U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Duodenal atresia

MedGen UID:
75602
Concept ID:
C0266174
Congenital Abnormality
Synonym: Duodenal atresia (disease)
SNOMED CT: Atresia of duodenum (51118003); Congenital atresia of duodenum (51118003); Duodenal atresia (51118003)
Modes of inheritance:
Unknown inheritance
MedGen UID:
989040
Concept ID:
CN307042
Finding
Source: Orphanet
Hereditary clinical entity whose mode of inheritance is unknown.
 
HPO: HP:0002247
Monarch Initiative: MONDO:0009126
OMIM®: 223400
Orphanet: ORPHA1203

Definition

A developmental defect resulting in complete obliteration of the duodenal lumen, that is, an abnormal closure of the duodenum. [from HPO]

Clinical features

From HPO
Duodenal atresia
MedGen UID:
75602
Concept ID:
C0266174
Congenital Abnormality
A developmental defect resulting in complete obliteration of the duodenal lumen, that is, an abnormal closure of the duodenum.

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVDuodenal atresia
Follow this link to review classifications for Duodenal atresia in Orphanet.

Conditions with this feature

Fryns syndrome
MedGen UID:
65088
Concept ID:
C0220730
Disease or Syndrome
Fryns syndrome is characterized by diaphragmatic defects (diaphragmatic hernia, eventration, hypoplasia, or agenesis); characteristic facial appearance (coarse facies, wide-set eyes, a wide and depressed nasal bridge with a broad nasal tip, long philtrum, low-set and anomalous ears, tented vermilion of the upper lip, wide mouth, and a small jaw); short distal phalanges of the fingers and toes (the nails may also be small); pulmonary hypoplasia; and associated anomalies (polyhydramnios, cloudy corneas and/or microphthalmia, orofacial clefting, renal dysplasia / renal cortical cysts, and/or malformations involving the brain, cardiovascular system, gastrointestinal system, and/or genitalia). Survival beyond the neonatal period is rare. Data on postnatal growth and psychomotor development are limited; however, severe developmental delay and intellectual disability are common.
Miller Dieker syndrome
MedGen UID:
78538
Concept ID:
C0265219
Disease or Syndrome
PAFAH1B1-related lissencephaly/subcortical band heterotopia (SBH) comprises a spectrum of severity. Affected newborns typically have mild-to-moderate hypotonia, feeding difficulties, and poor head control. During the first years, neurologic examination typically demonstrates poor visual tracking and response to sounds, axial hypotonia, and mild distal spasticity that can transition over time to more severe spasticity. Seizures occur in more than 90% of individuals with lissencephaly and often include infantile spasms. Seizures are often drug resistant, but even with good seizure control, the best developmental level achieved (excluding the few individuals with partial lissencephaly) is the equivalent of about age three to five months. In individuals with PAFAH1B1-related lissencephaly/SBH, developmental delay ranges from mild to severe. Other findings in PAFAH1B1-related lissencephaly/SBH include feeding issues and aspiration (which may result in need for gastrostomy tube placement), progressive microcephaly, and occasional developmental regression.
CHARGE association
MedGen UID:
75567
Concept ID:
C0265354
Disease or Syndrome
CHD7 disorder encompasses the entire phenotypic spectrum of heterozygous CHD7 pathogenic variants that includes CHARGE syndrome as well as subsets of features that comprise the CHARGE syndrome phenotype. The mnemonic CHARGE syndrome, introduced in the premolecular era, stands for coloboma, heart defect, choanal atresia, retarded growth and development, genital hypoplasia, ear anomalies (including deafness). Following the identification of the genetic cause of CHD7 disorder, the phenotypic spectrum expanded to include cranial nerve anomalies, vestibular defects, cleft lip and/or palate, hypothyroidism, tracheoesophageal anomalies, brain anomalies, seizures, and renal anomalies. Life expectancy highly depends on the severity of manifestations; mortality can be high in the first few years when severe birth defects (particularly complex heart defects) are present and often complicated by airway and feeding issues. In childhood, adolescence, and adulthood, decreased life expectancy is likely related to a combination of residual heart defects, infections, aspiration or choking, respiratory issues including obstructive and central apnea, and possibly seizures. Despite these complications, the life expectancy for many individuals can be normal.
Duodenal atresia
MedGen UID:
75602
Concept ID:
C0266174
Congenital Abnormality
A developmental defect resulting in complete obliteration of the duodenal lumen, that is, an abnormal closure of the duodenum.
Martinez-Frias syndrome
MedGen UID:
318628
Concept ID:
C1832443
Disease or Syndrome
The Martinez-Frias syndrome is characterized by pancreatic hypoplasia, intestinal atresia, and gallbladder aplasia or hypoplasia, with or without tracheoesophageal fistula. There is considerable phenotypic overlap between Martinez-Frias syndrome and Mitchell-Riley syndrome (MTCHRS; 615710), the latter being characterized by neonatal diabetes in addition to the features of the Martinez-Frias syndrome, but without tracheoesophageal fistula (Smith et al., 2010).
Heterotaxy, visceral, 1, X-linked
MedGen UID:
336609
Concept ID:
C1844020
Disease or Syndrome
Heterotaxy Heterotaxy ('heter' meaning 'other' and 'taxy' meaning 'arrangement'), or situs ambiguus, is a developmental condition characterized by randomization of the placement of visceral organs, including the heart, lungs, liver, spleen, and stomach. The organs are oriented randomly with respect to the left-right axis and with respect to one another (Srivastava, 1997). Heterotaxy is a clinically and genetically heterogeneous disorder. Multiple Types of Congenital Heart Defects Congenital heart defects (CHTD) are among the most common congenital defects, occurring with an incidence of 8/1,000 live births. The etiology of CHTD is complex, with contributions from environmental exposure, chromosomal abnormalities, and gene defects. Some patients with CHTD also have cardiac arrhythmias, which may be due to the anatomic defect itself or to surgical interventions (summary by van de Meerakker et al., 2011). Reviews Obler et al. (2008) reviewed published cases of double-outlet right ventricle and discussed etiology and associations. Genetic Heterogeneity of Visceral Heterotaxy See also HTX2 (605376), caused by mutation in the CFC1 gene (605194) on chromosome 2q21; HTX3 (606325), which maps to chromosome 6q21; HTX4 (613751), caused by mutation in the ACVR2B gene (602730) on chromosome 3p22; HTX5 (270100), caused by mutation in the NODAL gene (601265) on chromosome 10q22; HTX6 (614779), caused by mutation in the CCDC11 gene (614759) on chromosome 18q21; HTX7 (616749), caused by mutation in the MMP21 gene (608416) on chromosome 10q26; HTX8 (617205), caused by mutation in the PKD1L1 gene (609721) on chromosome 7p12; HTX9 (618948), caused by mutation in the MNS1 gene (610766) on chromosome 15q21; HTX10 (619607), caused by mutation in the CFAP52 gene (609804) on chromosome 17p13; HTX11 (619608), caused by mutation in the CFAP45 gene (605152) on chromosome 1q23; and HTX12 (619702), caused by mutation in the CIROP gene (619703) on chromosome 14q11. Genetic Heterogeneity of Multiple Types of Congenital Heart Defects An X-linked form of CHTD, CHTD1, is caused by mutation in the ZIC3 gene on chromosome Xq26. CHTD2 (614980) is caused by mutation in the TAB2 gene (605101) on chromosome 6q25. A form of nonsyndromic congenital heart defects associated with cardiac rhythm and conduction disturbances (CHTD3; 614954) has been mapped to chromosome 9q31. CHTD4 (615779) is caused by mutation in the NR2F2 gene (107773) on chromosome 15q26. CHTD5 (617912) is caused by mutation in the GATA5 gene (611496) on chromosome 20q13. CHTD6 (613854) is caused by mutation in the GDF1 gene (602880) on chromosome 19p13. CHTD7 (618780) is caused by mutation in the FLT4 gene (136352) on chromosome 5q35.
Fanconi anemia complementation group B
MedGen UID:
336901
Concept ID:
C1845292
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
Mosaic variegated aneuploidy syndrome 1
MedGen UID:
338026
Concept ID:
C1850343
Disease or Syndrome
Mosaic variegated aneuploidy (MVA) syndrome is a rare disorder in which some cells in the body have an abnormal number of chromosomes instead of the usual 46 chromosomes, a situation known as aneuploidy. Most commonly, cells have an extra chromosome, which is called trisomy, or are missing a chromosome, which is known as monosomy. In MVA syndrome, some cells are aneuploid and others have the normal number of chromosomes, which is a phenomenon known as mosaicism. Typically, at least one-quarter of cells in affected individuals have an abnormal number of chromosomes. Because the additional or missing chromosomes vary among the abnormal cells, the aneuploidy is described as variegated.\n\nIn MVA syndrome, growth before birth is slow (intrauterine growth restriction). After birth, affected individuals continue to grow at a slow rate and are shorter than average. In addition, they typically have an unusually small head size (microcephaly). Another common feature of MVA syndrome is an increased risk of developing cancer in childhood. Cancers that occur most frequently in affected individuals include a cancer of muscle tissue called rhabdomyosarcoma, a form of kidney cancer known as Wilms tumor, and a cancer of the blood-forming tissue known as leukemia.\n\nLess commonly, people with MVA syndrome have eye abnormalities or distinctive facial features, such as a broad nasal bridge and low-set ears. Some affected individuals have brain abnormalities, the most common of which is called Dandy-Walker malformation. Intellectual disability, seizures, and other health problems can also occur in people with MVA syndrome.\n\nThere are at least three types of MVA syndrome, each with a different genetic cause. Type 1 is the most common and displays the classic signs and symptoms described above. Type 2 appears to have slightly different signs and symptoms than type 1, although the small number of affected individuals makes it difficult to define its characteristic features. Individuals with MVA syndrome type 2 grow slowly before and after birth; however, their head size is typically normal. Some people with MVA syndrome type 2 have unusually short arms. Individuals with MVA syndrome type 2 do not seem to have an increased risk of cancer. Another form of MVA syndrome is characterized by a high risk of developing Wilms tumor. Individuals with this form may also have other signs and symptoms typical of MVA syndrome type 1.
Stromme syndrome
MedGen UID:
340938
Concept ID:
C1855705
Disease or Syndrome
Stromme syndrome is an autosomal recessive congenital disorder affecting multiple systems with features of a ciliopathy. Affected individuals typically have some type of intestinal atresia, variable ocular abnormalities, microcephaly, and sometimes involvement of other systems, including renal and cardiac. In some cases, the condition is lethal in early life, whereas other patients show normal survival with or without mild cognitive impairment (summary by Filges et al., 2016).
Hypoplastic pancreas-intestinal atresia-hypoplastic gallbalder syndrome
MedGen UID:
411637
Concept ID:
C2748662
Disease or Syndrome
Mitchell-Riley syndrome is characterized by neonatal diabetes, pancreatic hypoplasia, intestinal atresia, and gallbladder aplasia or hypoplasia. There is considerable phenotypic overlap between Mitchell-Riley syndrome and Martinez-Frias syndrome (601346), the latter being characterized by the features of the Mitchell-Riley syndrome except for neonatal diabetes, and including tracheoesophageal fistula in some patients (Smith et al., 2010).
Alveolar capillary dysplasia with pulmonary venous misalignment
MedGen UID:
755478
Concept ID:
C2960310
Congenital Abnormality
Congenital alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is characterized histologically by failure of formation and ingrowth of alveolar capillaries that then do not make contact with alveolar epithelium, medial muscular thickening of small pulmonary arterioles with muscularization of the intraacinar arterioles, thickened alveolar walls, and anomalously situated pulmonary veins running alongside pulmonary arterioles and sharing the same adventitial sheath. Less common features include a reduced number of alveoli and a patchy distribution of the histopathologic changes. The disorder is associated with persistent pulmonary hypertension of the neonate and shows varying degrees of lability and severity (Boggs et al., 1994). Affected infants present with respiratory distress resulting from pulmonary hypertension in the early postnatal period, and the disease is uniformly fatal within the newborn period (Vassal et al., 1998). Additional features of ACDMPV include multiple congenital anomalies affecting the cardiovascular, gastrointestinal, genitourinary, and musculoskeletal systems, as well as disruption of the normal right-left asymmetry of intrathoracic or intraabdominal organs (Sen et al., 2004).
Mosaic variegated aneuploidy syndrome 2
MedGen UID:
481473
Concept ID:
C3279843
Disease or Syndrome
Mosaic variegated aneuploidy syndrome is an autosomal recessive disorder characterized by poor growth and variable phenotypic manifestations, such as facial dysmorphism and congenital heart defects, associated with mosaic aneuploidies resulting from defects in cell division (summary by Snape et al., 2011). See also MVA1 (257300), caused by mutation in the BUB1B gene (602860) on chromosome 15q15.
Fanconi anemia complementation group F
MedGen UID:
854016
Concept ID:
C3469526
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
Heterotaxy, visceral, 5, autosomal
MedGen UID:
501198
Concept ID:
C3495537
Congenital Abnormality
Heterotaxy ('heter' meaning 'other' and 'taxy' meaning 'arrangement'), or situs ambiguus, is a developmental condition characterized by randomization of the placement of visceral organs, including the heart, lungs, liver, spleen, and stomach. The organs are oriented randomly with respect to the left-right axis and with respect to one another (Srivastava, 1997). Heterotaxy is a clinically and genetically heterogeneous disorder. For a discussion of genetic heterogeneity of visceral heterotaxy, see HTX1 (306955).
Neurodevelopmental disorder with or without anomalies of the brain, eye, or heart
MedGen UID:
934739
Concept ID:
C4310772
Disease or Syndrome
RERE-related disorders are characterized by neurodevelopmental problems with or without structural anomalies of the eyes, heart, kidneys, and genitourinary tract and mild sensorineural hearing loss. Hypotonia and feeding problems are common among affected individuals. Developmental delay and intellectual disability range from mild to profound. Behavior problems may include attention-deficit/hyperactivity disorder, self-injurious behavior, and autism spectrum disorder. A variety of eye anomalies (coloboma, optic nerve anomalies, microphthalmia, and/or Peter's anomaly) and vision issues (myopia, anisometropia, astigmatism, exotropia, esotropia) have been reported. Congenital heart defects, most commonly septal defects, have also been described. Genitourinary abnormalities include vesicoureteral reflux, and cryptorchidism and hypospadias in males. Sensorineural hearing loss can be unilateral or bilateral.
Fanconi anemia, complementation group W
MedGen UID:
1621245
Concept ID:
C4521564
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
Intellectual disability, autosomal dominant 53
MedGen UID:
1623344
Concept ID:
C4540481
Mental or Behavioral Dysfunction
Townes-Brocks syndrome 1
MedGen UID:
1635275
Concept ID:
C4551481
Disease or Syndrome
Townes-Brocks syndrome (TBS) is characterized by the triad of imperforate anus (84%), dysplastic ears (87%; overfolded superior helices and preauricular tags; frequently associated with sensorineural and/or conductive hearing impairment [65%]), and thumb malformations (89%; triphalangeal thumbs, duplication of the thumb [preaxial polydactyly], and rarely hypoplasia of the thumbs). Renal impairment (42%), including end-stage renal disease (ESRD), may occur with or without structural abnormalities (mild malrotation, ectopia, horseshoe kidney, renal hypoplasia, polycystic kidneys, vesicoutereral reflux). Congenital heart disease occurs in 25%. Foot malformations (52%; flat feet, overlapping toes) and genitourinary malformations (36%) are common. Intellectual disability occurs in approximately 10% of individuals. Rare features include iris coloboma, Duane anomaly, Arnold-Chiari malformation type 1, and growth retardation.
Feingold syndrome type 1
MedGen UID:
1637716
Concept ID:
C4551774
Disease or Syndrome
Feingold syndrome 1 (referred to as FS1 in this GeneReview) is characterized by digital anomalies (shortening of the 2nd and 5th middle phalanx of the hand, clinodactyly of the 5th finger, syndactyly of toes 2-3 and/or 4-5, thumb hypoplasia), microcephaly, facial dysmorphism (short palpebral fissures and micrognathia), gastrointestinal atresias (primarily esophageal and/or duodenal), and mild-to-moderate learning disability.
Holoprosencephaly 13, X-linked
MedGen UID:
1714826
Concept ID:
C5393308
Disease or Syndrome
X-linked holoprosencephaly-13 (HPE13) is a neurologic disorder characterized by midline developmental defects that mainly affect the brain and craniofacial structure. The severity and manifestations are variable: some patients may have full alobar HPE with cyclopia, whereas others have semilobar HPE or septooptic dysplasia. Dysmorphic features include microcephaly, hypotelorism, low-set ears, micrognathia, and cleft lip/palate. Patients with a more severe phenotype may die in the newborn period, whereas those with a less severe phenotype show global developmental delay. Additional variable features include congenital heart defects and vertebral anomalies. Phenotypic variability may be related to the type of mutation, X-inactivation status, and possible incomplete penetrance. The STAG2 protein is part of the multiprotein cohesin complex involved in chromatid cohesion during DNA replication and transcriptional regulation; HPE13 can thus be classified as a 'cohesinopathy' (summary by Kruszka et al., 2019). For a discussion of genetic heterogeneity of holoprosencephaly, see HPE1 (236100).
Diets-Jongmans syndrome
MedGen UID:
1714920
Concept ID:
C5394263
Disease or Syndrome
Diets-Jongmans syndrome (DIJOS) is an autosomal dominant disorder characterized by mild to moderately impaired intellectual development with a recognizable facial gestalt (summary by Diets et al., 2019).
Vertebral, cardiac, tracheoesophageal, renal, and limb defects
MedGen UID:
1788069
Concept ID:
C5543189
Disease or Syndrome
VCTERL syndrome is characterized by anomalies of the vertebrae, heart, trachea, esophagus, kidneys, and limbs. Some patients also exhibit craniofacial abnormalities. Incomplete penetrance and markedly variable disease expression have been observed, including intrafamilial variability (Martin et al., 2020).
Heterotaxy, visceral, 11, autosomal, with male infertility
MedGen UID:
1794229
Concept ID:
C5562019
Disease or Syndrome
Visceral heterotaxy-11 (HTX11) is characterized by a failure to generate normal left-right visceral asymmetry during embryogenesis, which can result in heterotaxy syndrome or situs inversus totalis. Affected individuals may experience mild chronic respiratory symptoms, but do not fulfill the criteria for primary ciliary dyskinesia (see 244400). Male infertility associated with reduced flagellar motility has been reported (Dougherty et al., 2020). For a discussion of genetic heterogeneity of visceral heterotaxy, see HTX1 (306955).
Gastrointestinal defects and immunodeficiency syndrome 1
MedGen UID:
988754
Concept ID:
CN306406
Disease or Syndrome
Gastrointestinal defects and immunodeficiency syndrome-1 (GIDID1) is characterized by multiple intestinal atresia, in which atresia occurs at various levels throughout the small and large intestines. Surgical outcomes are poor, and the condition is usually fatal within the first month of life. Some patients exhibit inflammatory bowel disease (IBD), with or without intestinal atresia, and in some cases, the intestinal features are associated with either mild or severe combined immunodeficiency (Samuels et al., 2013; Avitzur et al., 2014; Lemoine et al., 2014). Genetic Heterogeneity of GIDID See also GIDID2 (619708), caused by mutation in the PI4KA gene (600286) on chromosome 22q11.

Recent clinical studies

Etiology

Zrinyi A, Lum Min SA, Bello EA, Singh C, Keijzer R
Pediatr Surg Int 2023 Jan 18;39(1):84. doi: 10.1007/s00383-022-05359-w. PMID: 36653532
Weller JH, Engwall-Gill AJ, Westermann CR, Patel PP, Kunisaki SM, Rhee DS
J Surg Res 2022 Nov;279:803-808. Epub 2022 Apr 27 doi: 10.1016/j.jss.2022.04.028. PMID: 35487775
Hosokawa T, Tanami Y, Sato Y, Ishimaru T, Kawashima H, Oguma E
J Med Ultrason (2001) 2022 Apr;49(2):299-309. Epub 2022 Jan 6 doi: 10.1007/s10396-021-01176-1. PMID: 34988762
Toyama C, Masahata K, Ibuka S, Nara K, Soh H, Usui N
Pediatr Surg Int 2021 Jul;37(7):929-935. Epub 2021 Mar 25 doi: 10.1007/s00383-021-04890-6. PMID: 33768347
Bishop JC, McCormick B, Johnson CT, Miller J, Jelin E, Blakemore K, Jelin AC
Fetal Diagn Ther 2020;47(2):98-103. Epub 2019 Jun 5 doi: 10.1159/000500471. PMID: 31167209Free PMC Article

Diagnosis

Zrinyi A, Lum Min SA, Bello EA, Singh C, Keijzer R
Pediatr Surg Int 2023 Jan 18;39(1):84. doi: 10.1007/s00383-022-05359-w. PMID: 36653532
Hosokawa T, Tanami Y, Sato Y, Ishimaru T, Kawashima H, Oguma E
J Med Ultrason (2001) 2022 Apr;49(2):299-309. Epub 2022 Jan 6 doi: 10.1007/s10396-021-01176-1. PMID: 34988762
Toyama C, Masahata K, Ibuka S, Nara K, Soh H, Usui N
Pediatr Surg Int 2021 Jul;37(7):929-935. Epub 2021 Mar 25 doi: 10.1007/s00383-021-04890-6. PMID: 33768347
Qiang S, Fan M, Cui Q, Li Z, Zhou Y, Li Q, Li F
Medicine (Baltimore) 2020 Jul 31;99(31):e21439. doi: 10.1097/MD.0000000000021439. PMID: 32756156Free PMC Article
Bishop JC, McCormick B, Johnson CT, Miller J, Jelin E, Blakemore K, Jelin AC
Fetal Diagn Ther 2020;47(2):98-103. Epub 2019 Jun 5 doi: 10.1159/000500471. PMID: 31167209Free PMC Article

Therapy

Weller JH, Engwall-Gill AJ, Westermann CR, Patel PP, Kunisaki SM, Rhee DS
J Surg Res 2022 Nov;279:803-808. Epub 2022 Apr 27 doi: 10.1016/j.jss.2022.04.028. PMID: 35487775
Watanabe S, Manabe M, Miyata M, Naoe A, Suzuki T
J Neonatal Perinatal Med 2021;14(3):437-440. doi: 10.3233/NPM-200504. PMID: 33325401
Goh MFJ, Mak MHW, Low Y, Ong CCP
BMJ Case Rep 2019 Aug 28;12(8) doi: 10.1136/bcr-2019-231021. PMID: 31466956Free PMC Article
Mentessidou A, Saxena AK
World J Surg 2017 Aug;41(8):2178-2184. doi: 10.1007/s00268-017-3937-3. PMID: 28258456
Wu H, Huang Z, Ji M, Li Y, Zhao R
Clin Nucl Med 2017 Feb;42(2):140-142. doi: 10.1097/RLU.0000000000001524. PMID: 28060781

Prognosis

Calcaterra V, Chiricosta L, Mazzon E, Gugnandolo A, Alberti D, Maestri L, Meroni M, Vestri E, Verduci E, Dilillo D, Zuccotti G, Pelizzo G
Orphanet J Rare Dis 2021 Oct 29;16(1):455. doi: 10.1186/s13023-021-02093-9. PMID: 34715892Free PMC Article
Toyama C, Masahata K, Ibuka S, Nara K, Soh H, Usui N
Pediatr Surg Int 2021 Jul;37(7):929-935. Epub 2021 Mar 25 doi: 10.1007/s00383-021-04890-6. PMID: 33768347
Qiang S, Fan M, Cui Q, Li Z, Zhou Y, Li Q, Li F
Medicine (Baltimore) 2020 Jul 31;99(31):e21439. doi: 10.1097/MD.0000000000021439. PMID: 32756156Free PMC Article
Vinycomb T, Browning A, Jones MLM, Hutson JM, King SK, Teague WJ
J Pediatr Surg 2020 Oct;55(10):2111-2114. Epub 2019 Dec 28 doi: 10.1016/j.jpedsurg.2019.11.017. PMID: 31955988
Bishop JC, McCormick B, Johnson CT, Miller J, Jelin E, Blakemore K, Jelin AC
Fetal Diagn Ther 2020;47(2):98-103. Epub 2019 Jun 5 doi: 10.1159/000500471. PMID: 31167209Free PMC Article

Clinical prediction guides

Zrinyi A, Lum Min SA, Bello EA, Singh C, Keijzer R
Pediatr Surg Int 2023 Jan 18;39(1):84. doi: 10.1007/s00383-022-05359-w. PMID: 36653532
Calcaterra V, Chiricosta L, Mazzon E, Gugnandolo A, Alberti D, Maestri L, Meroni M, Vestri E, Verduci E, Dilillo D, Zuccotti G, Pelizzo G
Orphanet J Rare Dis 2021 Oct 29;16(1):455. doi: 10.1186/s13023-021-02093-9. PMID: 34715892Free PMC Article
Toyama C, Masahata K, Ibuka S, Nara K, Soh H, Usui N
Pediatr Surg Int 2021 Jul;37(7):929-935. Epub 2021 Mar 25 doi: 10.1007/s00383-021-04890-6. PMID: 33768347
Bishop JC, McCormick B, Johnson CT, Miller J, Jelin E, Blakemore K, Jelin AC
Fetal Diagn Ther 2020;47(2):98-103. Epub 2019 Jun 5 doi: 10.1159/000500471. PMID: 31167209Free PMC Article
Ordorica-Flores R, Orpinel-Armendariz E, Rodríguez-Reyna R, Pérez-Escamirosa F, Castro-Luna R, Minor-Martínez A, Nieto-Zermeño J
Surg Innov 2019 Dec;26(6):738-743. Epub 2019 Oct 11 doi: 10.1177/1553350619881068. PMID: 31603039

Recent systematic reviews

Zhang J, Xu X, Wang X, Zhao L, Lv Y, Chen K
Pediatr Surg Int 2022 Nov;38(11):1507-1515. Epub 2022 Sep 2 doi: 10.1007/s00383-022-05209-9. PMID: 36053328
Miscia ME, Lauriti G, Di Renzo D, Riccio A, Lisi G, Lelli Chiesa P
Eur J Pediatr Surg 2021 Oct;31(5):445-451. Epub 2020 Sep 28 doi: 10.1055/s-0040-1716884. PMID: 32987434
Miscia ME, Lauriti G, Lelli Chiesa P, Zani A
Pediatr Surg Int 2019 Jan;35(1):151-157. Epub 2018 Nov 1 doi: 10.1007/s00383-018-4387-1. PMID: 30386906
Mentessidou A, Saxena AK
World J Surg 2017 Aug;41(8):2178-2184. doi: 10.1007/s00268-017-3937-3. PMID: 28258456
Chung PH, Wong CW, Ip DK, Tam PK, Wong KK
J Pediatr Surg 2017 Mar;52(3):498-503. Epub 2016 Aug 30 doi: 10.1016/j.jpedsurg.2016.08.010. PMID: 27622585

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center