Perspectives in pediatric pathology最新文献

Two hundred thirty-seven autopsy cases of SUA and 1,242 unselected perinatal autopsies from military hospitals were reviewed and statistically analyzed. Results were correlated with those found in a comprehensive literature review. Incidence: The incidence of SUA in prospective deliveries is about 1%. Incidence is related to the portion of the umbilical cord examined, the method of cord examination (gross or microscopic), and to the race of the population base. The incidence of SUA in autopsy series is about twice the incidence in prospective series. SUA has a much higher incidence amont malformed, stillborn, or spontaneous abortuses than among apparently normal, liveborn, or induced abortuses. The incidence of SUA is less among very early embryos than among newborns because of the likelihood that SUA results from secondary atrophy of a preexisting normally formed second artery. As gestation proceeds, more cases will have become manifest to increase the incidence of SUA. There is no evidence of a familial tendency for SUA. SUA occurs slightly more frequently in females than in males, although there is a greater tendency for males with SUA to be malformed. The prognosis for SUA males is worse than for SUA females but no worse than that for male infants, in general. There is no relationship between the incidence of SUA and the month of the mother's last menstrual period. SUA and multiple births: The incidence of twins among SUA infants is at least three times greater than the overall incidence of twins. SUA occurs three to four times more frequently among twins than among Singletons. Although twin infants are subject to twice the expected incidence of malformations, twin SUA infants have no greater incidence of associated malformations than SUA singletons. Most SUA twins are discordant for the anomaly with SUA occurring in the smaller twin. The increased incidence of SUA among twin infants is not due to a greater incidence among monozygotic twins, since there is little difference from the usual proportion of monozygotic and dizygotic twins among twins with SUA. Mortality: In prospective series the mean perinatal mortality is about 20.0%. Approximately two-thirds of the perinatal deaths are stillborn and one-third are liveborn; and of the stillborn SUA infants, approximately three-quarters die antepartum and one-quarter die intrapartum. Mortality of SUA infants is related to associated fetal and placental malformations, prematurity and low birth weight, and intrauterine growth retardation. Although associated malformations are the primary cause of the high perinatal mortality, even nonmalformed SUA infants have an increased mortality rate.(ABSTRACT TRUNCATED AT 400 WORDS)

This classification of spontaneous abortions, based on placental rather than embryonic or fetal morphology, does not entail detailed embryological or histological techniques. It is readily adaptable to routine pathological laboratory practice. The advantages that may accrue from proper examination of spontaneous abortions are numerous and include provision of both clinical and epidemiological data pertinent to the immediate management of the aborting patient, as well as basic information that may clarify the mechanisms underlying the major complications of pregnancy which contribute to perinatal mortality in developed societies. The pathology of the placenta in groups 1 and 2 is seen as a possible indicator of the mechanisms leading to spontaneous abortions in man. The lesions are not seen in isolation but are viewed as a logical progression related to the time at which normal development ceases. The key and unifying concept in the hypothesis is the role of the villous circulation in the maintenance of normal trophoblastic function. In the earliest abortions, the villous circulation never develops, resulting in microscopic hydatidiform or hydropic change within the villus and attenuation of the trophoblast, while embryonic or fetal death following the establishment of a villous circulation results in the sequential changes characteristic of group 2 cases. Although the majority of embryonic and fetal deaths still remain unexplained, the hypothesis suggests a mechanism by which the abnormal conceptus may determine the outcome of pregnancy without invoking the concept of maternal rejection. Verification and extension of this hypothesis will require correlation of clinical, endocrinological, and morphological data. The histopathologist has failed to keep pace with advances in modern obstetrics during the last decade, particularly in the field of early pregnancy wastage, thus reinforcing the clinical opinion that morphological examination of abortions has little to offer in the clinical management of these cases. If counseling and therapy are to be based on scientific concepts rather than on empirical data, it is essential that this deficiency be rectified.

Ventricular septal defect (VSD) is the most common congenital cardiac lesion, occurring either in isolation or in hearts containing more complex lesions. Usually, the defect is between two ventricles, each of which is connected to a separate atrium and to a separate great artery, and surgical or spontaneous closure of the VSD basically corrects the circulation if the effects of any associated lesion are ignored. In other situations, the VSD is an integral part of the circulation, either because the atria connect to only one ventricle or because the ventricles give rise to only one patent great artery or else both great arteries arise from the same ventricle. When in such circumstances the circulation is VSD-dependent and the defect cannot be surgically closed without bypassing it with a conduit or similar device. In all of these situations, the VSD takes one of three basic forms. Usually, the VSD abuts directly upon the fibrous skeleton of the heart formed by the conjoined rings of the cardiac valves. The membranous part of the ventricular septum is an integral part of this skeleton, and these defects are termed perimembranous. These defects do not always occupy the same part of the septum. They may extend mostly into either the inlet, trabecular, or outlet parts of the muscular septum, or else be confluent extending into two or all these parts. Less commonly, VSD may be exclusively contained within the muscular septum. Such muscular defects can also be confined to either the inlet, trabecular, or outlet parts of the septum. They may be multiple or coexist with one of the other types. The third and least common type is a VSD which is roofed by the conjoined rings of the aortic and pulmonary valves because of absence of the outer septum. Such a defect may have a muscular posteroinferior rim or may extend to become perimembranous. Identifying a defect as perimembranous or muscular, together with its location relative to the different parts of the muscular septum, gives at the same time information concerning the site of the conduction axis in relation to the defect and its chances of spontaneous closure.

In this article we have described for a pathologist without forensic experience the need to describe meticulously all the injuries an abused child has suffered; the reasons for this required detail and attention; the need to exclude natural disease as the cause of death; the common radiographic features and morphology of injuries found in an abused child; the responsibility of the pathologist to the dead child and any living siblings; and have given an intimation of the legal processes which may follow.