U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Diastasis recti

MedGen UID:
113171
Concept ID:
C0221766
Disease or Syndrome
Synonyms: Divarication of recti; Divarification of recti; Gap between large left and right abdominal muscles
SNOMED CT: Diastasis recti (62629000); Divarification of recti (62629000); Divarication of recti (62629000)
 
HPO: HP:0001540

Definition

A separation of the rectus abdominis muscle into right and left halves (which are normally joined at the midline at the linea alba). [from HPO]

Term Hierarchy

Conditions with this feature

Beckwith-Wiedemann syndrome
MedGen UID:
2562
Concept ID:
C0004903
Disease or Syndrome
Beckwith-Wiedemann syndrome (BWS) is a growth disorder variably characterized by neonatal hypoglycemia, macrosomia, macroglossia, hemihyperplasia, omphalocele, embryonal tumors (e.g., Wilms tumor, hepatoblastoma, neuroblastoma, and rhabdomyosarcoma), visceromegaly, adrenocortical cytomegaly, renal abnormalities (e.g., medullary dysplasia, nephrocalcinosis, medullary sponge kidney, and nephromegaly), and ear creases/pits. BWS is considered a clinical spectrum, in which affected individuals may have many of these features or may have only one or two clinical features. Early death may occur from complications of prematurity, hypoglycemia, cardiomyopathy, macroglossia, or tumors. However, the previously reported mortality of 20% is likely an overestimate given better recognition of the disorder along with enhanced treatment options. Macroglossia and macrosomia are generally present at birth but may have postnatal onset. Growth rate slows around age seven to eight years. Hemihyperplasia may affect segmental regions of the body or selected organs and tissues.
5p partial monosomy syndrome
MedGen UID:
41345
Concept ID:
C0010314
Disease or Syndrome
Cri-du-chat syndrome was first described by Lejeune et al. (1963) as a hereditary congenital syndrome associated with deletion of part of the short arm of chromosome 5. The deletions can vary in size from extremely small and involving only band 5p15.2 to the entire short arm. Although the majority of deletions arise as new mutations, approximately 12% result from unbalanced segregation of translocations or recombination involving a pericentric inversion in one of the parents.
Focal dermal hypoplasia
MedGen UID:
42055
Concept ID:
C0016395
Disease or Syndrome
Focal dermal hypoplasia is a multisystem disorder characterized primarily by involvement of the skin, skeletal system, eyes, and face. Skin manifestations present at birth include atrophic and hypoplastic areas of skin; cutis aplasia; fat nodules in the dermis manifesting as soft, yellow-pink cutaneous nodules; and pigmentary changes. Verrucoid papillomas of the skin and mucous membranes may appear later. The nails can be ridged, dysplastic, or hypoplastic; hair can be sparse or absent. Limb malformations include oligo-/syndactyly and split hand/foot. Developmental abnormalities of the eye can include anophthalmia/microphthalmia, iris and chorioretinal coloboma, and lacrimal duct abnormalities. Craniofacial findings can include facial asymmetry, notched alae nasi, cleft lip and palate, and pointed chin. Occasional findings include dental anomalies, abdominal wall defects, diaphragmatic hernia, and renal anomalies. Psychomotor development is usually normal; some individuals have cognitive impairment.
Mucopolysaccharidosis type 7
MedGen UID:
43108
Concept ID:
C0085132
Disease or Syndrome
Mucopolysaccharidosis type VII (MPS7) is an autosomal recessive lysosomal storage disease characterized by the inability to degrade glucuronic acid-containing glycosaminoglycans. The phenotype is highly variable, ranging from severe lethal hydrops fetalis to mild forms with survival into adulthood. Most patients with the intermediate phenotype show hepatomegaly, skeletal anomalies, coarse facies, and variable degrees of mental impairment (Shipley et al., 1993). MPS VII was the first autosomal mucopolysaccharidosis for which chromosomal assignment was achieved.
Weaver syndrome
MedGen UID:
120511
Concept ID:
C0265210
Disease or Syndrome
EZH2-related overgrowth includes EZH2-related Weaver syndrome at one end of the spectrum and tall stature at the other. Although most individuals diagnosed with a heterozygous EZH2 pathogenic variant have been identified because of a clinical suspicion of Weaver syndrome, a minority have been identified through molecular genetic testing of family members of probands or individuals with overgrowth who did not have a clinical diagnosis of Weaver syndrome. Thus, the extent of the phenotypic spectrum associated with a heterozygous EZH2 pathogenic variant is not yet known. Weaver syndrome is characterized by tall stature, variable intellect (ranging from normal intellect to severe intellectual disability), characteristic facial appearance, and a range of associated clinical features including advanced bone age, poor coordination, soft doughy skin, camptodactyly of the fingers and/or toes, umbilical hernia, abnormal tone, and hoarse low cry in infancy. Brain MRI has identified abnormalities in a few individuals with EZH2-related overgrowth. Neuroblastoma occurs at a slightly increased frequency in individuals with a heterozygous EZH2 pathogenic variant but data are insufficient to determine absolute risk. There is currently no evidence that additional malignancies (including hematologic malignancies) occur with increased frequency.
Peters plus syndrome
MedGen UID:
163204
Concept ID:
C0796012
Disease or Syndrome
Peters plus syndrome is characterized by anterior chamber eye anomalies, short limbs with broad distal extremities, characteristic facial features, cleft lip/palate, and variable developmental delay / intellectual disability. The most common anterior chamber defect is Peters' anomaly, consisting of central corneal clouding, thinning of the posterior cornea, and iridocorneal adhesions. Cataracts and glaucoma are common. Developmental delay is observed in about 80% of children; intellectual disability can range from mild to severe.
3MC syndrome 3
MedGen UID:
208657
Concept ID:
C0796032
Disease or Syndrome
The term '3MC syndrome' encompasses 4 rare autosomal recessive disorders that were previously designated the Carnevale, Mingarelli, Malpuech, and Michels syndromes, respectively. The main features of these syndromes are facial dysmorphism that includes hypertelorism, blepharophimosis, blepharoptosis, and highly arched eyebrows, which are present in 70 to 95% of cases. Cleft lip and palate, postnatal growth deficiency, cognitive impairment, and hearing loss are also consistent findings, occurring in 40 to 68% of cases. Craniosynostosis, radioulnar synostosis, and genital and vesicorenal anomalies occur in 20 to 30% of cases. Rare features include anterior chamber defects, cardiac anomalies, caudal appendage, umbilical hernia (omphalocele), and diastasis recti (summary by Rooryck et al., 2011). For a discussion of genetic heterogeneity of 3MC syndrome, see 3MC1 (257920).
3MC syndrome 1
MedGen UID:
167100
Concept ID:
C0796059
Disease or Syndrome
The term '3MC syndrome' encompasses 4 rare autosomal recessive disorders that were previously designated the Carnevale, Mingarelli, Malpuech, and Michels syndromes, respectively. The main features of these syndromes are facial dysmorphism that includes hypertelorism, blepharophimosis, blepharoptosis, and highly arched eyebrows, which are present in 70 to 95% of cases. Cleft lip and palate, postnatal growth deficiency, cognitive impairment, and hearing loss are also consistent findings, occurring in 40 to 68% of cases. Craniosynostosis, radioulnar synostosis, and genital and vesicorenal anomalies occur in 20 to 30% of cases. Rare features include anterior chamber defects, cardiac anomalies, caudal appendage, umbilical hernia (omphalocele), and diastasis recti (summary by Rooryck et al., 2011). Genetic Heterogeneity of 3MC Syndrome Also see 3MC syndrome-2 (3MC2; 265050), caused by mutation in the COLEC11 gene (612502), and 3MC syndrome-3 (3MC3; 248340), caused by mutation in the COLEC1 gene (607620).
Simpson-Golabi-Behmel syndrome type 1
MedGen UID:
162917
Concept ID:
C0796154
Disease or Syndrome
Simpson-Golabi-Behmel syndrome type 1 (SGBS1) is characterized by pre- and postnatal macrosomia; distinctive craniofacial features (including macrocephaly, coarse facial features, macrostomia, macroglossia, and palatal abnormalities); and commonly, mild-to-severe intellectual disability with or without structural brain anomalies. Other variable findings include supernumerary nipples, diastasis recti / umbilical hernia, congenital heart defects, diaphragmatic hernia, genitourinary defects, and gastrointestinal anomalies. Skeletal anomalies can include vertebral fusion, scoliosis, rib anomalies, and congenital hip dislocation. Hand anomalies can include large hands and postaxial polydactyly. Affected individuals are at increased risk for embryonal tumors including Wilms tumor, hepatoblastoma, adrenal neuroblastoma, gonadoblastoma, hepatocellular carcinoma, and medulloblastoma.
3MC syndrome 2
MedGen UID:
167115
Concept ID:
C0796279
Disease or Syndrome
The term '3MC syndrome' encompasses 4 rare autosomal recessive disorders that were previously designated the Carnevale, Mingarelli, Malpuech, and Michels syndromes, respectively. The main features of these syndromes are facial dysmorphism that includes hypertelorism, blepharophimosis, blepharoptosis, and highly arched eyebrows, which are present in 70 to 95% of cases. Cleft lip and palate, postnatal growth deficiency, cognitive impairment, and hearing loss are also consistent findings, occurring in 40 to 68% of cases. Craniosynostosis, radioulnar synostosis, and genital and vesicorenal anomalies occur in 20 to 30% of cases. Rare features include anterior chamber defects, cardiac anomalies, caudal appendage, umbilical hernia (omphalocele), and diastasis recti (summary by Rooryck et al., 2011). For a discussion of genetic heterogeneity of 3MC syndrome, see 3MC1 (257920).
SCARF syndrome
MedGen UID:
326461
Concept ID:
C1839321
Disease or Syndrome
Syndrome with the association of skeletal abnormalities, cutis laxa, craniostenosis, ambiguous genitalia, psychomotor retardation and facial abnormalities. So far, it has been described in two males (maternal first cousins). The mode of inheritance was suggested to be X-linked recessive.
Alport syndrome-intellectual disability-midface hypoplasia-elliptocytosis syndrome
MedGen UID:
337424
Concept ID:
C1846242
Disease or Syndrome
The AMME complex is an X-linked contiguous gene deletion syndrome with features of Alport syndrome (see 301050), impaired intellectual development, midface hypoplasia, and elliptocytosis in affected males (summary by Meloni et al., 2002).
Primary intraosseous venous malformation
MedGen UID:
376071
Concept ID:
C1847197
Disease or Syndrome
Primary intraosseous vascular malformation (VMPI), previously called intraosseous hemangioma, is a rare malformation that usually involves the vertebral column and the skull. The most commonly affected bones in the skull are the mandible and the maxilla, and life-threatening bleeding after a simple tooth extraction is frequent (Vargel et al., 2002).
Ehlers-Danlos syndrome, musculocontractural type
MedGen UID:
356497
Concept ID:
C1866294
Disease or Syndrome
Bleeding problems are common in the vascular type of Ehlers-Danlos syndrome and are caused by unpredictable tearing (rupture) of blood vessels and organs. These complications can lead to easy bruising, internal bleeding, a hole in the wall of the intestine (intestinal perforation), or stroke. During pregnancy, women with vascular Ehlers-Danlos syndrome may experience rupture of the uterus. Additional forms of Ehlers-Danlos syndrome that involve rupture of the blood vessels include the kyphoscoliotic, classical, and classical-like types.\n\nOther types of Ehlers-Danlos syndrome have additional signs and symptoms. The cardiac-valvular type causes severe problems with the valves that control the movement of blood through the heart. People with the kyphoscoliotic type experience severe curvature of the spine that worsens over time and can interfere with breathing by restricting lung expansion. A type of Ehlers-Danlos syndrome called brittle cornea syndrome is characterized by thinness of the clear covering of the eye (the cornea) and other eye abnormalities. The spondylodysplastic type features short stature and skeletal abnormalities such as abnormally curved (bowed) limbs. Abnormalities of muscles, including hypotonia and permanently bent joints (contractures), are among the characteristic signs of the musculocontractural and myopathic forms of Ehlers-Danlos syndrome. The periodontal type causes abnormalities of the teeth and gums.\n\nMany people with the Ehlers-Danlos syndromes have soft, velvety skin that is highly stretchy (elastic) and fragile. Affected individuals tend to bruise easily, and some types of the condition also cause abnormal scarring. People with the classical form of Ehlers-Danlos syndrome experience wounds that split open with little bleeding and leave scars that widen over time to create characteristic "cigarette paper" scars. The dermatosparaxis type of the disorder is characterized by loose skin that sags and wrinkles, and extra (redundant) folds of skin may be present.\n\nAn unusually large range of joint movement (hypermobility) occurs in most forms of Ehlers-Danlos syndrome, and it is a hallmark feature of the hypermobile type. Infants and children with hypermobility often have weak muscle tone (hypotonia), which can delay the development of motor skills such as sitting, standing, and walking. The loose joints are unstable and prone to dislocation and chronic pain. In the arthrochalasia type of Ehlers-Danlos syndrome, infants have hypermobility and dislocations of both hips at birth.\n\nThe various forms of Ehlers-Danlos syndrome have been classified in several different ways. Originally, 11 forms of Ehlers-Danlos syndrome were named using Roman numerals to indicate the types (type I, type II, and so on). In 1997, researchers proposed a simpler classification (the Villefranche nomenclature) that reduced the number of types to six and gave them descriptive names based on their major features. In 2017, the classification was updated to include rare forms of Ehlers-Danlos syndrome that were identified more recently. The 2017 classification describes 13 types of Ehlers-Danlos syndrome.\n\nEhlers-Danlos syndrome is a group of disorders that affect connective tissues supporting the skin, bones, blood vessels, and many other organs and tissues. Defects in connective tissues cause the signs and symptoms of these conditions, which range from mildly loose joints to life-threatening complications.
Mucolipidosis type II
MedGen UID:
435914
Concept ID:
C2673377
Disease or Syndrome
GNPTAB-related disorders comprise the phenotypes mucolipidosis II (ML II) and mucolipidosis IIIa/ß (ML IIIa/ß), and phenotypes intermediate between ML II and ML IIIa/ß. ML II is evident at birth and slowly progressive; death most often occurs in early childhood. Orthopedic abnormalities present at birth may include thoracic deformity, kyphosis, clubfeet, deformed long bones, and/or dislocation of the hip(s). Growth often ceases in the second year of life; contractures develop in all large joints. The skin is thickened, facial features are coarse, and gingiva are hypertrophic. All children have cardiac involvement, most commonly thickening and insufficiency of the mitral valve and, less frequently, the aortic valve. Progressive mucosal thickening narrows the airways, and gradual stiffening of the thoracic cage contributes to respiratory insufficiency, the most common cause of death. ML IIIa/ß becomes evident at about age three years with slow growth rate and short stature; joint stiffness and pain initially in the shoulders, hips, and fingers; gradual mild coarsening of facial features; and normal to mildly impaired cognitive development. Pain from osteoporosis becomes more severe during adolescence. Cardiorespiratory complications (restrictive lung disease, thickening and insufficiency of the mitral and aortic valves, left and/or right ventricular hypertrophy) are common causes of death, typically in early to middle adulthood. Phenotypes intermediate between ML II and ML IIIa/ß are characterized by physical growth in infancy that resembles that of ML II and neuromotor and speech development that resemble that of ML IIIa/ß.
Diastasis recti and weakness of the linea alba
MedGen UID:
394255
Concept ID:
C2677303
Disease or Syndrome
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).
Macrocephaly-intellectual disability-neurodevelopmental disorder-small thorax syndrome
MedGen UID:
899689
Concept ID:
C4225259
Disease or Syndrome
Smith-Kingsmore syndrome (SKS) is a rare autosomal dominant syndromic intellectual disability syndrome characterized by macrocephaly, seizures, umbilical hernia, and facial dysmorphic features including frontal bossing, midface hypoplasia, small chin, hypertelorism with downslanting palpebral fissures, depressed nasal bridge, smooth philtrum, and thin upper lip (Smith et al., 2013; Baynam et al., 2015).
Gonadal dysgenesis, dysmorphic facies, retinal dystrophy, and myopathy
MedGen UID:
1679397
Concept ID:
C5193085
Disease or Syndrome
Myoectodermal gonadal dysgenesis syndrome (MEGD) is characterized by 46,XY complete or partial gonadal dysgenesis, or 46,XX gonadal dysgenesis, in association with extragonadal anomalies, including low birth weight, typical facies, rod and cone dystrophy, sensorineural hearing loss, omphalocele, anal atresia, renal agenesis, skeletal abnormalities, dry and scaly skin, severe myopathy, and neuromotor delay. Dysmorphic facial features along with muscular habitus are the hallmarks of the syndrome. Abnormal hair patterning with frontal upsweep and additional whorls, eyebrow abnormalities comprising broad, arched, and sparse or thick eyebrows, underdeveloped alae nasi, smooth philtrum, and low-set ears with overfolded helices facilitate a gestalt diagnosis. (Guran et al., 2019; Altunoglu et al., 2022).
Developmental and epileptic encephalopathy, 77
MedGen UID:
1684735
Concept ID:
C5231405
Disease or Syndrome
Multiple congenital anomalies-hypotonia-seizures syndrome-4 (MCAHS4) is an autosomal recessive neurologic disorder characterized by onset of refractory seizures in the first months of life. Patients have severe global developmental delay, and may have additional variable features, including dysmorphic or coarse facial features, visual defects, and mild skeletal or renal anomalies. At the cellular level, the disorder is caused by a defect in the synthesis of glycosylphosphatidylinositol (GPI), and thus affects the expression of GPI-anchored proteins at the cell surface (summary by Starr et al., 2019). For a discussion of genetic heterogeneity of MCAHS, see MCAHS1 (614080). For a discussion of genetic heterogeneity of DEE, see 308350. For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Tolchin-Le Caignec syndrome
MedGen UID:
1724999
Concept ID:
C5436509
Disease or Syndrome
Tolchin-Le Caignec syndrome (TOLCAS) is a developmental disorder characterized by mildly to moderately impaired intellectual development and behavioral problems, such as autism, ADHD, labile mood, and aggressive episodes. Many patients have bony abnormalities, including osteochondroma, craniosynostosis, dysmorphic facies, arachnodactyly, and large head circumference. Rarely, additional congenital anomalies may also be observed. These additional features and the bony defects are highly variable (summary by Tolchin et al., 2020).
Intellectual disability, autosomal dominant 40
MedGen UID:
1810363
Concept ID:
C5676894
Disease or Syndrome
Neurodevelopmental disorder with hypotonia, impaired language, and dysmorphic features (NEDHILD) is a rare neurodevelopmental disorder associated with impaired intellectual development, speech and language impairment, microcephaly, seizures, hypotonia, ophthalmologic issues, constipation/gastroesophageal reflux, and behavioral problems, including autism and sleep disturbances (summary by Garrity et al., 2021).
Paternal uniparental disomy of chromosome 14
MedGen UID:
1843450
Concept ID:
C5680251
Disease or Syndrome
Kagami-Ogata syndrome (KOS) is a rare imprinting disorder characterized prenatally by polyhydramnios, macrosomia, and placentomegaly. After birth, infants often have respiratory distress, feeding difficulties, and postnatal growth retardation. Thoracic abnormalities include small bell-shaped thorax, 'coat-hanger' ribs, narrow chest wall, and cardiac anomalies. Abdominal wall defects include omphalocele, diastasis recti, and inguinal hernias. Hepatoblastoma is present in some patients. Dysmorphic facial features include frontal bossing, depressed nasal bridge, hairy forehead, anteverted nares, micrognathia, and a short neck. Developmental findings include hypotonia, speech and/or motor delays, and normal to mildly impaired intellectual development (summary by Prasasya et al., 2020).

Professional guidelines

PubMed

Fiori F, Ferrara F, Gobatti D, Gentile D, Stella M
Hernia 2021 Aug;25(4):871-882. Epub 2020 Jun 20 doi: 10.1007/s10029-020-02252-0. PMID: 32564225
Michalska A, Rokita W, Wolder D, Pogorzelska J, Kaczmarczyk K
Ginekol Pol 2018;89(2):97-101. doi: 10.5603/GP.a2018.0016. PMID: 29512814
Mommers EHH, Ponten JEH, Al Omar AK, de Vries Reilingh TS, Bouvy ND, Nienhuijs SW
Surg Endosc 2017 Dec;31(12):4934-4949. Epub 2017 Jun 8 doi: 10.1007/s00464-017-5607-9. PMID: 28597282Free PMC Article

Recent clinical studies

Etiology

Gluppe SB, Ellström Engh M, Bø K
J Physiother 2023 Jul;69(3):160-167. Epub 2023 Jun 5 doi: 10.1016/j.jphys.2023.05.017. PMID: 37286390
Gluppe S, Engh ME, Bø K
Braz J Phys Ther 2021 Nov-Dec;25(6):664-675. Epub 2021 Jul 21 doi: 10.1016/j.bjpt.2021.06.006. PMID: 34391661Free PMC Article
Thabet AA, Alshehri MA
J Musculoskelet Neuronal Interact 2019 Mar 1;19(1):62-68. PMID: 30839304Free PMC Article
Lawson S, Sacks A
J Midwifery Womens Health 2018 Jul;63(4):410-417. Epub 2018 May 19 doi: 10.1111/jmwh.12736. PMID: 29778086
Michalska A, Rokita W, Wolder D, Pogorzelska J, Kaczmarczyk K
Ginekol Pol 2018;89(2):97-101. doi: 10.5603/GP.a2018.0016. PMID: 29512814

Diagnosis

Gluppe SB, Ellström Engh M, Bø K
J Physiother 2023 Jul;69(3):160-167. Epub 2023 Jun 5 doi: 10.1016/j.jphys.2023.05.017. PMID: 37286390
Kaya AK, Menek MY
Eur J Obstet Gynecol Reprod Biol 2023 Jun;285:24-30. Epub 2023 Apr 1 doi: 10.1016/j.ejogrb.2023.03.040. PMID: 37031572
Gluppe SB, Engh ME, Bø K
Phys Ther 2020 Aug 12;100(8):1372-1383. doi: 10.1093/ptj/pzaa070. PMID: 32302393
Gluppe SL, Hilde G, Tennfjord MK, Engh ME, Bø K
Phys Ther 2018 Apr 1;98(4):260-268. doi: 10.1093/ptj/pzy008. PMID: 29351646Free PMC Article
Fernandes da Mota PG, Pascoal AG, Carita AI, Bø K
Man Ther 2015 Feb;20(1):200-5. Epub 2014 Sep 19 doi: 10.1016/j.math.2014.09.002. PMID: 25282439

Therapy

Gluppe SB, Ellström Engh M, Bø K
J Physiother 2023 Jul;69(3):160-167. Epub 2023 Jun 5 doi: 10.1016/j.jphys.2023.05.017. PMID: 37286390
Gluppe S, Engh ME, Bø K
Braz J Phys Ther 2021 Nov-Dec;25(6):664-675. Epub 2021 Jul 21 doi: 10.1016/j.bjpt.2021.06.006. PMID: 34391661Free PMC Article
Keshwani N, Mathur S, McLean L
Physiother Theory Pract 2021 Sep;37(9):1018-1033. Epub 2019 Oct 23 doi: 10.1080/09593985.2019.1675207. PMID: 31642725
Thabet AA, Alshehri MA
J Musculoskelet Neuronal Interact 2019 Mar 1;19(1):62-68. PMID: 30839304Free PMC Article
Benjamin DR, van de Water AT, Peiris CL
Physiotherapy 2014 Mar;100(1):1-8. Epub 2013 Oct 5 doi: 10.1016/j.physio.2013.08.005. PMID: 24268942

Prognosis

Swanson E
Ann Plast Surg 2023 Feb 1;90(2):180-188. Epub 2022 Dec 21 doi: 10.1097/SAP.0000000000003387. PMID: 36688862Free PMC Article
Denizoglu Kulli H, Gurses HN
Eur J Obstet Gynecol Reprod Biol 2022 Dec;279:40-44. Epub 2022 Oct 5 doi: 10.1016/j.ejogrb.2022.10.001. PMID: 36242869
Harada BS, De Bortolli TT, Carnaz L, De Conti MHS, Hijaz A, Driusso P, Marini G
Physiother Theory Pract 2022 Oct;38(10):1538-1544. Epub 2020 Dec 7 doi: 10.1080/09593985.2020.1849476. PMID: 33283590
Veríssimo P, Nahas FX, Barbosa MV, de Carvalho Gomes HF, Ferreira LM
Aesthetic Plast Surg 2014 Apr;38(2):379-86. Epub 2014 Jan 30 doi: 10.1007/s00266-014-0272-z. PMID: 24477520
Moesbergen T, Law A, Roake J, Lewis DR
Vascular 2009 Nov-Dec;17(6):325-9. doi: 10.2310/6670.2009.00047. PMID: 19909679

Clinical prediction guides

Gluppe SB, Ellström Engh M, Bø K
J Physiother 2023 Jul;69(3):160-167. Epub 2023 Jun 5 doi: 10.1016/j.jphys.2023.05.017. PMID: 37286390
Kaya AK, Menek MY
Eur J Obstet Gynecol Reprod Biol 2023 Jun;285:24-30. Epub 2023 Apr 1 doi: 10.1016/j.ejogrb.2023.03.040. PMID: 37031572
Kim S, Yi D, Yim J
Int J Environ Res Public Health 2022 Jun 8;19(12) doi: 10.3390/ijerph19127031. PMID: 35742279Free PMC Article
Cuccomarino S, Bonomo LD, Aprà F, Toscano A, Jannaci A
Surg Endosc 2022 Feb;36(2):1302-1309. Epub 2021 Mar 4 doi: 10.1007/s00464-021-08405-1. PMID: 33661382
Keshwani N, Mathur S, McLean L
Physiother Theory Pract 2021 Sep;37(9):1018-1033. Epub 2019 Oct 23 doi: 10.1080/09593985.2019.1675207. PMID: 31642725

Recent systematic reviews

Benjamin DR, Frawley HC, Shields N, Peiris CL, van de Water ATM, Bruder AM, Taylor NF
Physiotherapy 2023 Jun;119:54-71. Epub 2023 Mar 5 doi: 10.1016/j.physio.2023.02.002. PMID: 36934466
Sokunbi G, Camino-Willhuber G, Paschal PK, Olufade O, Hussain FS, Shue J, Abjornson C, Zelenty WD, Lebl DR, Cammisa FP, Girardi FP, Hughes AP, Sama AA
World Neurosurg 2023 Jun;174:119-125. Epub 2023 Mar 8 doi: 10.1016/j.wneu.2023.03.014. PMID: 36894002
Gluppe S, Engh ME, Bø K
Braz J Phys Ther 2021 Nov-Dec;25(6):664-675. Epub 2021 Jul 21 doi: 10.1016/j.bjpt.2021.06.006. PMID: 34391661Free PMC Article
Mommers EHH, Ponten JEH, Al Omar AK, de Vries Reilingh TS, Bouvy ND, Nienhuijs SW
Surg Endosc 2017 Dec;31(12):4934-4949. Epub 2017 Jun 8 doi: 10.1007/s00464-017-5607-9. PMID: 28597282Free PMC Article
Benjamin DR, van de Water AT, Peiris CL
Physiotherapy 2014 Mar;100(1):1-8. Epub 2013 Oct 5 doi: 10.1016/j.physio.2013.08.005. PMID: 24268942

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...