<unk>  was first discovered by Meadow et al. in 1968. Manson and Frederic clarified the teratogenic effects of<unk>  in their epidemiological studies in 1973 and Hanson and Smith in 1975.<unk> , characterized by altered growth and development, has been well described in recent years in the fetus of epileptic mothers taking phenytoin or other<unk>  anticonvulsants during the gestational period.It is understood that<unk> s are the result of infants born to mothers with seizure disorders treated with anticonvulsant medications during pregnancy. There is also an association with EPHX1 has been suggested. Although the exact pathogenesis of phenytoin (PTN) embryotoxicity is not clear, some possible mechanisms have been proposed. Phenytoin inhibits sodium (Na) and calcium (Ca) channels which act as membrane stabilizers, as a result of which free radicals are released and cause endothelial damage, myocardial depression, bradycardia, and consequently fetal hypoxia. Phenytoin induces cytochrome P450 activation which ends up within the release of teratogenic free radicals, sourced via the metabolism of epoxides, folate, and vitamin K within the liver. The severity of associated abnormalities will vary greatly from one infant to another. The characteristic features of<unk>  include abnormalities of growth such as pre and postnatal growth deficiency and microcephaly abnormalities of performance such as developmental delay or dull mentality to frank mental deficiency; and dysmorphic craniofacial features commonly including short nose with broad depressed bridge and inner epicanthic folds, mild ocular hypertelorism, ptosis of the eyelid, strabismus, wide mouth, sutural ridging, and short neck with mild webbing; less commonly cleft lip and palate, and limb anomalies including hypoplasia of the nails and distal phalanges with an increased frequency of low arch digital dermal ridge patterns, and fingerlike thumb. Less commonly children displaying these dysmorphic craniofacial and limb features were reported to have major anomalies in other systems, including cardiac anomalies. It was also shown an increased incidence of major genitourinary and central nervous system anomalies, more serious limb reduction defects, and diaphragmatic hernia.<unk>  may be caused by a combination of specific genetic and environmental factors. Common causes of<unk>  may include the anti-seizure(anticonvulsant) drug phenytoin (Dilantin) during pregnancy.<unk>  must be differentiated from other diseases that cause Hypoplastic nails and growth retardation along with some similar facial features are also found in the Coffin-Siris, Hypoplasia of distal phalanges in Noonan's syndrome, and Nail hypoplasia in Robinson's disease. The exact incidence and prevalence of<unk>  are unknown. The risk appears to be 2-3 times greater than normal in the children of epileptic women taking anticonvulsant drugs than in the general population. The exact incidence and prevalence of<unk>  are unknown.The risk appears to be 2-3 times greater than normal in the children of epileptic women taking anticonvulsant drugs than in the general population. The risk of neurological impairment estimated to be 1% to 11% is 2 to 3 times higher than in the general population. The risk of oral clefts and cardiac anomalies is 5 times that of others in<unk>  exposed infants. Less frequently observed abnormalities include microcephaly, ocular defects, hypospadias, umbilical and inguinal hernias.<unk>  affects males and females equally. Common risk factors in the development of<unk>  include exposure of the fetus to antiepileptic drugs phenytoin(Dilantin). There is insufficient evidence to recommend routine screening for<unk> . But In case the fetus is exposed in utero to phenytoin, screening by cytogenetic analysis, a careful screening by morphological ultrasound was recommended. Without termination of pregnancy, the patient will develop conditions of severe respiratory distress, multiple congenital anomalies, including the imperforate anus, ambiguous genitalia, dislocated hips, clubfeet, hypoplastic fingernails, a short neck, and a barrel-shaped thorax, swollen thigh, decreased breath sound and cardiac murmur which may eventually lead to neonatal death. Common complications of<unk>  are microcephaly, growth deficiency, congenital heart defects, systemic abnormalities (nervous, renal, GI systems). The diagnosis is based on the clinical features along with a history of phenytoin exposure during pregnancy. Ultrasound may be helpful in the diagnosis of<unk> . Findings on ultrasound suggestive of<unk>  include gastroschisis, sacral meningomyelocele, absence of the upper limb lower limb, clubfoot, Pectus carinatum, dilated right/left heart with pericardial effusion. Treatment of individuals with<unk>  depends on the particular manifestation of the disease. Individuals with congenital heart disease may require to undergo major corrective surgery soon after birth. Other individuals who have relatively minor health problems require no therapy. Patients with<unk>  require follow-up and close monitoring of growth, psychomotor craniofacial evaluation, cardiac evaluation.
Fetal hydantoin syndrome
Fetal methotrexate syndrome
Fetal alcohol syndrome
Neonatal sepsis
Shaken baby syndrome
Small for gestational age
Large for gestational age
Fetus in fetu