Biomedical subjects
Publications and source records attributed to R Bejar.
The experience of the Special Care Nursery of the University of California Medical Center, San Diego, in the management of the high risk newborn with progressive ventricular enlargement is reviewed, and the physiopathological basis of progressive ventricular enlargement is analyzed.
Fifty-three low birth weight high risk newborns who developed progressive hydrocephalus despite a trial period of intermittent lumbar punctures underwent cribside ventriculoperitoneal shunt placement. They all weighed less than 2000 g at the time of shunting (mean, 1308.6 g +/- 398.2 SD). The operative procedures were performed at a mean age of 31.5 days +/- 16.1 (SD). There were no deaths in this series. During the nursery stay, 14 patients required operative revisions for obstruction. The most common problem was infection, which occurred in 13 (24.5%) after the primary intervention and in another 5 of the 14 (35.7%) patients who required revision. The overall infection rate/patient was 26.9%. Shunt removal and intensive antibiotic therapy cured the infection in all but 1 patient. Premature, low birth weight newborns may undergo ventriculoperitoneal shunting, but close follow-up for complications such as infection and shunt obstruction is always required.
Hypoxanthine, the end product of purine metabolism, is usually very elevated in body fluids during severe hypoxia. We measured hypoxanthine in the cerebrospinal fluid of hydrocephalic preterm infants (12 with posthemorrhagic, one with congenital hydrocephalus) to determine whether hydrocephalus is associated with anaerobic metabolism of brain tissue. Cerebrospinal fluid hypoxanthine was undetectable in normal infants. In hydrocephalic infants, the concentration of hypoxanthine ranged from 7.5 mumol/L to 28 mumol (means = 14.3 mumol/L). The hypoxanthine concentrations fell from a mean of 12.8 mumol/L to a mean of 2.0 mumol/L (P less than 0.05) with successful treatment of the ventriculomegaly by lumbar puncture or by ventriculoperitoneal shunt. Patients with acute posthemorrhagic hydrocephalus had similar concentrations of hypoxanthine (means = 14.5 mumol/L) as patients with late or with congenital hydrocephalus (means = 13.8 mumol/L), indicating that brain hypoxia is probably a consequence of the ventriculomegaly and not of the hemorrhagic insult.
Real-time ultrasonography is being used increasingly to establish the diagnosis of and serially assess intraventricular hemorrhage and hydrocephalus in neonates. The procedure requires an open fontanel because scatter from the bone occurs from direct application of the transducer to the skull and bone density precludes satisfactory imaging. With an adult, under circumstances where a bone flap is left out after intracranial procedures and the patient's clinical status is such that the patient cannot be transferred for computed tomographic scanning, real-time ultrasonography allows a safe, noninvasive, bedside demonstration of ventricular size, degree of shift of midline structures, and intraparenchymal and intraventricular lesions.
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Human term labor is thought to be initiated by amniotic and chorionic phospholipase A2, an enzyme that liberates arachidonic acid esters from the phospholipids of these membranes, leading to the synthesis of prostaglandins by the placental membranes. The striking association of premature labor with intrauterine infection or contamination, urinary tract infection, and early neonatal sepsis led us to study the microorganisms present in these infections for phospholipase A2 activity. Activity was found in Bacteroides fragilis, Peptostreptococcus, Fusobacterium necrophorum, Streptococcus viridans, Streptococcus fecalis, Streptococcus A and B, Escherichia coli, Klebsiella, Staphylococcus epidermidis, Pneumococcus, Lactobacillus, and Mycoplasma hominis. Bacteroides fragilis, Peptostreptococcus, Fusobacterium, and S viridans had the highest activities. The specific activities of phospholipase A2 from these organisms were several times higher than that of the membrane phospholipase A2 of the amnion and chorion. We postulate that premature labor may be initiated by microorganisms with phospholipase A2 activity from endocervical and/or intrauterine contamination or infection, producing deacylation of arachidonic acid from amniotic phospholipids with increased concentrations of free arachidonic acid and increased prostaglandin synthesis, which triggers labor.
Amnion and chorion from premature and term placentas after both spontaneous labor and elective cesarean section were assayed for phospholipids and fatty acid composition by 2-dimensional thin-layer chromatography and gas-liquid chromatography. In preterm placental phospholipids, phosphorus concentrations were higher in amnion than in chorion, whereas at term the membranes were similar owing to an increase in phospholipid concentration in the chorion late in gestation. PHosphatidylcholine (PC) accounted for 47% of the total phospholipid phosphorus, followed by sphingomyelin at 20%, phosphatidylethanolamine (PE) at 15%, phosphatidylserine (PS) at 12%, and phosphatidylinositol (PI) at 5%. These percentages were similar for amnion and chorion and they did not change during gestation. The percentage of arachidonic acid (AA) was higher in PS (40 to 65%) than in PE (30 to 53%) and PC (10 to 13%). The percentage of AA was significantly higher in PC, PE, and PS from the amnion in premature pregnancies than in those of the premature chorion. At term, these amnionic and chorionic phospholipids had similar concentrations of AA owing to a significant increase in AA in the chorion late in gestation. Amnionic PE from term and preterm elective cesarean section had a significantly higher percentage of AA than that from preterm and term labor. These data suggest that AA is consumed during labor and that amnionic phospholipids, particularly PE, may be its principal source. The amnion seems to be more important for the storage of AA than the chorion, particularly in preterm pregnancies in which the concentrations of phospholipids and the percentages of AA in PC, PE, and PS were significantly higher than in the chorion.
A technique to diagnose subependymal hemorrhage (SEH), intraventricular hemorrhage (IVH), intracerebral hemorrhage, and posthemorrhage hydrocephalus in tiny infants, using real time ultrasound studies of the brain ventricular system, is described. This is a bedside technique that visualizes the brain through the fontanelles and the sutures, in three planes: coronal, sagittal, and horizontal. Excellent visualization of the ventricular system, caudate nuclei, the thalamus, the choroid plexus, the corpus callosum, and the foramen of Monro is obtained. This method has good definition using high frequency transducers since there is no bone interference. The ultrasound diagnosis correlated well with computed tomography (CT) and with direct pathologic studies. This technique was more sensitive in diagnosing small IVH/SEH and organized clots than were CT studies. IVH/SEH were found in 90% of 113 infants less than or equal to 34 weeks of gestation; 49% of the hemorrhages were large and 41% were small. Most hemorrhages were found in the first scan, usually shortly after birth. Twenty-one premature infants who never had perinatal asphyxia or respiratory distress syndrome had IVH/SEH. The hemorrhages were followed until disappearance, usually in one to three months in cases of large hemorrhages.
The first report of a 7-month-old male with pseudohypoaldosteronism in which unresponsiveness to mineralocorticoids has been demonstrated in the kidney, colon, and sweat and salivary glands is presented here. This is documented by urinary, salivary, and sweat sodium wasting in the presence of elevated urinary aldosterone excretion, plasma aldosterone concentration, and PRA. There was no mineralocorticoid response in the kidney or salivary or sweat glands to the administration of high doses of 9 alpha-flurocortisol. Furthermore, in this patient, the colonic mucosal cells failed to respond to exogenous aldosterone administration. Repeat evaluation at 25 months of age showed persistence of the sodium wasting and multiple target organ insensitivity to administered mineralocorticoid. Since this patient has defective mineralocorticoid response in the major sodium-conserving organs, the only therapy possible was administration of sodium to compensate for total sodium loss.
The study of metabolism of muscle electrolyte in children with the salt-losing form of congenital adrenal hyperplasia reveals two types of alterations. After admission and during initial therapy with salt and desoxycorticosterone, the changes are typical of those seen in experimental animals with adrenalectomy and excessive replacement therapy. Discontinuation of the sodium supplement after three months of therapy resulted in a return of muscle electrolyte values to normal. During the period of poor growth common to these patients a different pattern was observed. Sodium and water accumulated without alteration in tissue potassium. The mechanism of this alteration is not clear; however, it is consistent with the known effects of excess cortisone on muscle composition. These observations permit the conclusion that at least two fractions of sodium are present in muscle fibers, that which exchanges potassium and that which is independent of potassium metabolism.
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Eleven preterm infants (gestational ages 27-35 weeks) with echogenic paraventricular white matter identified shortly after birth were studied with serial echoencephalograms to fully delineate the sonographic findings characterizing the pathologic stages of white-matter necrosis. Echoencephalograms were compared with autopsy findings and CT scans. Cerebral function was assessed by electroencephalograms and later by neurodevelopmental evaluations. Echogenic areas were observed in the paraventricular white matter in the acute stage. Microscopically, the echogenic white matter consisted of vascular congestion and petechial hemorrhages, but not always with foci of necrosis. Anechoic areas, which characterized the chronic stage, corresponded to cavitary lesions, and these generally appeared within 2 weeks of birth. However, six infants had anechoic lesions by day 4, suggesting that the onset of white-matter damage was antenatal. CT showed mildly decreased attenuation when paraventricular echogenic areas alone or in association with small anechoic areas were observed. Markedly decreased attenuation on CT scans corresponded to large anechoic areas. Resolution of the sonographic and CT findings did not indicate normalization of the white matter since all surviving infants were neurologically abnormal at 1 year. Electroencephalograms with central (rolandic) positive sharp waves were associated with echogenic white matter alone or with evolving anechoic areas. All patients with positive sharp waves on electroencephalograms had large anechoic areas in later studies. Early and serial echoencephalograms are necessary to evaluate white-matter necrosis in preterm infants. When echogenic white matter is identified, electroencephalography can suggest the presence of white-matter necrosis.
In a randomized study, indomethacin was administered either by an intravenous rapid infusion or by a 30-minute intravenous infusion to preterm infants. Ten infants were randomly assigned to the rapid infusion group and nine to the other group. Time-averaged mean systolic, mean flow velocity, and mean diastolic blood flow velocities were measured in the internal carotid artery with a pulsed Doppler. Blood flow velocities, arterial blood gases, intraarterial blood pressures, and transcutaneous PO2 and PCO2 were measured at 5 and 1 minutes before indomethacin and then at 5, 10, 20, 30, 35, 40, 50, 60, and 90 minutes after indomethacin administration. Intravenous indomethacin either by rapid or slow infusion caused a significant decrease in the blood flow velocities. The blood flow velocities were significantly lower 5 minutes after rapid infusion and by 30 minutes in the slow-infusion group. In both groups, the blood flow velocities remained depressed up to 90 minutes. The blood pressures increased concomitantly to the blood flow velocities in the rapid-administration group only. Because indomethacin given for 30 minutes does not avoid the decrease in the blood flow velocities, further studies are necessary to ascertain the safest method of administration.