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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tellurium dioxide (TeO2) induces hydrocephalus, edema, exophthalmia, ocular hemorrhage, umbilical hernia, undescended testes and small kidneys in day 20 Wistar rat fetuses when administered s.c. to pregnant dams from gestational day 15 to 19. At doses of 500 mumole/kg or greater, a 100% incidence of these findings and a reduction in maternal weight gain were observed. A pair-fed study at the dose of 500 mumole/kg of TeO2 was conducted to establish if the effects of tellurium were a result of a reduction in food intake or other maternal toxic responses. Two additional control groups of rats receiving tellurium or vehicle were fed ad libitum. After a comparable maternal weight gain from day 0 to 15, weight gain was significantly reduced in the treated groups and the pair-fed control. There was a reduction of fetal weight in the treated groups (p less than 0.01) and in the pair-fed control (p less than 0.02). There was a 100% incidence of the above anomalies in the litters of the two treated groups, but none in the pair-fed and control groups. No histological alterations other than a mild centrolobular fatty change in the liver were detected in the other organs from the tellurium exposed dams. Thus, tellurium induces both maternal toxicity and teratogenic effects in the rat where the teratogenicity is not mediated by alterations in the diet.
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PMID:Maternal toxicity and teratogenicity of tellurium dioxide in the Wistar rat: relationship to pair-feeding. 298 Apr 2

The effects of multiple maternal subcutaneous injections of tellurium dioxide (TeO2) suspended in olive oil (0-1,000 mumol/kg) from day 15 to day 19 of gestation were evaluated in the Wistar rat. External and internal soft-tissue examinations were performed on day 20 fetuses. Multiple maternal injections, at doses higher than 10 mumol/kg, resulted in a dose-related appearance of hydrocephalus, edema, exophthalmia, ocular hemorrhage, umbilical hernia, undescended testis, and small kidneys in fetuses on day 20 of gestation. At 500 mumol/kg, reduction in maternal weight gain was also observed. At this level, the incidence of the above anomalies was 100%. The 100 mumol/kg dose of Te, which did not produce apparent maternal toxic responses, resulted in a 100% incidence of hydrocephalus and edema but no fetal mortality. Thus, tellurium can be teratogenic to the rat fetus without concomitant maternal toxicity. Also, the fetal period may be more sensitive than the organogenic period for the induction of hydrocephalus. Such evidence is consistent with the development of the choroid plexus and an effect of TeO2 on the production/resorption of cerebrospinal fluid.
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PMID:Teratogenicity of tellurium dioxide: prenatal assessment. 313 38

We present a foetus, 46,XY, with holoprosencephaly, hydrocephaly, unilateral lower limb post axial polydactyly, clubhands, auricular septal defect, umbilical cord hernia. The differential diagnosis of the condition is discussed: especially the hydrolethalus syndrome, and the Young and Madders' syndrome reported in 1987.
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PMID:[Holoprosencephaly, polydactyly, cardiopathy: new syndrome or a new case of hydrolethalus?]. 321 92

Twenty-nine newborn infants with diaphragmatic hernia have been received in a neonatal intensive care unit over a seven year period. In three cases, clinical signs appeared after the first day: they all survived. Six infants died before surgery: five of them had major pulmonary hypoplasia. Surgery was performed in twenty cases: nine of these infants died. Death occurred during the first twelve post-surgical hours in six cases with major pulmonary hypoplasia. Fourteen infants were followed from 6 to 24 months; two developed post-anoxic hydrocephaly with poor neurological development in one case. A pH above 7.1 and an adequate hemodynamic status obtained before surgery are simple criteria of a good prognosis. When these criteria are not obtained, prognosis is poor as they are in favor of major pulmonary hypoplasia.
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PMID:[Diaphragmatic hernia: the role of perioperative resuscitation]. 358 79

Of 99 children in the Royal Blind School, Edinburgh (which serves Scotland and part of N E England), 15 had optic atrophy (hydrocephalus 4, intracranial haemorrhage 2, prematurity 2, fetal distress 2, birth asphyxia 2, cerebral atrophy 1, cardiac arrest during hernia operation 1, and leukaemia 1). Fourteen had congenital cataract, 12 congenital retinal aplasia (Leber's congenital amaurosis) and 11 retinopathy of prematurity. There were small numbers in many other diagnostic categories, including three with non-accidental head injury. Mental retardation, spasticity, and nystagmus were frequent other correlates in all diagnostic categories. 'Very probably hereditary' was a conservative attribution in 36, while 'probable' seemed appropriate for 12-that is, almost 48% were hereditary. Only about 11 cases might have been prevented through genetic counselling, which testifies to the frequency of autosomal recessive hereditary disease, although no parents were consanguineous.
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PMID:Blindness in schoolchildren: importance of heredity, congenital cataract, and prematurity. 365 73

Experience in fetal invasive therapeutic procedures is currently nearly entirely based on animal experimental research. Structural defects in the human fetus which are potentially amenable to intrauterine surgical treatment are obstructive uropathy, hydrocephaly and diaphragmatic hernia. The results from closed procedures such as shunting of urine or CNS fluid to the amniotic fluid compartment under ultrasound monitoring is as yet not very encouraging. This is partly determined by technical inadequacies, and partly due to insufficient information available on the possible presence of associated anomalies and functional aspects of the affected organ systems. The risks of invasive procedures for the mother and in particular the fetus must be weighed up against the advantages for the fetus if surgery has been successful. It seems that the development of open surgical procedures will determine the future of fetal surgery.
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PMID:[Prenatal diagnosis and therapeutic intervention]. 367 83

Recent developments and improvements in prenatal diagnostic methods, and in particular antenatal ultrasonography, have made intrauterine detection of fetal abnormalities possible. Most defects are best treated after birth, only a few disorders are potentially amenable to surgical treatment in utero. Studies in animal models have helped us to define the pathophysiology, to recognize the interference of the abnormality with organ development and to determine whether elimination of the anomaly might allow fetal development to proceed normally. In-utero repair of congenital diaphragmatic hernia has been practiced on a fetal lamb model but has not yet been attempted in human beings. Treatment of fetal hydrocephalus has been investigated in sheep and rhesus monkeys, and the pathophysiology and intrauterine treatment of fetal hydrocephalus has been studied in fetal lambs and monkeys, but the question of the reversibility of renal dysplasia has not been resolved. Animal models have been described for possible intrauterine treatment of skeletal abnormalities like spina bifida. But more knowledge of embryology and of the pathophysiology of the malformation is needed, as well as about the efficacy and feasibility of this method before it can be attempted in human beings. Prerequisites for fetal surgery include the selection of those fetuses who might benefit from intrauterine treatment, counselling of the family concerned, and a highly experienced multidisciplinary team including a perinatal obstetrician, an ultrasonographer, a pediatric surgeon and a neonatologist. In human beings intrauterine treatment has been performed in erythroblastosis fetalis, urinary tract obstruction and hydrocephalus with encouraging results. There are many ethical, legal and social questions which cannot be answered; new guidelines and rules will have to be laid down.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Problems of and possibilities in fetal surgery]. 389 50

Contemporary neonatal intensive care has resulted in survival of many seriously ill preterm and older infants that frequently present with symptomatic inguinal hernia. Controversy exists concerning timing and safety of early repair in prematures or other neonates, especially those hospitalized with concurrent illness. This study examines this topic by evaluating predisposing factors, presentation, and postoperative complications in 100 recent consecutive hernia repairs in previously hospitalized infants less than 2 months of age. There were 85 boys and 15 girls. Thirty percent were premature (less than 36 wks gestation). Forty-two infants were hospitalized for RDS with assisted ventilation in 16 infants, hydrocephalus and ventriculoperitoneal (VP) shunt in 7 infants, and congenital heart disease (CHD) in 19 infants. Clinical presentation was on the right side in 44 infants, bilateral in 42, and on the left side in 14. Incarceration occurred in 31 cases with nine babies having overt intestinal obstruction. The incidence of cryptorchidism was 12.9%. All (VP) shunt, CHD patients, and incarcerated cases were treated with preoperative antibiotics. Following discharge, 49 preterm or previously ill infants developed a symptomatic hernia at home and were readmitted. Nine full-term infants were treated as outpatients. Bilateral inguinal exploration was performed in 92 cases with second hernia or patent processus found in 81. Seven of eight with unilateral exploration had acute incarceration with obstruction at the time of the procedure. Three subsequently required a second hernia repair. Two infants with incarceration and cryptorchid testis or ovarian slider had gonadal infarction. There were eight postoperative complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inguinal hernia repair in the perinatal period and early infancy: clinical considerations. 652 Jun 82

The antimitotic drug hydroxyurea (HU) has been evaluated as a positive standard for teratological screening in rats. Single intraperitoneal administration of HU to pregnant Sprague Dawley rats at the dose level of 750 mg/kg induced embryolethality or specific anomalies depending on the day of treatment: HU administration on days 7, 8, 9, 10 or 11 produced lethal effects in a high percentage of embryos; cardiovascular malformations were specifically induced by a single dose on day 10, ocular anomalies on day 10 or 11, palatoschisis or diaphragmatic hernia on day 12, limb or paw deformities on day 10, 11, 12 or 13. This experiment demonstrated the high susceptibility of the genotype of our colony of rats to the embryotoxic potential of HU. Repeated oral administration of HU during the organogenetic period (from day 6 to day 15 of gestation), at dose levels ranging from 50 to 450 mg/kg, led to a dose dependent embryolethal and teratogenic effect. Live foetuses at term generally showed severe ocular and craniofacial anomalies; hydrocephalus, cardiovascular anomalies, vertebral and costal defects were also registered. Limb malformations were not frequent and paw abnormalities were totally absent. In our experimental conditions, the dose level of 300 mg/kg is regarded as a suitable positive control dosage in teratological testing of new molecules by oral route.
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PMID:Hydroxyurea as a reference standard in teratological screening. Comparison of the embryotoxic and teratogenic effects following single intraperitoneal or repeated oral administrations to pregnant rats. 693 10

Herniation of the hindbrain occurs when the lowest parts of the cerebellum and sometimes part of the medulla are moved downwards through the foramen magnum, a pressure difference acting across the foramen magnum moulding the tissues into a plug. It is suggested that the clinical course in both adults and babies with spina bifida may be explained by the hindbrain hernia acting as a valve.The term 'Chiari Type I deformity' is commonly used for an abnormality in which the tonsils and lowermost parts of the cerebellar hemispheres are prolapsed through a normal foramen magnum. Acute herniation may occur as a result of space-occupying lesions. Chronic herniation may be morphologically identical although it tends to be more severe. Sometimes it will produce few symptoms which often may be delayed so that the original causative lesion may not be apparent. Causes include bone softening, tumour, or previous meningitis. Birth injury is probably the commonest cause of the deformity, which presents clinically in adults.In infants with severe forms of spina bifida a hindbrain herniation is present. This abnormality may be called 'Chiari Type II deformity' or Arnold-Chiari deformity and is an intra-uterine abnormality in which the fourth ventricle and medulla are grotesquely herniated before they are properly developed and the foramen magnum is enlarged.The commonest clinical presentation of Chiari Type I deformity is syringomyelia, which is usually not diagnosed until adult life. Other presentations include syringobulbia, headache, oscillopsia, attacks of giddiness, lower cranial nerve palsies, and ataxia. Particularly characteristic are cough headache and cough syncope. Syringomyelia and syringobulbia in particular may be irreversible by the time they are diagnosed. Nevertheless, surgical decompression may be successful in relieving symptoms of headache, cough syncope, and long-tract compression; most cases of syringomyelia show some improvement and in others progression of the disease is arrested. Operative techniques for hindbrain herniation are discussed.Chiari Type II deformity is probably responsible for the progression of hydrocephalus after birth in the majority of babies with spina bifida. Measurement of pressure in the cerebrospinal fluid above and below the foramen magnum shows that intermittent pressure difference is commonly present at times of neurological deterioration. Surgical decompression of the hernia in adults allows correction of the valvular effect, which may be monitored by pressure measurements. In babies the associated hydrocephalus is usually so gross that it requires separate treatment, but pressure monitoring may be of value in assessing the state of the disease.
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PMID:Chronic herniation of the hindbrain. 701 51


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