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OBJECTIVE: To distinguish the fact from artifact of an isolated, large, intracranial cyst on prenatal sonography (PSG). BACKGROUND: The use of PSG is rapidly increasing with most obstetric ultrasounds occurring in general community settings like small hospitals and clinics with personnel who have variable training, experience, and interest levels. In contrast, most PSG articles and books are produced in large subspecialty centers with concentrated referral bases plus both highly-trained and experienced personnel. DESIGN/METHODS: We report a series of 2 normal newborn patients who had a large prenatal unilateral intracranial cyst diagnosed by PSG in the 10 years between July of 1989 and 1999 at a rural community hospital. The newborns had imaging studies at birth and their neurodevelopmental progress was followed for several years. Textbook, bibliography and computerized Medline (1966-present) searches including prenatal ultrasound, observer variation, diagnostic errors, reproducibility of results, sensitivity and specificity, accuracy, central nervous system, false-positive, prenatal diagnosis, and brain were examined starting in August 1996 for reports. RESULTS: There were 4079 obstetric ultrasounds performed in 3.5 years, January 1996 through July 1999 at this rural community facility. This rate extrapolates to a total of 11 654 obstetric ultrasounds over the 10-year study period in which the 2 cases of intracranial cyst artifact occurred. Thus, the incidence of 2 intracranial cyst artifacts was estimated as 2/11 654 PSG, a .0002% false-positive rate. CONCLUSIONS: This is the first report of the occurrence of PSG artifacts in a community facility. Artifact is a real problem and needs to be specified in differential diagnoses. There are ways to decrease sonographic artifact-or at least to recognize it-so our estimates at a community hospital for its occurrence are presented with the relevant technical and ethical issues. None of these issues have been previously reported in the pediatric literature. Our false-positive rate for large intracranial cyst compares favorably with other reports. Our estimate may inflate our denominator by reporting scans rather than the number of fetuses scanned, and our numerator may miss cases that moved from the community. Confusion differentiating PSG artifact from reality often occurs when interpreting static or frozen real-time images. The signs that sonogram images may be artifacts include defects that: extend outside the fetal body; change shape, size and echogenecity with different scan planes; are not seen on all examinations; and are isolated in an otherwise normal fetus. Failure to offer quality PSG in clinical settings where it is available restricts access of pregnant women to the diagnosis of fetal anomalies, and therefore restricts access to the options of pregnancy termination, fetal therapy like fetal surgery, and delivery options of timing, setting, and mode. We suggest a multidisciplinary approach to prenatal abnormalities like isolated third trimester unilateral intracranial cyst in both primary and tertiary care settings aids interpretation followed by expectant conservative management without elaborate, risky, or terminal interventions.

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Spinal muscular atrophy (SMA) or Werdnig-Hoffmann disease is the second most common neuromuscular disease, with 25% of cases presenting in infancy. Deletions in the survival motor neuron gene are believed responsible for autosomal-recessive SMA. SMA affects about 1 in 10,000 births. Symptomatic newborns have severe hypotonia, may have respiratory distress, may be unable to feed, and rapidly progress to death early in infancy. This paper describes another early pulmonary manifestation of SMA, i.e., migrating or rotating atelectasis, in 2 patients with infantile SMA. Migrating or rotating atelectasis may suggest the diagnosis of SMA.

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Fetal origins of coronary disease were proposed recently on the basis of evidence that intrauterine growth retardation predisposed to precocious coronary disease. Recent ultrastructural studies suggest a pathogenesis supporting perinatal origins of coronary atherosclerosis. Half of infants show coronary intimal lesions with foam cells. Intimal proliferative lesions, precursive to lipid insudation of coronary arteries, have been reported in fetuses and newborns. Acute hypertension increases and promotes the progression of preexisting modified smooth muscle cell plaques in perinatal animals by developing prominent fibroplasia and collagenization. Such perinatal surges in blood pressure may be involved in the perinatal initiation of atherogenesis. Modification of naturally occurring lesions may depend on perinatal circumstances superimposed on the transition between fetal and adult patterns of circulation. Unusual perinatal stresses involving anoxia or catecholamine release in the mother, fetus, or newborn may predispose to the development of precocious coronary atherosclerosis later in life.

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Activated platelets rapidly internalize ligand-alpha(IIb)beta 3 complexes and particulates. The platelets sequester these primarily to the surface-connected canalicular system (SCCS), alpha-granules or evaginated surfaces. This occurs swiftly as activation initiates shape change, internal transformation, and secretion out of the platelet SCCS. The transmembrane signaling mechanism for internalization is through the platelet submembranous, detergent-resistant, cytochalasin B-resistant cytoskeletal filaments, not cytoplasmic actin filaments. This work proposes the model that platelet internalization responses contribute in the retraction of clots and participate in vivo in thrombus development at sites of coronary artery injury. In isometric clot retraction, the retracting platelets show internalization of fibrinogen-gold and fibrin while spreading on the polymerizing fibrin strands. The combination of platelet internalization (retracting) with evagination (spreading) on fibrin strands appear to approximate and organize nearby platelets into the developing thrombi. Ex vivo findings are similar under flowing conditions on denuded rabbit aortic endothelium with fibrinogen-gold markers. Early thrombi developing in vivo at sites of congenital coronary artery lesions in perinatal piglets show fibrin strands internalized into the SCCS of platelets. A thrombogenesis model is proposed that shows that platelet internalization responses anchor fibrin and approximate platelets, thus enhancing thrombus development and retraction.

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The fine structure and ultrastructure of the anterior descending coronary artery were studied in a series of perinatal piglets at 1 week prior to birth, and at 8, 24, 72 and 168 h after birth. In the anterior descending coronary artery, at or just distal to the branch point of the left circumflex artery, early plaque-like intimal lesions were present in the majority of animals. These consisted of subendothelial edema, fragmentation and dissolution of the internal elastic lamella, and the appearance of intimal myoid cells known as modified smooth muscle cells (MSMCs). These changes were present in all piglets at and before 8 h of age. They persisted and progressed during the first week of life in about half of the piglets. Beginning at 72 h and continuing through 168 h, there was an increase in MSMCs and the appearance of fibroblasts. Both fibroblasts and MSMCs were associated with the elaboration of dense collagen fibrils. Foamy macrophages appeared within the subendothelial intima having the appearance of lipophages. While the prevalence of these changes at birth indicates that they may be part of normal development, their persistence in half the piglets and structural features suggest reaction to intimal injury beginning prenatally. The lesions may be precursive of coronary atherosclerosis later in life and may parallel the early stages of atherogenesis in humans.

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OBJECTIVE: To determine if selective newborn cord blood testing (NCBT) could contain costs without increasing morbidity of hemolytic disease of the newborn (HDN). DESIGN: A national telephone survey confirmed the common practice of routine blood type and Coombs' NCBT. Two 12-month study arms, retrospective and prospective, were conducted. Hemolytic disease of the newborn was studied retrospectively under an unrestricted NCBT policy. Then, HDN was studied after a policy change that restricted NCBT to patients in newborn intensive care units and normal newborns with clinical jaundice or Rh-negative mothers, and/or positive maternal antibody screenings, or unavailable maternal blood testing. PARTICIPANTS: All newborns (N = 8501) at the Metro-Health Medical Center, Cleveland, Ohio, were studied (retrospective arm, all 1989 admissions; prospective arm, all July 1990 to June 1991 admissions). OUTCOME MEASURES: Blood type and Coombs' NCBT, maternal blood type and antibody screening, Hobel risk scores for clinical severity of newborn hospitalization, duration of hospitalizations, and peak serum bilirubin levels. RESULTS: No quantitative or qualitative increases in morbidity from jaundice were detected by retrospective analysis with unrestricted NCBT, or prospectively after selective testing on 4498 newborns. Each study arm resulted in 15 readmissions for jaundice; these included two patients with ABO HDN. Furthermore, selective testing resulted in performance of NCBTs on only 390 infants in the "normal" nursery (24% of the original sample). Estimates projected on 1991 US births (4,111,000) showed that selective NCBT offers potential yearly savings above $30.8 million of patient charges, savings above $11.3 million of hospital costs, and the reassignment of more than 112 personnel full-time equivalents. CONCLUSION: Selective NCBT decreases the use of resources and costs without apparent additional patient morbidity from HDN.

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Newborn piglets were subjected to 45 min of sustained norepinephrine-induced hypertension and then monitored for 4 hr at baseline conditions. They were then sacrificed and the anterior descending coronary artery was serially sectioned for study by light and electron microscopy. Other groups were sacrificed after 72 and 168 hr of baseline conditions. Changes were limited to the endothelium and subendothelial intima of the most proximal segment of the anterior descending coronary artery. As similar changes are normally present in perinatal piglets, the experimental animals were compared with sham-operated controls to determine if there was a modification of the naturally occurring congenital lesions. Although the prevalence of coronary lesions in control and experimental animals was not significantly different, the experimental groups showed unique features. At 4 hr, there was marked intimal edema and disruption of the endothelium with fragmentation and dissolution of the internal elastic lamina. There was selective invasion of the intima by platelets and monocytemacrophages. After 72 and 168 hr, there was an increase and progression in preexisting modified smooth muscle cell plaques in which there developed prominent fibroplasia and collagenization. It is proposed that acute hypertension may be responsible for these changes. Such perinatal surges in blood pressure may be involved in the initiation of atherogenesis.

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Obtaining hematocrit and bilirubin determinations is associated with infection risks, including human immunodeficiency virus infection. This study describes two simple procedures to decrease the risk of infection to health care providers while obtaining hematocrit and bilirubin determinations. Using readily available, inexpensive items (nonsterile gauze, a standard file, and plastic holder) and some simple techniques, the risk of infection can be decreased without increasing the time required. We believe these procedures are very reasonable and simple solutions to a common nursery problem.

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Human platelets were incubated with gold particles coupled to fibrinogen to label the glycoprotein IIb-IIIa (GPIIb-IIIa) receptor after initial activation of the cells by contact with formvar-coated grid and glass surfaces. Fibrinogen-gold (Fgn-Au) markers were absent on discoid platelets, but diffusely spread over the surface and extended pseudopods of early dendritic cells. Conversion to spread platelets resulted in movement of ligand-receptor complexes away from the cell margin toward cell centres. However, Fgn-Au gold did not concentrate in the central region. Rather, the Fgn-Au, GPIIb-IIIa complexes in the middle of spread platelets appeared to move toward a belt-like, intermediate zone, as did the ligand receptor complexes from the cell margin and pseudopods. The ultimate destination of the mobile receptor-ligand complexes, however, appeared to be channels of the surface-connected open canalicular system (OCS). Fgn-Au was concentrated in OCS channels of most dendritic and a small proportion of spread platelets. The decreased frequency of Fgn-Au filled channels in more transformed platelets may have been due to collapse or evagination of the OCS. Examination of platelets exposed to Fgn-Au after spreading on glass and then prepared for thin sections confirmed that the OCS was the final destination for mobile ligand receptor complexes on surface-activated platelets. Findings of this study are consistent with previous work showing clearance of mobile receptor-ligand complexes to the OCS of platelets activated in suspension.

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