), the major gut chloride secretory ion channel. 13 More likely, the chloride loss is caused by impaired chloride absorption as a result of rapid transit through the gut. It is possible that a high rate of gastrin chloride secretion (stimulated by high gastrin levels) could also be a contributing factor. We have no information about gastric acid secretion or serum gastrin levels in these patients, but it is note worthy that in both patients, proton pump inhibition was ineffective in reducing ileostomy output. Patient 2 had only 10 cm of ileum remaining, and it is likely that she was in a precarious balance with regard to ileal absorption at all times, so that any cause of increased ileal volume drainage tipped her into alkalosis and volume depletion. On the other hand, patient 1 had virtually all his ileum. He had presumed pancreaticin sufficiency, but this should not have affected his ability to absorb chloride from the smallbowel.

                                                            [J.AJKD,2008;(10)1053]

參考譯文

這些病例說明做過回腸造痿術(shù)的患者，會(huì)迅速發(fā)展為急性水電解質(zhì)紊亂和酸堿平衡失調(diào)，同時(shí)伴隨回腸引流液增加。水電解質(zhì)紊亂和酸堿平衡失調(diào)的程度，取決于切除部分的回腸的生理特性，但幾乎在所有的病例中都持續(xù)存在伴有細(xì)胞外液量減少而發(fā)生的腎小球?yàn)V過率降低。2例伴有代謝性堿中毒的患者，與這個(gè)特別相關(guān)。之前僅報(bào)道過2例患者代謝性堿中毒與回腸造口術(shù)后大量引流的相關(guān)性。其中1例是有回腸纖維糞性病的嬰兒，在進(jìn)行回腸造口術(shù)后迅速發(fā)生代謝性堿中毒。研究者認(rèn)為回腸纖維囊性病與代謝性堿中毒存在線性關(guān)系,但是沒有推測(cè)出它的原因。在上面提到的病例和本文的2例病例中,回腸引流物不但量很大，而且有異常高的氯化物，也許可以說明的酸堿平衡失調(diào)的本質(zhì)。在此前報(bào)道的1例成人回腸造口術(shù)后,日回腸引流量1.5~2L.并迅速發(fā)生代謝性堿中毒(血清碳酸氫鹽32mmol/L)。

我們推測(cè)所有患者的代謝性堿中毒,都是由于回腸造口引流選擇性的丟失氯化物。選擇性氯化物丟失是最為常見的代謝性堿中毒原因。目前尚不清楚是什么原因?qū)е禄啬c引流液中大量高氯化合物丟失?；颊卟淮罂赡艽罅糠置诼然锏侥c道中,因?yàn)檫@些患者缺乏纖維囊性細(xì)胞膜調(diào)節(jié)因子,而這些因子是腸道氯離子分泌的主要離子通道。氯化物的大量丟失更有可能是氯離子快速通過腸道時(shí)的吸收障礙。另外有一種可能是氯化物的大量分泌(由于高水平胃泌素刺激)。我們雖然沒有胃酸和血清胃泌素的數(shù)據(jù),這也是沒有價(jià)值的,因?yàn)槲覀兪褂觅|(zhì)子泵抑制藥并沒有減少回腸引流物。病例2只保留了10cm長(zhǎng)的回腸,這極有可能是她在任何時(shí)候都不能保持回腸吸收的平衡，以至于大量回腸液丟失，導(dǎo)致代謝性堿中毒和血容量下降。另一方面，病例1事實(shí)上是保留了他的全部回腸，我們推測(cè)他的大量分泌胰島素，但這不足以促使從小腸吸收氯化物。

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