Congenital heart lesions, Down syndrome, club foot, congenital gut lesions, hypospadias, microcephaly, harelip and cleft palate, congenital hip, hemangioma, undescended testicles, polydactyly, conjoined twins and teratomatous malformation, patent ductus arteriosus, amaurosis, arteriovenous fistula, inguinal hernia, umbilical hernia, syndactyly, pectus excavatum, myopathy, dermoid cyst of scalp, omphalocele, spina bifida occulta, ichthyosis, and persistent lingual frenulum.
Abstract Pancuronium bromide PB is used in neonates and pregnant women to induce limp, flaccid paralysis in order to allow mechanical ventilation during intensive care.
Such non-depolarizing neuromuscular blocking drugs are administered to 0. In this study, we examined PB effects on skeletal development in chick embryos. PB treatment Development of deformities skeletal deformities associated with significant reduction in longitudinal growth of all appendicular elements.
This was associated with greater cartilage to bone ratios, indicating a preferential reduction in osteogenesis. PB also increased the incidence of knee joint flexion and tibiotarsal joint hyperextension. In addition to limb, spinal and craniofacial deformities, flaccid immobility appears to convert the normal geometric pattern of weight gain to a simple arithmetic accretion.
This novel study highlights the potentially harmful effects of pharmacologically induced flaccid immobility on chick embryonic skeletal development. Whilst in ovo avian development clearly differs from human, our findings may have implications for the fetus, premature and term neonate receiving such non-depolarizing neuromuscular blocking drugs.
The administration of these muscle relaxants is commonly used in order to induce the immobilization necessary to reduce resistance to mechanical ventilation during respiratory distress.
These drugs function by combining with postjunctional acetylcholine ACh receptors and competitively antagonize the endplate transmitter action of ACh Rang et al. This favourable pattern of pharmacological characteristics has led to the broad clinical use of PB.
These studies have shown that nutrition and preprogrammed growth are necessary but not sufficient for normal bone growth and development.
An interest in the mechanisms of skeletal deformity as well as a desire to determine the factors regulating musculoskeletal development stimulated a search for appropriate animal models capable of shedding light on such phenomena. Such treatment also caused reduced birth weights and produced multiple positional deformities of the extremities fetal akinesia deformation sequence Moessinger In humans, neonatal contractures with micrognathia and neck webbing have been described after day maternal treatment for tetanus with d-TC administered between 10 and 12 weeks gestation Jago Although PB-like drugs are more commonly used in neonates suffering from respiratory distress, their effects on the developing musculoskeletal system in this context are very difficult to assess.
An association between the mechanism of action of such drugs and the acquisition of neonatal contractures has nonetheless already been made Jago ; Vincent et al.
Despite this, the possibility that PB administration may exert side effects on the developing skeleton remains unaddressed. We have previously found that PB treatment rapidly induces a state of flaccid paralysis in the developing embryonic chick Osborne et al.
By administering PB in ovo, it has been possible to study the role of movement on limb development. This study is the first to report that the PB treatment induces a significant range of fixed, and diverse, positional deformities.
Prolonged administration with PB also resulted in decreased body weight, accompanied by profound changes in skeletal growth. In addition to limb, spinal and craniofacial deformities, such treatment during the second half of gestation appears to convert a normal geometric pattern of weight gain to a simple arithmetic accretion.
Analysis of the bones reveals significant reductions in limb length with an increase in cartilage to bone ratio indicating that flaccid paralysis also selectively provokes aberrations in the normal process of endochondral ossification.
Finally, it is tempting to speculate that the skeletal phenotype induced by PB treatment in ovo represents a longer term consequence of isolating embryos from the sequelae of normal mobility during musculoskeletal development, and if parallels can be drawn between chick and human development then it raises questions regarding the prolonged use of such drugs in preterm neonates.
Another three groups of chicks received TS, as a control, at the same times. One day after the final treatment at stages 37, 40 and 44, respectivelychicks were killed by Schedule 1 procedure conforming to the Animal Scientific Procedures act About 3% to 4% of all babies born in the United States have congenital abnormalities that will affect the way they look, develop, or function—in some cases for the rest of their lives.
Congenital abnormalities are caused by problems during the fetus's development before birth. It is important for. Paediatric Orthopaedic conditions are relatively common. In most cases the observed abnormalities are simply variations of normal development and with growth these deformities undergo spontaneous correction (physiological deformity).
Pediatric foot deformity is a term that includes a range of conditions that may affect the bones, tendons, and muscles of the foot. Among those most frequently treated at HSS are cavus foot, tarsal coalition, clubfoot, accessory navicular, and juvenile bunion.
Causes and development of the “pollybeak-deformity“. a) Risk-factors are deep nasofrontal angle (1), high cartilaginous dorsum (2) and under-projection of n. Amphibian deformities have remained one of the most prominent and controversial environmental issues of the past fifteen years.
During this time we have presented strong evidence that suggests the proximate causes for anuran hind limb deformities featuring supernumerary limbs and segments are caused by parasitic infection by the trematode Ribeiroia ondatrae.
Cankers on trees appear as isolated dead areas on the bark, stems, branches or twigs. Cankers may appear as discolored areas or depressed places on the bark.
A fungus that enters the tree and grows between the bark and the wood killing the bark generally causes cankers. However, cankers can also be.