Combined Cerebral and Renal Near-Infrared Spectroscopy After Congenital Heart Surgery

The maintenance of an adequate oxygen supply to tissues after congenital heart surgery is essential for good outcomes. The objective of this study was to assess the usefulness of near-infrared spectroscopy (NIRS) for estimating central venous oxygen saturation (ScvO₂) using both cerebral and renal measurements, explore its relation with cardiac output measurements and check its ability to detect low cardiac output. A prospective observational pilot study was conducted in patients weighing <10 kg undergoing cardiopulmonary bypass surgery. Spectroscopy probes were placed on the forehead and renal area, and serial cardiac output measurements were obtained by femoral transpulmonary thermodilution over the first 24 h after surgery. In the 15 patients studied, ScvO₂ was correlated with cerebral (r = 0.58), renal (r = 0.60) and combined (r = 0.71) measurements. Likewise, the systolic index was correlated with the NIRS signals: cerebral (r = 0.60), renal (r = 0.50) and combined (r = 0.66). Statistically significant differences were found in the NIRS measures registered in the 29 low cardiac output events detected by thermodilution: cerebral: 62 % (59–65) versus 69 % (63–76); renal: 83 % (70–89) versus 89 % (83–95); and combined 64 % (60–69) versus 72 % (67–76). In our series, combined cerebral and renal monitoring was correlated with central venous oxygen saturation and cardiac output; low cardiac output detection associated a different spectroscopy pattern.     

新生儿坏死性小肠结肠炎的研究进展

坏死性小肠结肠炎（NEC）是新生儿常见而严重的胃肠道急症。目前多认为早产、喂养不当与细菌移位、缺血后再灌注损伤、炎症介质作用等是NEC最重要的危险因素，这些危险因素共同作用导致NEC发生。NEC的预防主要应针对病因，如促进肠上皮细胞成熟、维持正常肠黏膜屏障和肠微生态系统平衡及抑制炎性介质释放和细菌移位的发生。表皮生长因子及肝素结合表皮生长因子、益生菌、谷氨酰胺和精氨酸、人类粒细胞集落刺激因子等对预防NEC的发生有一定作用。     

The Haematology of Neonatal Necrotizing Enterocolitis

The haematology of forty-four infants with necrotizing enterocolitis (NEC) has been reviewed. Normal values for neutrophil, band cell and platelet counts as well as coagulation profiles have been defined for normal term and preterm infants at varying postnatal ages. In NEC, the absolute neutrophil count was of no diagnostic or prognostic significance but serial counts were useful in following the course of disease process. Band cell and platelet counts were strong predictors of onset of disease and both were significantly different in infants who died compared with those who survived the disease. Disseminated intravascular coagulation occurred in 11% of cases of NEC, all of whom died. Hypovolaemic shock preceded NEC in 5 infants and 3 infants had preexisting polycythaemia. Severe thrombocytopenia was treated with platelet infusions. Exchange transfusion was carried out for disseminated intravascular coagulation.     

Neonatal Necrotizing Enterocolitis: Radiological Manifestations

The radiographic manifestations of necrotizing enterocolitis (NEC) were reviewed in 44 infants. As the clinical presentation of NEC could often not be distinguished from sepsis and/or surgical abdominal problems, abdominal X-ray is by far the most sensitive test for the presence of this disease. Nonspecific radiological findings which frequently accompanied or preceded the appearance of intramural gas include bowel distension, a foamy pattern and asymmetry of gas pattern. The presence of these findings is an indication to repeat radiological abdominal examinations as an adjunct in the early diagnosis of NEC. The radiological hallmark of NEC is intramural gas, though this may be absent in infants with fulminating disease. If pueumoperitoneum occurs, it is diagnosed almost always at the onset or within 24 hours of the disease. Portal venous gas may be a transient sign and is not as ominous as previously reported. Barium studies are not justified in the acute disease but the high incidence of intestinal stricture in survivors may warrant a contrast study during the recovery phase.     

新生儿坏死性小肠结肠炎的外科处理

目的 探讨新生儿坏死性小肠结肠炎外科手术指征、手术方法及术后并发症的预防。方法 回顾性分析1995年1月～2003年1月外科处理的24例新生儿坏死性小肠结肠炎的资料。结果 全部病例治愈18人，死亡6人，治愈率75％。结论 选择合适的手术时机及手术方法可以减少术后并发症的发生，提高治愈率。     

新生儿坏死性小肠结肠炎治疗中的矛盾与对策

新生儿坏死性小肠结肠炎(NEC)是新生儿常见且严重的胃肠道急症,是新生儿主要死亡原因之一,在其治疗中常遇到各种矛盾,如禁食与喂养、抗生素应用及益生菌应用、是否手术治疗等。现就NEC治疗中常见矛盾问题提出解决对策。     

新生儿坏死性小肠结肠炎的防治进展

新生儿坏死性小肠结肠炎(NEC)是新生儿时期严重的肠道炎症性疾病,是早产儿、低出生体重儿早期死亡的主要原因之一。随着对NEC发病机制的深入了解,除传统上禁食、全胃肠外营养、对症治疗及严重者外科治疗的应用等防治手段外,近年国外学者对该病病因、危险因素及发病机制进行了深入研究,并试图在NEC发病机制的几个环节上进行干预:病原菌感染和炎症的控制、微生态制剂的应用、营养因子促进肠道功能成熟、细胞因子干预。该文就近年有关这方面的干预研究进展作一综述。     

Neonatal Necrotizing Enterocolitis: Clinical Considerations and Pathogenetic Concepts

Necrotizing enterocolitis (NEC), a disease affecting predominantly premature infants, is a leading cause of morbidity and mortality in neonatal intensive care units. Although several predisposing factors have been identified, such as prematurity, enteral feeding, and infection, its pathogenesis remains elusive. In the past 20 years, we have established several animal models of NEC in rats and found several endogenous mediators, especially platelet-activating factor (PAF), which may play a pivotal role in NEC. Injection of PAF induces intestinal necrosis, and PAF antagonists prevent the bowel injury induced by bacterial endotoxin, hypoxia, or challenge with tumor necrosis factor-a (TNF) plus endotoxin in adult rats. The same is true for lesions induced by hypoxia and enteral feeding in neonatal animals. Human patients with NEC show high levels of PAF and decreased plasma PAF-acetylhydrolase, the enzyme degrading PAF. The initial event in our experimental models of NEC is probably polymorphonuclear leukocyte (PMN) activation and adhesion to venules in the intestine, which initiates a local inflammatory reaction involving proinflammatory mediators including TNF, complement, prostaglandins, and leukotriene C4. Subsequent norepinephrine release and mesenteric vasoconstriction result in splanchnic ischemia and reperfusion. Bacterial products (e.g., endotoxin) enter the intestinal tissue during local mucosal barrier breakdown, and endotoxin synergizes with PAF to amplify the inflammation. Reactive oxygen species produced by the activated leukocytes and by intestinal epithelial xanthine oxidase may be the final pathway for tissue injury. Protective mechanisms include nitric oxide produced by the constitutive (mainly neuronal) nitric oxide synthase, and indigenous probiotics such as Bifidobacteria infantis. The former maintains intestinal perfusion and the integrity of the mucosal barrier, and the latter keep virulent bacteria in check. The development of tissue injury depends on the balance between injurious and protective mechanisms.     

新生儿坏死性小肠结肠炎的防治进展

新生儿坏死性小肠结肠炎（NEC）是新生儿时期严重的肠道炎症性疾病,是早产儿、低出生体重儿早期死亡的主要原因之一.随着对NEC发病机制的深入了解,除传统上禁食、全胃肠外营养、对症治疗及严重者外科治疗的应用等防治手段外,近年国外学者对该病病因、危险因素及发病机制进行了深入研究,并试图在NEC发病机制的几个环节上进行干预：病原菌感染和炎症的控制、微生态制剂的应用、营养因子促进肠道功能成熟、细胞因子干预.该文就近年有关这方面的干预研究进展作一综述.     

Risk Factors and Outcome in Neonatal Necrotising Enterocolitis

Objectives

To analyze multiple risk factors of necrotizing enterocolitis (NEC) and the outcome.

Methods

Hundred neonates with NEC were compared with 100 normal neonates matched for sex, gestation and weight. Their data including antenatal, natal, course of illness, hospital stay, progress and outcome were collected. Univariate analysis and logistic regression were used to analyze the risk factors.

Results

Mean age of onset of NEC was 2.35?±?1.11 d. Stage I, II and III were noted in 48 %, 39 % and 13 % of cases respectively. Most common clinical features were abdominal distension (85 %) and feed intolerance (70 %). Important risk factors associated with NEC were sepsis, top feeding, perinatal asphyxia, respiratory distress and mechanical ventilation. Antenatal steroids and breast feeding had beneficial effect. No association was found with occurrence of NEC and cyanotic heart disease or administration of H₂ blockers. Outcome in stage III was very poor.

Conclusions

Early identification of risk factors and appropriate intervention may reduce the incidence and improve the outcome in NEC.     

坏死性小肠结肠炎早产儿病因及微生态制剂预防作用

目的探讨新生儿坏死性小肠结肠炎(NEC)病因及应用微生态制剂(培菲康)预防早产儿NEC的有效性及对体质量的影响。方法早产儿524例,随机分为预防组276例与非预防组248例。预防组予培菲康口服,0.5包/次,2次/d;非预防组仅予原发病治疗。观察二组NEC的发生情况及体质量变化。确诊NEC20例患儿为病例组,非NEC80例早产儿为对照组,对二组进行对照研究。结果预防组发生NEC5例,每日体质量增加(8.114±8.137)g;非预防组发生NEC17例,每日体质量增加(6.595±5.337)g。二组NEC发生率比较有显著差异(χ2=7.57P<0.01);二组每日体质量增加量比较有显著差异(t=2.497P<0.05)。Logistic多元回归分析提示:胎龄、HIE、败血症及病情危重症程度是NEC发生的危险因素,应用微生态制剂及免疫球蛋白(IVIG)是保护因素。结论避免NEC的危险因素,应用IVIG和微生态制剂能减少早产儿NEC的发生和促进体质量增长。     

谷氨酰胺和表皮生长因子对新生鼠坏死性小肠结肠炎的影响

目的探讨谷氨酰胺(Gln)和表皮生长因子(EGF)对新生鼠坏死性小肠结肠炎(NEC)肠黏膜修复的影响。方法新生1日龄Wistar大鼠40只随机分为4组,A组(正常对照组),B组(NEC模型组),C组(NEC Gln),D组(NEC EGF Gln)。建立NEC模型,4 d后分别取近回盲段2~3 cm肠道组织固定、包埋、切片。HE染色光镜下作病理学检查,应用免疫组织化学技术检测肠黏膜增殖细胞核抗原(PCNA)的表达,TUNEL法检测肠黏膜细胞凋亡。结果B组HE染色切片见肠黏膜损伤,病理评分的中位积分为3分;C、D组损伤程度较轻,病理评分的中位积分为1分。B组PCNA阳性细胞数低于A组(P<0.01);C、D组PCNA阳性细胞数高于B组(P<0.01);且D组PCNA阳性细胞数高于C组(P<0.05)。B组肠黏膜细胞凋亡数高于A组(P<0.01);C、D组肠黏膜细胞凋亡数低于B组(P<0.01);且D组肠黏膜细胞凋亡数低于C组(P<0.05)。结论NEC新生鼠肠黏膜受损,增殖减慢,细胞凋亡数增加;补充Gln和EGF可促进NEC新生鼠肠黏膜隐窝细胞的增殖,减少肠黏膜细胞的凋亡,加快肠黏膜修复。     

Role of Asphyxia and Feeding in a Neonatal Rat Model of Necrotizing Enterocolitis

Necrotizing enterocolitis (NEC) is a common gastrointestinal disorder affecting premature infants. To investigate critically the importance of the purported risk factors of NEC (formula feeding, asphyxia, bacteria, and prematurity), we developed a neonatal rat model that closely mimics the human disease. Full-term and premature newborn rats were stressed with formula feeding, asphyxia, and/or exogenous bacterial colonization and subsequently evaluated grossly and histologically for the development of intestinal injury. We found that most animals treated with asphyxia, formula feeding, and bacteria developed NEC (77%) and died (86%) by 96 h. All maternally fed animals treated with asphyxia and bacterial colonization survived and had normal intestinal histology. Furthermore, asphyxia was a critical instigating factor, because formula and bacterial exposure without asphyxia resulted in normal intestine and minimal mortality (12%). Enteral bacterial colonization was not a significant determinant of NEC in this model. We conclude that the neonatal rat model is an excellent test system for the study of NEC. As in the human disease, asphyxia and formula feeding play an important role in the pathophysiology of experimental NEC.     

应用微生态制剂预防早产儿坏死性小肠结肠炎412例

目的 探讨应用微生态制剂金双歧预防早产儿坏死性小肠结肠炎(NEC)的临床效果.方法 将2009年5月-2010年2月在本院住院的412例早产儿按病例对照研究分成2组(预防组、对照组),2组除病因治疗、合理喂养外,预防组在24 h内加金双歧口服.应用χ2检验或确切概率法比较2组不同胎龄、不同出生质量早产儿NEC患病率的差异.结果 预防组207例中3例诊断为NEC,患病率为1.45%;对照组205例中13例诊断为NEC,患病率为6.34%.预防组早产儿的NEC患病率明显低于对照组(χ2=6.60,P＜0.05).胎龄＜32周早产儿,2组NEC患病率比较差异无统计学意义(χ2=0.39,P＞0.10).2组极低出生体质量早产儿NEC患病率比较差异无统计学意义(P=0.58);2组低出生体质量早产儿NEC患病率比较差异有统计学意义(χ2=10.33,P＜0.05).结论 预防性应用微生态制剂金双歧可明显降低早产儿NEC的患病率,可能与金双歧可促进早产儿肠道正常菌群的定植和优势化有关.微生态制剂预防性保护作用随胎龄减小有渐减趋势.     

坏死性小肠结肠炎诱导新生大鼠全身炎症反应综合征动物模型的建立

目的将新生Wistar大鼠进行缺氧、低温、鼠乳代用品人工喂养、不同剂量脂多糖(LPS)灌胃等综合因素刺激,造成坏死性小肠结肠炎(NEC),并导致全身炎症反应综合征(SIRS)的动物模型。方法 40只新生Wistar大鼠,出生36～48h随机分成4组,每组各10只。A组为正常对照组,B、C、D组采用低温缺氧(给予1 L.L-1氮气缺氧90s,4℃冷刺激10 min,每天2次,连续2 d)、鼠乳代用品人工喂养、不同剂量LPS(5 mg.kg-1、10 mg.kg-1、20 mg.kg-1)灌胃。实验结束后处死动物,HE染色光镜下观察其回盲部近端肠组织形态学改变,采用肠损伤病理评分进行评价,组织学评分≥2分确定为NEC,根据血液白细胞总数及呼吸改变确定为SIRS。结果 B、C、D组大鼠逐渐出现腹泻、腹胀、活动减少,D组大鼠50%发生死亡。A、B、C、D4组肠损伤病理评分分别为(0.33±0.10)分、(2.03±1.16)分、(3.77±0.41)分、(3.13±0.69)分,组间差异有统计学意义(H=29.83,P<0.01)。NEC发病率分别为0%、50%、100%和100%;SIRS发生率分别为0%、30%、70%和70%。结论在鼠乳代用品人工喂养、缺氧低温刺激条件下,给予LPS灌胃可诱导新生鼠发生NEC,并导致SIRS发生,本模型与新生儿SIRS病理改变接近,是一种比较理想的研究新生儿SIRS的动物模型。     

Necrotizing Enterocolitis Induced by Local Circulatory Interruption in the Ileum of Neonatal Piglets

Occlusion of groups of vessels in the mesenteric vascular arcades of distal ileum for 48 h induced necrotizing enterocolitis lesions in low birth weight, spontaneously delivered, neonatal piglets. Lesion severity increased with numbers of adjacent groups of vessels occluded and with proximity to the ileocecal junction. A previously undescribed feature, “prepneumatosis,” was confined to the lymphatic vessels of the submucosa and serosa. This feature closely resembled the position, shape, and distribution of classical pneumatosis intestinalis. Occlusion of vessels for 30 min followed by reperfusion did not induce any detectable changes 48 h later. Identical procedures (48-h occlusions) did not induce any detectable changes in 35-kg pigs.     

新生儿过敏致坏死性小肠结肠炎3例

3例患儿均以呕吐、腹胀、腹泻、便血急转入我院。男2例，女1例；日龄1～3d。生后均喂以合适配比的配方奶（全牛奶配方）。其中1例有轻度围生期窒息病史，另2例生产史正常。首排胎便均正常。3例自喂养后6—8h开始出现呕吐、腹胀，随后出现腹泻、便血；1例出现阵发性发绀及发热，急诊入院。入院后立即予对症治疗，病情稍稳定后行立位胸腹X线检查，影像学检查提示为肠管扩张，肠管内可见多个细小气液平面，肠壁间隙增宽，出现“双轨征”，     

Relationship of Birth Weight to the Pathogenesis of Necrotizing Enterocolitis in the Neonatal Piglet

The relationship between birth weight and the development of necrotizing enterocolitis (NEC) was studied in the term-delivered neonatal piglet. Hypoxia (pO₂ less than 30% for 1 h) coupled with hyperviscosity (hematocrit more than 75%), with and without splenectomy, resulted in a high frequency and severity of NEC. This effect was most pronounced in low birth weight (LBW) animals. A statistically significant inverse relationship was found between birth weight and the number and severity of lesions. Splenectomy increased the incidence and severity of lesions particularly in LBW animals. A predominance of lesions was found in the distal ileum with occasional occurrences elsewhere in the small bowel and in the proximal colon.

The neonatal piglet is capable of producing the full spectrum of NEC under acceptable experimental conditions. LBW is a significant predisposing factor in the pathogenesis of NEC.