关键词: acidosis parenteral nutrition serial transverse enteroplasty

Mesh : Humans Child Child, Preschool Adolescent Acidosis, Lactic / etiology therapy Intestinal Volvulus / complications Case-Control Studies Retrospective Studies Intestinal Failure Acidosis / complications Short Bowel Syndrome / complications therapy Lactic Acid Digestive System Abnormalities

来  源:   DOI:10.1002/jpn3.12075   PDF(Pubmed)

Abstract:
BACKGROUND: D-lactic acidosis (DLA) is a serious complication of short bowel syndrome (SBS) in children with intestinal failure (IF). Malabsorbed carbohydrates are metabolized by bacteria in the intestine to D-lactate which can lead to metabolic acidosis and neurologic symptoms.
METHODS: A retrospective chart review was performed in children ≤18 years old with SBS who had one of the following criteria: unexplained metabolic acidosis, neurologic signs or symptoms, history of antibiotic therapy for small bowel bacterial overgrowth, or high clinical suspicion of DLA. Cases had serum D-lactate concentration >0.25 mmol/L; controls with concentrations ≤0.25 mmol/L.
RESULTS: Of forty-six children, median age was 3.16 (interquartile range (IQR): 1.98, 5.82) years, and median residual bowel length was 40 (IQR: 25, 59) cm. There were 23 cases and 23 controls. Univariate analysis showed that cases had significantly lower median bicarbonate (19 vs. 24 mEq/L, p = 0.001), higher anion gap (17 vs. 14 mEq/L, p < 0.001) and were less likely to be receiving parenteral nutrition, compared with children without DLA. Multivariable analysis identified midgut volvulus, history of intestinal lengthening procedure, and anion gap as significant independent risk factors. Midgut volvulus was the strongest independent factor associated with DLA (adjusted odds ratio = 17.1, 95% CI: 2.21, 133, p = 0.007).
CONCLUSIONS: DLA is an important complication of pediatric IF due to SBS. Patients with IF, particularly those with history of midgut volvulus, having undergone intestinal lengthening, or with anion gap acidosis, should be closely monitored for DLA.
摘要:
背景:D-乳酸性酸中毒(DLA)是肠衰竭(IF)儿童短肠综合征(SBS)的严重并发症。吸收不良的碳水化合物被肠道中的细菌代谢为D-乳酸,这可能导致代谢性酸中毒和神经系统症状。
方法:对符合以下标准之一的≤18岁SBS儿童进行回顾性分析:原因不明的代谢性酸中毒,神经系统体征或症状,抗生素治疗小肠细菌过度生长的历史,或临床高度怀疑DLA。病例血清D-乳酸浓度>0.25mmol/L;对照组浓度≤0.25mmol/L
结果:在46名儿童中,中位年龄为3.16(四分位数间距(IQR):1.98,5.82)岁,中位残余肠长为40(IQR:25,59)cm。有23例病例和23例对照。单变量分析表明,病例的碳酸氢盐中位数显着降低(19vs.24mEq/L,p=0.001),较高的阴离子间隙(17与14mEq/L,p<0.001),并且不太可能接受肠外营养,与没有DLA的儿童相比。多变量分析确定了中肠扭转,肠延长手术史,阴离子差作为显著的独立危险因素。中肠扭转是与DLA相关的最强的独立因素(校正比值比=17.1,95%CI:2.21,133,p=0.007)。
结论:DLA是SBS引起的小儿IF的重要并发症。IF患者,特别是那些有中肠扭转病史的人,经历了肠道延长,或者阴离子间隙酸中毒,应该密切监测DLA。
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