Risk factors for concurrent sepsis in neonates with necrotizing enterocolitis
AN Yao, LIU Li, LI Qiu-Yu, RAN Ya-Lin, LI Lu-Quan
Neonatal Diagnosis and Treatment Center, Children's Hospital of Chongqing Medical University/National Demonstration Base of Standardized Training Base for Resident Physicians/Ministry of Education Key Laboratory of Child Development and Disorders/Key Laboratory of Pediatrics in Chongqing/Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing 400014, China
Abstract:Objective To investigate the risk factors for concurrent sepsis in neonates with necrotizing enterocolitis (NEC). Methods A retrospective analysis was performed for the clinical data of 273 neonates with NEC. The risk factors for concurrent sepsis were analyzed from the aspects of perinatal factors and treatment regimen before the diagnosis of NEC. Results The incidence rate of concurrent sepsis in NEC was 32.2% (88/273). The neonates with stage Ⅲ NEC had a significantly higher incidence rate of concurrent sepsis than those with stage Ⅱ NEC (69.0% vs 15.9%; P < 0.05). Of all neonates with sepsis, 62.5% experienced sepsis within 3 days after the diagnosis of NEC, and 37.5% experienced sepsis more than 3 days after the diagnosis. Compared with those without concurrent sepsis, the neonates with concurrent sepsis had significantly lower gestational age and birth weight (P < 0.05). The neonates who had scleredema, had stage Ⅲ NEC, needed gastrointestinal decompression after the diagnosis of NEC, and experienced a long time of gastrointestinal decompression tended to develop sepsis more easily (P < 0.05). Scleredema (OR=9.75, 95%CI:2.84-33.52, P < 0.001), stage Ⅲ NEC (OR=12.94, 95%CI:6.82-24.55, P < 0.001), and gastrointestinal decompression (OR=2.27, 95%CI:1.14-4.5, P=0.02) were independent risk factors for concurrent sepsis in NEC. Conclusions Scleredema, stage Ⅲ NEC, and gastrointestinal decompression are independent risk factors for concurrent sepsis in neonates with NEC.
Clark RH,Gordon P,Walker WM,et al.Characteristics of patients who die of necrotizing enterocolitis[J].J Perinatol,2012,32(3):199-204.
[1]
Kawajiri S,Saiki S,Sato S,et al.Genetic mutations and functions of PINK1[J].Trends Pharmacol Sci,2011,32(10):573-580.
[4]
Wu SF,Caplan M,Lin HC.Necrotizing enterocolitis:old problem with new hope[J].Pediatr Neonatol,2012,53(3):158-163.
[2]
Pickrell AM,Youle RJ.The roles of PINK1,parkin,and mitochondrial fidelity in Parkinson's disease[J].Neuron,2015,85(2):257-273.
[3]
Durcan TM,Fon EA.The three ‘P’s of mitophagy:PARKIN,PINK1,and post-translational modifications[J].Genes Dev,2015,29(10):989-999.
[5]
Bizzarro MJ,Ehrenkranz RA,Gallagher PG.Concurrent bloodstream infections in infants with necrotizing enterocolitis[J].J Pediatr,2014,164(1):61-66.
[4]
Puschmann A.Monogenic Parkinson's disease and parkinsonism:clinical phenotypes and frequencies of known mutations[J].Parkinsonism Relat Disord,2013,19(4):407-415.
Zhou C,Huang Y,Shao Y,et al.The kinase domain of mitochondrial PINK1 faces the cytoplasm[J].Proc Natl Acad Sci U S A,2008,105(33):12022-12027.
[7]
Chaaban H,Shin M,Sirya E,et al.Inter-alpha inhibitor protein level in neonatal predicts necrotizing entericolitis[J].J Pediatr,2010,157(5):757-761.
[6]
Trempe JF,Fon EA.Structure and function of parkin,PINK1,and DJ-1,the three musketeers of neuroprotection[J].Front Neurol,2013,4:38.
[8]
Arnold M,Moore SW,Sidler D,et al.Long-term outcome of surgically managed necrotizing enterocolitis in a developing country[J].Pediatr Surg Int,2010,26(4):355-360.
[9]
Miner CA,Fullmer S,Eggett DL,et al.Factors affecting the severity of necrotizing enterocolitis[J].J Matern Fetal Neonatal Med,2013,26(17):1715-1719.
[7]
Sim CH,Gabriel K,Mills RD,et al.Analysis of the regulatory and catalytic domains of PTEN-induced kinase-1(PINK1)[J].Hum Mutat,2012,33(10):1408-1422.
[10]
Walsh MC,Kliegman RM.Necrotizing enterocolitis:treatment based on staging criteria[J].Pediatr Clin North Am,1986,33(1):179-201.
Wust R,Maurer B,Hauser K,et al.Mutation analyses and association studies to assess the role of the presenilin-associated rhomboid-like gene in Parkinson's disease[J].Neurobiol Aging,2016,39:217 el3-el5.
[9]
Bandres-Ciga S,Mencacci NE,Duran R,et al.Analysis of the genetic variability in Parkinson's disease from Southern Spain[J].Neurobiol Aging,2016,37:210 el-e5.
[10]
Ye M,Zhou D,Zhou Y,et al.Parkinson's disease-associated PINK1 G309D mutation increases abnormal phosphorylation of Tau[J].IUBMB Life,2015,67(4):286-290.
[12]
Anand RJ,Leaphart CL,Mollen KP,et al.The role of the intestinal barrier in the pathogenesis of necrotizing enterocolitis[J].Shock,2007,27(2):124-133.
[13]
Krediet TG,van Lelyveld N,Vijlbrief DC,et al.Microbiological factors associated with neonatal necrotizing enterocolitis:protective effect of early antibiotic treatment[J].Acta Paediatr,2003,92(10):1180-1182.
[14]
Sharma R,Tepas JJ,Hudak ML,et al.Neonatal gut injury and infection rate:impact of surgical debridement on outcome[J].Pediatr Surg Int,2005,21(12):977-982.
[15]
Heida FH,Hulscher JBF,Schurink M,et al.Bloodstream infections during the onset of necrotizing enterocolitis and their relation with the pro-inflammatory response,gut wall integrity and severity of disease in NEC[J].Pediatr Surg,2015,50(11):1837-1841.
Thompson AM,Bizzarro MJ.Necrotizing enterocolitis in newborns pathogenesis,prevention and management[J].Drugs,2008,68(9):1227-1238.
[18]
Vongbhavit K,Underwood MA.Prevention of necrotizing enterocolitis through manipulation of the intestinal microbiota of the premature infant[J].Clin Ther,2016,38(4):716-732.
[19]
Eaton S,Rees CM,Hall NJ.Current research in necrotizing enterocolitis[J].Early Hum Dev,2016,97:33-39.
[11]
Rub C,Schroder N,Voos W.Biochemical properties of the kinase PINK1 as sensor protein for mitochondrial damage signalling[J].Biochem Soc Trans,2015,43(2):287-291.