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Fetal distress

MedGen UID:
5164
Concept ID:
C0015930
Pathologic Function
Synonyms: Fetal Distress; Fetal Status, Nonreassuring; Nonreassuring Fetal Status
SNOMED CT: Fetal distress (130955003); Nonreassuring fetal status (130955003)
 
HPO: HP:0025116

Definition

An intrauterine state characterized by suboptimal values in the fetal heart rate, oxygenation of fetal blood, or other parameters indicative of compromise of the fetus. Signs of fetal distress include repetitive variable decelerations, fetal tachycardia or bradycardia, late decelerations, or low biophysical profile. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Fetal distress

Conditions with this feature

FRAXE
MedGen UID:
155512
Concept ID:
C0751157
Disease or Syndrome
Intellectual developmental disorder-109 (MRX109) is characterized by mildly to moderately impaired intellectual development associated with learning difficulties, communication deficits, attention problems, hyperactivity, and autistic behavior (summary by Bensaid et al., 2009). The disorder, which is associated with a fragile site on chromosome Xq28 (FRAXE), can be caused either by silencing of the FMR2 gene as a consequence of a CCG expansion located upstream of this gene or by deletion within the gene (Stettner et al., 2011).
Pettigrew syndrome
MedGen UID:
162924
Concept ID:
C0796254
Disease or Syndrome
X-linked Dandy-Walker malformation with intellectual disability, basal ganglia disease and seizures (XDIBS), or Pettigrew syndrome is a central nervous system malformation characterized by severe intellectual deficit, early hypotonia with progression to spasticity and contractures, choreoathetosis, seizures, dysmorphic face (long face with prominent forehead), and brain imaging abnormalities such as Dandy-Walker malformation, and iron deposition. (From Mondo:0010574)
Hereditary cryohydrocytosis with reduced stomatin
MedGen UID:
332390
Concept ID:
C1837206
Disease or Syndrome
Stomatin-deficient cryohydrocytosis with neurologic defects is an autosomal dominant disorder characterized by delayed psychomotor development, seizures, cataracts, and pseudohyperkalemia resulting from defects in the red blood cell membrane. The disorder combines the neurologic features of Glut1 deficiency syndrome-1 (GLUT1DS1; 606777), resulting from impaired glucose transport at the blood-brain barrier, and hemolytic anemia/pseudohyperkalemia with stomatocytosis, resulting from a cation leak in erythrocytes (summary by Bawazir et al., 2012). For a discussion of clinical and genetic heterogeneity of red cell stomatocyte disorders, see 194380.
Midface hypoplasia, obesity, developmental delay, and neonatal hypotonia
MedGen UID:
325238
Concept ID:
C1837730
Disease or Syndrome
Pyridoxine-dependent epilepsy
MedGen UID:
340341
Concept ID:
C1849508
Disease or Syndrome
Pyridoxine-dependent epilepsy – ALDH7A1 (PDE-ALDH7A1) is characterized by seizures not well controlled with anti-seizure medication that are responsive clinically and electrographically to large daily supplements of pyridoxine (vitamin B6). This is true across a phenotypic spectrum that ranges from classic to atypical PDE-ALDH7A1. Intellectual disability is common, particularly in classic PDE-ALDH7A1. Classic PDE-ALDH7A1. Untreated seizures begin within the first weeks to months of life. Dramatic presentations of prolonged seizures and recurrent episodes of status epilepticus are typical; recurrent self-limited events including partial seizures, generalized seizures, atonic seizures, myoclonic events, and infantile spasms also occur. Electrographic seizures can occur without clinical correlates. Atypical PDE-ALDH7A1. Findings in untreated individuals can include late-onset seizures beginning between late infancy and age three years, seizures that initially respond to anti-seizure medication and then become intractable, seizures during early life that do not respond to pyridoxine but are subsequently controlled with pyridoxine several months later, and prolonged seizure-free intervals (=5 months) that occur after discontinuation of pyridoxine.
Congenital lactic acidosis, Saguenay-Lac-Saint-Jean type
MedGen UID:
387801
Concept ID:
C1857355
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 5 (MC4DN5) is an autosomal recessive severe metabolic multisystemic disorder with onset in infancy. Features include delayed psychomotor development, impaired intellectual development with speech delay, mild dysmorphic facial features, hypotonia, ataxia, and seizures. There is increased serum lactate and episodic hypoglycemia. Some patients may have cardiomyopathy, abnormal breathing, or liver abnormalities, reflecting systemic involvement. Brain imaging shows lesions in the brainstem and basal ganglia, consistent with a diagnosis of Leigh syndrome (see 256000). Affected individuals tend to have episodic metabolic and/or neurologic crises in early childhood, which often lead to early death (summary by Debray et al., 2011). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Diamond-Blackfan anemia 7
MedGen UID:
436451
Concept ID:
C2675512
Disease or Syndrome
Diamond-Blackfan anemia (DBA) is characterized by a profound normochromic and usually macrocytic anemia with normal leukocytes and platelets, congenital malformations in up to 50%, and growth deficiency in 30% of affected individuals. The hematologic complications occur in 90% of affected individuals during the first year of life. The phenotypic spectrum ranges from a mild form (e.g., mild anemia or no anemia with only subtle erythroid abnormalities, physical malformations without anemia) to a severe form of fetal anemia resulting in nonimmune hydrops fetalis. DBA is associated with an increased risk for acute myelogenous leukemia (AML), myelodysplastic syndrome (MDS), and solid tumors including osteogenic sarcoma.
Sterile multifocal osteomyelitis with periostitis and pustulosis
MedGen UID:
411230
Concept ID:
C2748507
Disease or Syndrome
Chronic recurrent multifocal osteomyelitis-2 with periostitis and pustulosis (CRMO2) is an autosomal recessive multisystemic autoinflammatory disorder characterized by onset of symptoms in early infancy. Affected individuals present with joint swelling and pain, pustular rash, oral mucosal lesions, and fetal distress. The disorder progresses in severity to generalized severe pustulosis or ichthyosiform lesions and diffuse bone lesions. Radiographic studies show widening of the anterior rib ends, periosteal elevation along multiple long bones, multifocal osteolytic lesions, heterotopic ossification, and metaphyseal erosions of the long bones. Laboratory studies show elevation of inflammatory markers. The disorder results from unopposed activation of the IL1 inflammatory signaling pathway. Treatment with the interleukin-1 receptor antagonist anakinra may result in clinical improvement (Aksentijevich et al., 2009). For a discussion of genetic heterogeneity of CRMO, see 609628.
Multiple congenital anomalies-hypotonia-seizures syndrome 2
MedGen UID:
477139
Concept ID:
C3275508
Disease or Syndrome
Multiple congenital anomalies-hypotonia-seizures syndrome-2 (MCAHS2) is an X-linked recessive neurodevelopmental disorder characterized by dysmorphic features, neonatal hypotonia, early-onset myoclonic seizures, and variable congenital anomalies involving the central nervous, cardiac, and urinary systems. Some affected individuals die in infancy (summary by Johnston et al., 2012). The phenotype shows clinical variability with regard to severity and extraneurologic features. However, most patients present in infancy with early-onset epileptic encephalopathy associated with developmental arrest and subsequent severe neurologic disability; these features are consistent with a form of developmental and epileptic encephalopathy (DEE) (summary by Belet et al., 2014, Kato et al., 2014). The disorder is caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis. For a discussion of genetic heterogeneity of MCAHS, see MCAHS1 (614080). For a discussion of nomenclature and genetic heterogeneity of DEE, see 308350. For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Cholestasis, intrahepatic, of pregnancy, 1
MedGen UID:
762759
Concept ID:
C3549845
Disease or Syndrome
Intrahepatic cholestasis of pregnancy is a reversible form of cholestasis that occurs most often in the third trimester of pregnancy and recurs in 45 to 70% of subsequent pregnancies. Symptoms include pruritus, jaundice, increased serum bile salts, and abnormal liver enzymes, all of which resolve rapidly after delivery. However, the condition is associated with fetal complications, including placental insufficiency, premature labor, fetal distress, and intrauterine death. Some women with ICP may also be susceptible to oral contraceptive-induced cholestasis (OCIC) (summary by Pasmant et al., 2012). Genetic Heterogeneity of Intrahepatic Cholestasis of Pregnancy See also ICP3 (614972), caused by mutation in the ABCB4 gene (171060).
Methylmalonic acidemia with homocystinuria, type cblJ
MedGen UID:
766829
Concept ID:
C3553915
Disease or Syndrome
Combined methylmalonic aciduria (MMA) and homocystinuria is a genetically heterogeneous metabolic disorder of cobalamin (cbl; vitamin B12) metabolism, which is essential for hematologic and neurologic function. Biochemically, the defect causes decreased levels of the coenzymes adenosylcobalamin (AdoCbl) and methylcobalamin (MeCbl), which results in decreased activity of the respective enzymes methylmalonyl-CoA mutase (MUT; 609058) and methyltetrahydrofolate:homocysteine methyltransferase, also known as methionine synthase (MTR; 156570). The cblJ type is phenotypically and biochemically similar to the cblF type (MAHCF; 277380) (summary by Coelho et al., 2012).
Peroxisome biogenesis disorder 5A (Zellweger)
MedGen UID:
766854
Concept ID:
C3553940
Disease or Syndrome
The peroxisomal biogenesis disorder (PBD) Zellweger syndrome (ZS) is an autosomal recessive multiple congenital anomaly syndrome. Affected children present in the newborn period with profound hypotonia, seizures, and inability to feed. Characteristic craniofacial anomalies, eye abnormalities, neuronal migration defects, hepatomegaly, and chondrodysplasia punctata are present. Children with this condition do not show any significant development and usually die in the first year of life (summary by Steinberg et al., 2006). For a complete phenotypic description and a discussion of genetic heterogeneity of Zellweger syndrome, see 214100. Individuals with PBDs of complementation group 5 (CG5, equivalent to CG10 and CGF) have mutations in the PEX2 gene. For information on the history of PBD complementation groups, see 214100.
Cholestasis, intrahepatic, of pregnancy, 3
MedGen UID:
767155
Concept ID:
C3554241
Disease or Syndrome
Intrahepatic cholestasis of pregnancy is a reversible form of cholestasis that occurs most often in the third trimester of pregnancy and recurs in 45 to 70% of subsequent pregnancies. Symptoms include pruritus, jaundice, increased serum bile salts, and abnormal liver enzymes, all of which resolve rapidly after delivery. However, the condition is associated with fetal complications, including placental insufficiency, premature labor, fetal distress, and intrauterine death. Women with ICP are also susceptible to oral contraceptive-induced cholestasis (OCIC). Ursodeoxycholic acid (UDCA) is an effective treatment for conditions caused by ABCB4 mutations (summary by Pasmant et al., 2012). Mutation in the ABCB4 gene accounts for about 15% of ICP cases (summary by Ziol et al., 2008). For a discussion of genetic heterogeneity of ICP, see ICP1 (147480).
Tatton-Brown-Rahman overgrowth syndrome
MedGen UID:
862982
Concept ID:
C4014545
Disease or Syndrome
Tatton-Brown-Rahman syndrome (TBRS) is an overgrowth / intellectual disability syndrome characterized by length/height and/or head circumference =2 SD above the mean for age and sex, obesity / increased weight, intellectual disability that ranges from mild to severe, joint hypermobility, hypotonia, behavioral/psychiatric issues, kyphoscoliosis, and seizures. Individuals with TBRS have subtle dysmorphic features, including a round face with coarse features, thick horizontal low-set eyebrows, narrow (as measured vertically) palpebral fissures, and prominent upper central incisors. The facial gestalt is most easily recognizable in the teenage years. TBRS may be associated with an increased risk of developing acute myeloid leukemia. There are less clear associations with aortic root dilatation and increased risk of other hematologic and solid tumors.
Pancytopenia due to IKZF1 mutations
MedGen UID:
905078
Concept ID:
C4225173
Disease or Syndrome
Common variable immunodeficiency-13 (CVID13) is an autosomal dominant primary immunodeficiency disorder characterized by recurrent bacterial infections, mainly affecting the respiratory tract, and associated with hypogammaglobulinemia and decreased numbers of B cells. The age at onset of clinical features can range from infancy to adulthood, and some patients may have a mild disorder or even remain clinically asymptomatic (summary by Kuehn et al., 2016). For a general description and a discussion of genetic heterogeneity of common variable immunodeficiency, see CVID1 (607594).
Epilepsy, early-onset, vitamin B6-dependent
MedGen UID:
934599
Concept ID:
C4310632
Disease or Syndrome
Early-onset vitamin B6-dependent epilepsy-1 (EPEO1) is an autosomal recessive neurologic disorder characterized by onset of seizures in the neonatal period or first months of life. The seizures show favorable response to treatment with activated vitamin B6 (pyridoxal 5-prime-phosphate; PLP) and/or pyridoxine. However, most patients show delayed psychomotor development (Darin et al., 2016). Genetic Heterogeneity of Early-Onset Epilepsy EPEO2 (618832) is caused by mutation in the SETD1A gene (611052) on chromosome 16p11. EPEO3 (620465) is caused by mutation in the ATP6V0C gene (108745) on chromosome 16p13. EPEO4 (266100) is caused by mutation in the ALDH7A1 gene (107323) on chromosome 5q23.
Atypical glycine encephalopathy
MedGen UID:
934910
Concept ID:
C4310943
Disease or Syndrome
GLYT1 encephalopathy is characterized in neonates by severe hypotonia, respiratory failure requiring mechanical ventilation, and absent neonatal reflexes; encephalopathy, including impaired consciousness and unresponsiveness, may be present. Arthrogryposis or joint laxity can be observed. Generalized hypotonia develops later into axial hypotonia with limb hypertonicity and a startle-like response to vocal and visual stimuli which should not be confused with seizures. To date, three of the six affected children reported from three families died between ages two days and seven months; the oldest reported living child is severely globally impaired at age three years. Because of the limited number of affected individuals reported to date, the phenotype has not yet been completely described.
Pseudo-TORCH syndrome 2
MedGen UID:
1373355
Concept ID:
C4479376
Disease or Syndrome
Pseudo-TORCH syndrome-2 (PTORCH2) is an autosomal recessive multisystem disorder characterized by antenatal onset of intracranial hemorrhage, calcification, brain malformations, liver dysfunction, and often thrombocytopenia. Affected individuals tend to have respiratory insufficiency and seizures, and die in infancy. The phenotype resembles the sequelae of intrauterine infection, but there is no evidence of an infectious agent. The disorder results from inappropriate activation of the interferon (IFN) immunologic pathway (summary by Meuwissen et al., 2016). For a discussion of genetic heterogeneity of PTORCH, see PTORCH1 (251290).
Intellectual disability, autosomal dominant 46
MedGen UID:
1618560
Concept ID:
C4539851
Mental or Behavioral Dysfunction
Intellectual disability, autosomal dominant 54
MedGen UID:
1614787
Concept ID:
C4540484
Mental or Behavioral Dysfunction
Arterial calcification, generalized, of infancy, 1
MedGen UID:
1631685
Concept ID:
C4551985
Disease or Syndrome
Generalized arterial calcification of infancy (GACI) is characterized by infantile onset of widespread arterial calcification and/or narrowing of large and medium-sized vessels resulting in cardiovascular findings (which can include heart failure, respiratory distress, edema, cyanosis, hypertension, and/or cardiomegaly). Additional findings can include typical skin and retinal manifestations of pseudoxanthoma elasticum (PXE), periarticular calcifications, development of rickets after infancy, cervical spine fusion, and hearing loss. While mortality in infancy is high, survival into the third and fourth decades has occurred.
Chromosome 1p35 deletion syndrome
MedGen UID:
1632676
Concept ID:
C4693669
Disease or Syndrome
Pontocerebellar hypoplasia, type 1D
MedGen UID:
1648387
Concept ID:
C4748058
Disease or Syndrome
Pontocerebellar hypoplasia type 1D (PCH1D) is a severe autosomal recessive neurologic disorder characterized by severe hypotonia and a motor neuronopathy apparent at birth or in infancy. Patients have respiratory insufficiency, feeding difficulties, and severely delayed or minimal gross motor development. Other features may include eye movement abnormalities, poor overall growth, contractures. Brain imaging shows progressive cerebellar atrophy with relative sparing of the brainstem (summary by Burns et al., 2018). For a general phenotypic description and a discussion of genetic heterogeneity of PCH, see PCH1A (607596).
Mitochondrial complex 1 deficiency, nuclear type 22
MedGen UID:
1648347
Concept ID:
C4748796
Disease or Syndrome
Pontocerebellar hypoplasia, hypotonia, and respiratory insufficiency syndrome, neonatal lethal
MedGen UID:
1716458
Concept ID:
C5394137
Disease or Syndrome
Neonatal lethal pontocerebellar hypoplasia, hypotonia, and respiratory insufficiency syndrome (PHRINL) is an autosomal recessive multisystem disorder with onset in utero and death in the neonatal period. Rare patients may survive a few months. Affected infants show respiratory insufficiency and almost no spontaneous movement at birth, usually requiring mechanical ventilation and admission to the neonatal intensive care unit. Additional features include corneal clouding, seizures, dysmorphic facies, contractures, and progressive pontocerebellar hypoplasia with simplified gyral pattern and white matter abnormalities. Some patients may have cardiac anomalies or cardiac hypertrophy. Laboratory studies show evidence consistent with mitochondrial defects and/or abnormal cholesterol or lipid metabolism. Depending on the type of mutation or deletion, some patients may have a less severe disorder (see GENOTYPE/PHENOTYPE CORRELATIONS) (summary by Desai et al., 2017).
Neurodevelopmental disorder with dysmorphic facies and variable seizures
MedGen UID:
1784197
Concept ID:
C5543268
Disease or Syndrome
Neurodevelopmental disorder with dysmorphic facies and variable seizures (NEDDFAS) is an autosomal recessive disorder characterized by global developmental delay apparent in early childhood. Patients have mildly impaired intellectual development, often with speech delay or behavioral abnormalities. Some may have seizures. Most have nonspecific dysmorphic facial features. Additional findings may include brain imaging abnormalities, mild skeletal defects, and renal abnormalities, although the renal anomalies may be unrelated (summary by Shao et al., 2021).
Radio-Tartaglia syndrome
MedGen UID:
1778557
Concept ID:
C5543339
Disease or Syndrome
Radio-Tartaglia syndrome (RATARS) is a neurodevelopmental disorder characterized by global developmental delay with impaired intellectual development, speech delay, and variable behavioral abnormalities. Affected individuals show hypotonia, mild motor difficulties, and craniofacial dysmorphism. Brain imaging may show nonspecific defects; rare patients have seizures or pyramidal signs. A subset of individuals may have congenital heart defects, precocious puberty, and obesity in females. Some of the features are similar to those observed in patients with chromosome 1p36 deletion syndrome (607872) (summary by Radio et al., 2021).
VISS syndrome
MedGen UID:
1794165
Concept ID:
C5561955
Disease or Syndrome
VISS syndrome is a generalized connective tissue disorder characterized by early-onset thoracic aortic aneurysm and other connective tissue findings, such as aneurysm and tortuosity of other arteries, joint hypermobility, skin laxity, and hernias, as well as craniofacial dysmorphic features, structural cardiac defects, skeletal anomalies, and motor developmental delay (Van Gucht et al., 2021). Immune dysregulation has been observed in some patients (Ziegler et al., 2021).
Biliary, renal, neurologic, and skeletal syndrome
MedGen UID:
1794200
Concept ID:
C5561990
Disease or Syndrome
Biliary, renal, neurologic, and skeletal syndrome (BRENS) is an autosomal recessive complex ciliopathy with multisystemic manifestations. The most common presentation is severe neonatal cholestasis that progresses to liver fibrosis and cirrhosis. Most patients have additional clinical features suggestive of a ciliopathy, including postaxial polydactyly, hydrocephalus, retinal abnormalities, and situs inversus. Additional features of the syndrome may include congenital cardiac defects, echogenic kidneys with renal failure, ocular abnormalities, joint hyperextensibility, and dysmorphic facial features. Some patients have global developmental delay. Brain imaging typically shows dilated ventricles, hypomyelination, and white matter abnormalities, although some patients have been described with abnormal pituitary development (summary by Shaheen et al., 2020 and David et al., 2020).
Restrictive dermopathy 2
MedGen UID:
1801155
Concept ID:
C5676942
Disease or Syndrome
Restrictive dermopathy is a rare genodermatosis characterized mainly by intrauterine growth retardation, tight and rigid skin with erosions, prominent superficial vasculature and epidermal hyperkeratosis, facial dysmorphism (small mouth, small pinched nose and micrognathia), sparse/absent eyelashes and eyebrows, mineralization defects of the skull, thin dysplastic clavicles, pulmonary hypoplasia, multiple joint contractures, and an early neonatal lethal course. Liveborn children usually die within the first week of life (summary by Navarro et al., 2004). For a discussion of genetic heterogeneity of restrictive dermopathy, see RSDM1 (275210).
Muscular dystrophy, congenital, with or without seizures
MedGen UID:
1824047
Concept ID:
C5774274
Disease or Syndrome
Congenital muscular dystrophy with or without seizures (MYOS) is an autosomal recessive disorder characterized by severe muscle hypotonia apparent from birth, as well as developmental delay. Laboratory studies show increased serum creatine kinase and muscle biopsy shows nonspecific dystrophic features. Most patients develop seizures or have abnormal epileptiform findings on EEG studies; other variable findings may include feeding difficulties, nystagmus, myopathic facies, areflexia, and brain atrophy on MRI (summary by Larson et al., 2018 and Henige et al., 2021).
Microcephaly 30, primary, autosomal recessive
MedGen UID:
1824053
Concept ID:
C5774280
Disease or Syndrome
Autosomal recessive primary microcephaly-30 (MCPH30) is characterized by small head circumference, poor overall growth, and global developmental delay with variably impaired intellectual development. Affected individuals have been reported to have variable additional congenital anomalies, including atrial septal defect, dysmorphic facial features, tracheal stenosis, and anomalies of the skin and teeth (Carvalhal et al., 2022). For a general phenotypic description and a discussion of genetic heterogeneity of primary microcephaly, see MCPH1 (251200).
Mitochondrial complex IV deficiency, nuclear type 23
MedGen UID:
1840958
Concept ID:
C5830322
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 23 (MC4DN23) is an autosomal recessive disorder characterized by infantile-onset encephalopathy (Rius et al., 2022). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.

Professional guidelines

PubMed

Lees CC, Romero R, Stampalija T, Dall'Asta A, DeVore GA, Prefumo F, Frusca T, Visser GHA, Hobbins JC, Baschat AA, Bilardo CM, Galan HL, Campbell S, Maulik D, Figueras F, Lee W, Unterscheider J, Valensise H, Da Silva Costa F, Salomon LJ, Poon LC, Ferrazzi E, Mari G, Rizzo G, Kingdom JC, Kiserud T, Hecher K
Am J Obstet Gynecol 2022 Mar;226(3):366-378. Epub 2022 Jan 10 doi: 10.1016/j.ajog.2021.11.1357. PMID: 35026129Free PMC Article
Wong L, Kwan AHW, Lau SL, Sin WTA, Leung TY
Am J Obstet Gynecol 2021 Oct;225(4):357-366. Epub 2021 Jun 26 doi: 10.1016/j.ajog.2021.06.077. PMID: 34181893
Jones L, Othman M, Dowswell T, Alfirevic Z, Gates S, Newburn M, Jordan S, Lavender T, Neilson JP
Cochrane Database Syst Rev 2012 Mar 14;2012(3):CD009234. doi: 10.1002/14651858.CD009234.pub2. PMID: 22419342Free PMC Article

Recent clinical studies

Etiology

Obstet Gynecol 2021 Jun 1;137(6):e116-e127. doi: 10.1097/AOG.0000000000004410. PMID: 34011889
Brosens I, Benagiano G
Eur J Obstet Gynecol Reprod Biol 2016 Jan;196:57-9. Epub 2015 Nov 24 doi: 10.1016/j.ejogrb.2015.11.022. PMID: 26685798
Hofmeyr GJ, Kulier R
Cochrane Database Syst Rev 2012 Jun 13;2012(6):CD001064. doi: 10.1002/14651858.CD001064.pub2. PMID: 22696322Free PMC Article
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Obstet Gynecol Clin North Am 1999 Jun;26(2):259-74. doi: 10.1016/s0889-8545(05)70073-5. PMID: 10399760
Morrison EH
Am Fam Physician 1998 Nov 1;58(7):1593-604. PMID: 9824957

Diagnosis

Kale I
J Matern Fetal Neonatal Med 2022 Mar;35(6):1017-1022. Epub 2021 Apr 6 doi: 10.1080/14767058.2021.1906220. PMID: 33823730
Avagliano L, Massa V, Bulfamante G
Eur J Obstet Gynecol Reprod Biol 2021 Nov;266:55-62. Epub 2021 Sep 16 doi: 10.1016/j.ejogrb.2021.09.016. PMID: 34592650
Nageotte MP
Semin Fetal Neonatal Med 2015 Jun;20(3):144-8. Epub 2015 Mar 11 doi: 10.1016/j.siny.2015.02.002. PMID: 25769203
Tharmaratnam S
Baillieres Best Pract Res Clin Obstet Gynaecol 2000 Feb;14(1):155-72. doi: 10.1053/beog.1999.0069. PMID: 10789266
Morrison EH
Am Fam Physician 1998 Nov 1;58(7):1593-604. PMID: 9824957

Therapy

Lees CC, Romero R, Stampalija T, Dall'Asta A, DeVore GA, Prefumo F, Frusca T, Visser GHA, Hobbins JC, Baschat AA, Bilardo CM, Galan HL, Campbell S, Maulik D, Figueras F, Lee W, Unterscheider J, Valensise H, Da Silva Costa F, Salomon LJ, Poon LC, Ferrazzi E, Mari G, Rizzo G, Kingdom JC, Kiserud T, Hecher K
Am J Obstet Gynecol 2022 Mar;226(3):366-378. Epub 2022 Jan 10 doi: 10.1016/j.ajog.2021.11.1357. PMID: 35026129Free PMC Article
Al Wattar BH, Honess E, Bunnewell S, Welton NJ, Quenby S, Khan KS, Zamora J, Thangaratinam S
CMAJ 2021 Apr 6;193(14):E468-E477. doi: 10.1503/cmaj.202538. PMID: 33824144Free PMC Article
Walker KF, Chappell LC, Hague WM, Middleton P, Thornton JG
Cochrane Database Syst Rev 2020 Jul 27;7(7):CD000493. doi: 10.1002/14651858.CD000493.pub3. PMID: 32716060Free PMC Article
Middleton P, Shepherd E, Flenady V, McBain RD, Crowther CA
Cochrane Database Syst Rev 2017 Jan 4;1(1):CD005302. doi: 10.1002/14651858.CD005302.pub3. PMID: 28050900Free PMC Article
Rabie N, Magann E, Steelman S, Ounpraseuth S
Ultrasound Obstet Gynecol 2017 Apr;49(4):442-449. doi: 10.1002/uog.15929. PMID: 27062200

Prognosis

Fuchs S, Regev R, Harrington J
J Pediatr Endocrinol Metab 2021 Aug 26;34(8):1041-1044. Epub 2021 Apr 16 doi: 10.1515/jpem-2020-0594. PMID: 33866697
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Cochrane Database Syst Rev 2014 Jan 23;2014(1):CD000014. doi: 10.1002/14651858.CD000014.pub4. PMID: 24453049Free PMC Article
Phelan JP
Clin Obstet Gynecol 1990 Sep;33(3):432-7. doi: 10.1097/00003081-199009000-00007. PMID: 2225574
Danforth DN
JAMA 1985 Feb 8;253(6):811-8. PMID: 3881613

Clinical prediction guides

Duncan JR, Schenone CV, Običan SG
Curr Opin Obstet Gynecol 2022 Oct 1;34(5):292-299. Epub 2022 Jul 16 doi: 10.1097/GCO.0000000000000809. PMID: 35895911
Zhu M, Liu L
J Healthc Eng 2021;2021:7608785. Epub 2021 Sep 29 doi: 10.1155/2021/7608785. PMID: 34630995Free PMC Article
Guan P, Tang F, Sun G, Ren W
J Investig Med 2020 Mar;68(3):799-806. Epub 2020 Jan 24 doi: 10.1136/jim-2019-001175. PMID: 31980540Free PMC Article
Vollgraff Heidweiller-Schreurs CA, De Boer MA, Heymans MW, Schoonmade LJ, Bossuyt PMM, Mol BWJ, De Groot CJM, Bax CJ
Ultrasound Obstet Gynecol 2018 Mar;51(3):313-322. Epub 2018 Feb 5 doi: 10.1002/uog.18809. PMID: 28708272Free PMC Article
Penning S, Garite TJ
Obstet Gynecol Clin North Am 1999 Jun;26(2):259-74. doi: 10.1016/s0889-8545(05)70073-5. PMID: 10399760

Recent systematic reviews

de Medeiros KS, Sarmento ACA, Costa APF, Macêdo LTA, da Silva LAS, de Freitas CL, Simões ACZ, Gonçalves AK
Int J Gynaecol Obstet 2022 Mar;156(3):394-405. Epub 2021 Nov 19 doi: 10.1002/ijgo.14015. PMID: 34762735Free PMC Article
Al Wattar BH, Honess E, Bunnewell S, Welton NJ, Quenby S, Khan KS, Zamora J, Thangaratinam S
CMAJ 2021 Apr 6;193(14):E468-E477. doi: 10.1503/cmaj.202538. PMID: 33824144Free PMC Article
Vollgraff Heidweiller-Schreurs CA, De Boer MA, Heymans MW, Schoonmade LJ, Bossuyt PMM, Mol BWJ, De Groot CJM, Bax CJ
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