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MedGen UID:
Concept ID:
Anatomical Abnormality; Finding
Synonym: Hernias
SNOMED CT: Hernia (414403008); Herniated structure (414403008); Herniated tissue (414403008); Herniation (414403008)
HPO: HP:0100790


The protrusion of part of an organ or fibroadipose tissue through an abnormal opening. [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVHernia

Conditions with this feature

MedGen UID:
Concept ID:
Disease or Syndrome
Fucosidosis is an autosomal recessive lysosomal storage disease caused by defective alpha-L-fucosidase with accumulation of fucose in the tissues. Clinical features include angiokeratoma, progressive psychomotor retardation, neurologic signs, coarse facial features, and dysostosis multiplex. Fucosidosis has been classified into 2 major types. Type 1 is characterized by rapid psychomotor regression and severe neurologic deterioration beginning at about 6 months of age, elevated sweat sodium chloride, and death within the first decade of life. Type 2 is characterized by milder psychomotor retardation and neurologic signs, the development of angiokeratoma corporis diffusum, normal sweat salinity, and longer survival (Kousseff et al., 1976).
Mucopolysaccharidosis, MPS-III-C
MedGen UID:
Concept ID:
Disease or Syndrome
Mucopolysaccharidosis type III (MPS III) is a multisystem lysosomal storage disease characterized by progressive central nervous system degeneration manifest as severe intellectual disability (ID), developmental regression, and other neurologic manifestations including autism spectrum disorder (ASD), behavioral problems, and sleep disturbances. Disease onset is typically before age ten years. Disease course may be rapidly or slowly progressive; some individuals with an extremely attenuated disease course present in mid-to-late adulthood with early-onset dementia with or without a history of ID. Systemic manifestations can include musculoskeletal problems (joint stiffness, contractures, scoliosis, and hip dysplasia), hearing loss, respiratory tract and sinopulmonary infections, and cardiac disease (valvular thickening, defects in the cardiac conduction system). Neurologic decline is seen in all affected individuals; however, clinical severity varies within and among the four MPS III subtypes (defined by the enzyme involved) and even among members of the same family. Death usually occurs in the second or third decade of life secondary to neurologic regression or respiratory tract infections.
Hurler syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
Mucopolysaccharidosis type I (MPS I) is a progressive multisystem disorder with features ranging over a continuum of severity. While affected individuals have traditionally been classified as having one of three MPS I syndromes (Hurler syndrome, Hurler-Scheie syndrome, or Scheie syndrome), no easily measurable biochemical differences have been identified and the clinical findings overlap. Affected individuals are best described as having either a phenotype consistent with either severe (Hurler syndrome) or attenuated MPS I, a distinction that influences therapeutic options. Severe MPS I. Infants appear normal at birth. Typical early manifestations are nonspecific (e.g., umbilical or inguinal hernia, frequent upper respiratory tract infections before age 1 year). Coarsening of the facial features may not become apparent until after age one year. Gibbus deformity of the lower spine is common and often noted within the first year. Progressive skeletal dysplasia (dysostosis multiplex) involving all bones is universal, as is progressive arthropathy involving most joints. By age three years, linear growth decreases. Intellectual disability is progressive and profound but may not be readily apparent in the first year of life. Progressive cardiorespiratory involvement, hearing loss, and corneal clouding are common. Without treatment, death (typically from cardiorespiratory failure) usually occurs within the first ten years of life. Attenuated MPS I. Clinical onset is usually between ages three and ten years. The severity and rate of disease progression range from serious life-threatening complications leading to death in the second to third decade, to a normal life span complicated by significant disability from progressive joint manifestations and cardiorespiratory disease. While some individuals have no neurologic involvement and psychomotor development may be normal in early childhood, learning disabilities and psychiatric manifestations can be present later in life. Hearing loss, cardiac valvular disease, respiratory involvement, and corneal clouding are common.
Freeman-Sheldon syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
Freeman-Sheldon syndrome (FSS), or DA2A, is phenotypically similar to DA1. In addition to contractures of the hands and feet, FSS is characterized by oropharyngeal abnormalities, scoliosis, and a distinctive face that includes a very small oral orifice (often only a few millimeters in diameter at birth), puckered lips, and an H-shaped dimple of the chin; hence, FSS has been called 'whistling face syndrome.' The limb phenotypes of DA1 and FSS may be so similar that they can only be distinguished by the differences in facial morphology (summary by Bamshad et al., 2009). For a general phenotypic description and a discussion of genetic heterogeneity of distal arthrogryposis, see DA1 (108120).
MedGen UID:
Concept ID:
Disease or Syndrome
Aspartylglucosaminuria (AGU) is a severe autosomal recessive lysosomal storage disorder that involves the central nervous system and causes skeletal abnormalities as well as connective tissue lesions. The most characteristic feature is progressive mental retardation. The disorder is caused by deficient activity of the lysosomal enzyme glycosylasparaginase, which results in body fluid and tissue accumulation of a series of glycoasparagines, i.e., glycoconjugates with an aspartylglucosamine moiety at the reducing end. AGU belongs to the group of disorders commonly referred to as the Finnish disease heritage (summary by Mononen et al., 1993 and Arvio and Arvio, 2002).
Ehlers-Danlos syndrome, classic type, 2
MedGen UID:
Concept ID:
Disease or Syndrome
Classic Ehlers-Danlos syndrome (cEDS) is a connective tissue disorder characterized by skin hyperextensibility, atrophic scarring, and generalized joint hypermobility (GJH). The skin is soft and doughy to the touch, and hyperextensible, extending easily and snapping back after release (unlike lax, redundant skin, as in cutis laxa). The skin is fragile, as manifested by splitting of the dermis following relatively minor trauma, especially over pressure points (knees, elbows) and areas prone to trauma (shins, forehead, chin). Wound healing is poor, and stretching of scars after apparently successful primary wound healing is characteristic. Complications of joint hypermobility, such as dislocations of the shoulder, patella, digits, hip, radius, and clavicle, usually resolve spontaneously or are easily managed by the affected individual. Other features include hypotonia with delayed motor development, fatigue and muscle cramps, and easy bruising. Mitral valve prolapse can occur infrequently, but tends to be of little clinical consequence. Aortic root dilatation has been reported, appears to be more common in young individuals, and rarely progresses.
Toriello-Carey syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
Toriello-Carey syndrome is a multiple congenital anomaly disorder with variable systemic manifestations, most commonly including mental retardation, agenesis of the corpus callosum, postnatal growth delay, cardiac defects, usually septal defects, distal limb defects, and urogenital anomalies in affected males. Patients have facial dysmorphic features, micrognathia, including full cheeks, hypertelorism, flattened nasal bridge, anteverted nares, and short neck. Not all features are found in all patients and some patients may have additional features such as anal anomalies or hernias (summary by Toriello et al., 2003). In a review of the Toriello-Carey syndrome, Toriello et al. (2016) stated that while corpus callosum abnormalities and micrognathia with highly arched or cleft palate are seen in most patients, other manifestations are widely variable. They noted that etiologic heterogeneity has been observed in reported patients, with at least 20% of patients having chromosome anomalies, and that no good candidate genes have been identified by exome sequencing. The authors commented that this condition might not be a unitary diagnostic entity. They recommended chromosome microarray for any child suspected of having the condition, followed by standard of care by genetic testing.
Megalencephaly-capillary malformation-polymicrogyria syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
PIK3CA-related overgrowth spectrum (PROS) encompasses a range of clinical findings in which the core features are congenital or early-childhood onset of segmental/focal overgrowth with or without cellular dysplasia. Prior to the identification of PIK3CA as the causative gene, PROS was separated into distinct clinical syndromes based on the tissues and/or organs involved (e.g., MCAP [megalencephaly-capillary malformation] syndrome and CLOVES [congenital lipomatous asymmetric overgrowth of the trunk, lymphatic, capillary, venous, and combined-type vascular malformations, epidermal nevi, skeletal and spinal anomalies] syndrome). The predominant areas of overgrowth include the brain, limbs (including fingers and toes), trunk (including abdomen and chest), and face, all usually in an asymmetric distribution. Generalized brain overgrowth may be accompanied by secondary overgrowth of specific brain structures resulting in ventriculomegaly, a markedly thick corpus callosum, and cerebellar tonsillar ectopia with crowding of the posterior fossa. Vascular malformations may include capillary, venous, and less frequently, arterial or mixed (capillary-lymphatic-venous or arteriovenous) malformations. Lymphatic malformations may be in various locations (internal and/or external) and can cause various clinical issues, including swelling, pain, and occasionally localized bleeding secondary to trauma. Lipomatous overgrowth may occur ipsilateral or contralateral to a vascular malformation, if present. The degree of intellectual disability appears to be mostly related to the presence and severity of seizures, cortical dysplasia (e.g., polymicrogyria), and hydrocephalus. Many children have feeding difficulties that are often multifactorial in nature. Endocrine issues affect a small number of individuals and most commonly include hypoglycemia (largely hypoinsulinemic hypoketotic hypoglycemia), hypothyroidism, and growth hormone deficiency.
Cutis laxa, autosomal dominant 3
MedGen UID:
Concept ID:
Disease or Syndrome
Autosomal dominant cutis laxa-3 is characterized by thin skin with visible veins and wrinkles, cataract or corneal clouding, clenched fingers, pre- and postnatal growth retardation, and moderate intellectual disability. In addition, patients exhibit a combination of muscular hypotonia with brisk muscle reflexes (Fischer-Zirnsak et al., 2015). For a general phenotypic description and discussion of genetic heterogeneity of autosomal dominant cutis laxa, see ARCL1 (123700).
Bone marrow failure syndrome 3
MedGen UID:
Concept ID:
Disease or Syndrome
Bone marrow failure syndrome-3 is an autosomal recessive disorder characterized by onset of pancytopenia in early childhood. Patients may have additional variable nonspecific somatic abnormalities, including poor growth, microcephaly, and skin anomalies (summary by Tummala et al., 2016). BMFS3 has a distinct phenotype and may include features that overlap with Shwachman-Diamond syndrome (SDS1; 260400), such as pancreatic insufficiency and short stature, and with dyskeratosis congenita (see, e.g., DKCA1, 127550), such as dental and hair abnormalities and shortened telomeres. In addition, some patients may have joint and skeletal abnormalities, impaired development, and retinal dysplasia (summary by D'Amours et al., 2018). For a discussion of genetic heterogeneity of BMFS, see BMFS1 (614675).

Professional guidelines


Yadlapati R, Gyawali CP, Pandolfino JE; CGIT GERD Consensus Conference Participants
Clin Gastroenterol Hepatol 2022 May;20(5):984-994.e1. Epub 2022 Feb 2 doi: 10.1016/j.cgh.2022.01.025. PMID: 35123084Free PMC Article
Shakil A, Aparicio K, Barta E, Munez K
Am Fam Physician 2020 Oct 15;102(8):487-492. PMID: 33064426
HerniaSurge Group
Hernia 2018 Feb;22(1):1-165. Epub 2018 Jan 12 doi: 10.1007/s10029-017-1668-x. PMID: 29330835Free PMC Article

Recent clinical studies


Sæter AH, Fonnes S, Rosenberg J, Andresen K
Surg Endosc 2022 Nov;36(11):7961-7973. Epub 2022 May 31 doi: 10.1007/s00464-022-09327-2. PMID: 35641700
Perez AJ, Campbell S
J Am Med Dir Assoc 2022 Apr;23(4):563-567. Epub 2022 Mar 5 doi: 10.1016/j.jamda.2022.02.008. PMID: 35259338
Alayon-Rosario M, Schlosser K, Griscom T, Bolton W, Hall A, Augenstein V, Cobb WS, Warren JA, Carbonell AM
Hernia 2021 Dec;25(6):1621-1628. Epub 2020 Apr 24 doi: 10.1007/s10029-020-02194-7. PMID: 32333211
Ramachandran V, Edwards CF, Bichianu DC
Neoreviews 2020 Jun;21(6):e392-e403. doi: 10.1542/neo.21-6-e392. PMID: 32482701
Simons MP, Aufenacker T, Bay-Nielsen M, Bouillot JL, Campanelli G, Conze J, de Lange D, Fortelny R, Heikkinen T, Kingsnorth A, Kukleta J, Morales-Conde S, Nordin P, Schumpelick V, Smedberg S, Smietanski M, Weber G, Miserez M
Hernia 2009 Aug;13(4):343-403. Epub 2009 Jul 28 doi: 10.1007/s10029-009-0529-7. PMID: 19636493Free PMC Article


Musbahi A, Mahawar K
Br J Surg 2023 Mar 30;110(4):401-402. doi: 10.1093/bjs/znac449. PMID: 36610072
Nnadozie UU, Onyeyirichi O, Maduba CC, Ekwesianya AC
Ghana Med J 2021 Sep;55(3):229-231. doi: 10.4314/gmj.v55i3.9. PMID: 35950172Free PMC Article
Am Fam Physician 2020 Oct 15;102(8):Online. PMID: 33064435
Park HR, Park SB, Lee ES, Park HJ
Clin Imaging 2016 Sep-Oct;40(5):949-55. Epub 2016 May 3 doi: 10.1016/j.clinimag.2016.04.017. PMID: 27209238
Spangen L
World J Surg 1989 Sep-Oct;13(5):573-80. doi: 10.1007/BF01658873. PMID: 2683401


Haladu N, Alabi A, Brazzelli M, Imamura M, Ahmed I, Ramsay G, Scott NW
Surg Endosc 2022 Jul;36(7):4685-4700. Epub 2022 Mar 14 doi: 10.1007/s00464-022-09161-6. PMID: 35286471Free PMC Article
Aiolfi A, Cavalli M, Ferraro SD, Manfredini L, Bonitta G, Bruni PG, Bona D, Campanelli G
Ann Surg 2021 Dec 1;274(6):954-961. doi: 10.1097/SLA.0000000000004735. PMID: 33427757
Kavak Akelma F, Altınsoy S, Arslan MT, Ergil J
Anaesthesist 2020 Mar;69(3):198-204. Epub 2020 Feb 11 doi: 10.1007/s00101-020-00731-8. PMID: 32047952
Lockhart K, Dunn D, Teo S, Ng JY, Dhillon M, Teo E, van Driel ML
Cochrane Database Syst Rev 2018 Sep 13;9(9):CD011517. doi: 10.1002/14651858.CD011517.pub2. PMID: 30209805Free PMC Article
Dietz UA, Menzel S, Lock J, Wiegering A
Dtsch Arztebl Int 2018 Jan 19;115(3):31-37. doi: 10.3238/arztebl.2018.0031. PMID: 29366450Free PMC Article


De Alwis D, Ades A, Nanayakkara P
Obstet Gynecol Surv 2021 Dec;76(12):751-759. doi: 10.1097/OGX.0000000000000961. PMID: 34942651
Barutcu AG, Klein D, Kilian M, Biebl M, Raakow R, Pratschke J, Raakow J
Surg Endosc 2020 Jan;34(1):126-132. Epub 2019 Mar 12 doi: 10.1007/s00464-019-06739-5. PMID: 30863926
Wang Y, Honeyford K, Aylin P, Bottle A, Giuliani S
BJS Open 2019 Jun;3(3):305-313. Epub 2019 Jan 31 doi: 10.1002/bjs5.50135. PMID: 31183446Free PMC Article
Lesinski J, Zielonka TM, Wajtryt O, Peplinska K, Kaszynska A
Adv Respir Med 2019;87(1):54-62. Epub 2019 Mar 4 doi: 10.5603/ARM.a2019.0009. PMID: 30830959
Rubikas R
Eur J Cardiothorac Surg 2001 Jul;20(1):53-7. doi: 10.1016/s1010-7940(01)00753-9. PMID: 11423274

Clinical prediction guides

Ono R, Kitagawa I
Gastroenterology 2021 Aug;161(2):427-428. Epub 2021 May 5 doi: 10.1053/j.gastro.2021.04.072. PMID: 33961884
Li X, Wen D, Li X, Yao C, Chong W, Chen H
Front Immunol 2020;11:1678. Epub 2020 Sep 3 doi: 10.3389/fimmu.2020.01678. PMID: 33013820Free PMC Article
Chatterjee D, Ing RJ, Gien J
Anesth Analg 2020 Sep;131(3):808-821. doi: 10.1213/ANE.0000000000004324. PMID: 31335403
Park HR, Park SB, Lee ES, Park HJ
Clin Imaging 2016 Sep-Oct;40(5):949-55. Epub 2016 May 3 doi: 10.1016/j.clinimag.2016.04.017. PMID: 27209238
Cohn RM, Lerebours F, Strauss EJ
Bull Hosp Jt Dis (2013) 2015 Jun;73(2):90-9. PMID: 26517161

Recent systematic reviews

Deerenberg EB, Henriksen NA, Antoniou GA, Antoniou SA, Bramer WM, Fischer JP, Fortelny RH, Gök H, Harris HW, Hope W, Horne CM, Jensen TK, Köckerling F, Kretschmer A, López-Cano M, Malcher F, Shao JM, Slieker JC, de Smet GHJ, Stabilini C, Torkington J, Muysoms FE
Br J Surg 2022 Nov 22;109(12):1239-1250. doi: 10.1093/bjs/znac302. PMID: 36026550Free PMC Article
Sæter AH, Fonnes S, Rosenberg J, Andresen K
Surg Endosc 2022 Nov;36(11):7961-7973. Epub 2022 May 31 doi: 10.1007/s00464-022-09327-2. PMID: 35641700
Cirocchi R, Burini G, Avenia S, Tebala G, Palumbo P, Cianci MC, Morabito A, Bruzzone P
ANZ J Surg 2022 Oct;92(10):2433-2441. Epub 2022 Mar 26 doi: 10.1111/ans.17594. PMID: 35338686
Solaini L, Cavaliere D, Avanzolini A, Rocco G, Ercolani G
J Robot Surg 2022 Aug;16(4):775-781. Epub 2021 Oct 5 doi: 10.1007/s11701-021-01312-6. PMID: 34609697Free PMC Article
Aiolfi A, Cavalli M, Ferraro SD, Manfredini L, Bonitta G, Bruni PG, Bona D, Campanelli G
Ann Surg 2021 Dec 1;274(6):954-961. doi: 10.1097/SLA.0000000000004735. PMID: 33427757

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