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Biomedical subjects

J M Perlman

Publications and source records attributed to J M Perlman.

At least 73 records · Page 4Linked to original sources
PubMed1988

Renal injury in the asphyxiated newborn infant: relationship to neurologic outcome.

The relationship of renal and central nervous system injury was prospectively evaluated in 120 asphyxiated infants. Renal evaluation findings were considered abnormal if there was oliguria (urine output less than 1 ml/kg/hr), which was designated transient if present in the first 24 hours only and persistent if present for at least 36 hours, or if the urinary beta 2-microglobulin concentration from first-void urine was elevated: (1) Thirteen infants had persistent oliguria; the urinary beta 2-microglobulin level was elevated in all. The six term infants had clinical signs consistent with hypoxic-ischemic encephalopathy (HIE); all six had ultrasonographic abnormalities. The outcome was poor (i.e., death or long-term neurologic deficits) in five of six infants. The seven preterm infants with persistent oliguria had clinical evidence of HIE, and three infants had intraventricular hemorrhage; all seven infants died. (2) Fifteen infants had transient oliguria (beta 2-microglobulin level was elevated in eight infants). Two of the eight term infants had evidence for HIE; the cranial ultrasound scan was normal in all. At follow-up, seven term infants are normal and one is abnormal. Six of the seven preterm infants with transient oliguria had clinical evidence of HIE; three infants had intraventricular hemorrhage. Three infants died, and the four survivors are normal at follow-up. (3) Ninety-two infants had normal urine output. Of the 22 term infants, two developed signs of HIE, and the ultrasound scan was abnormal in three infants. Of the 70 preterm infants, eight (11%) had clinical signs consistent with HIE, the ultrasound scan was abnormal in 20 of 64 (31%) infants scanned, and 14 (20%) infants died. Most of the followed infants are normal. Thus oliguria was significantly associated with clinical signs of HIE, including seizures, death (specifically in the premature infant), and long-term neurologic deficits. These data suggest that oliguria in the perinatal period is a sensitive indicator of infants at risk for long-term neurologic deficits.

Apgar Score↗
PubMed1988

Renal failure in sick hypertensive premature infants receiving captopril therapy.

A retrospective study of nine sick premature infants with chronic lung disease who received captopril for control of systemic hypertension (systolic blood pressure (BP) greater than 113 mm Hg) was carried out to determine efficacy of therapy and associated complications. All nine infants had markedly elevated peripheral renin values, 134.3 +/- 128.1 ng/mL/hr (mean +/- SD). Five infants had abnormal renal sonographic and perfusion scans with evidence of renal artery thrombosis, parenchymal disease, or both. Captopril therapy (0.3 mg/kg) was instituted at a postnatal age of 123 +/- 108 days. After the initial dose, the systolic BP decreased significantly in all infants, the decrease ranging from 21% to 58% of the pretreatment value. Dosage was subsequently halved in all infants. Seventeen episodes of unpredictable decreases in BP more than 40% from baseline occurred during the reduced maintenance therapy. Four infants had a total of seven episodes during which the BP decreased by 57 +/- 10% from baseline; this decrease persisted for 17 +/- 6 hours and was unresponsive to volume reexpansion and inotropic therapy. All seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/hr) that persisted for 18 +/- 12 hours. These episodes were accompanied by neurologic signs (subtle seizures, lethargy, and/or apnea) within 18 +/- 6 hours after the onset of oliguria. The remaining five infants had a total of 13 episodes of decreased BP of 50 +/- 8% of baseline, which were of significantly shorter duration and responded to volume reexpanders, inotropic therapy, or both and were unaccompanied by oliguria. These data suggest the need for close observation of BP in infants receiving maintenance captopril therapy.

Acute Kidney Injury↗
PubMed1988

Seizures in the neonatal intensive care unit of the 1980s. Types, Etiologies, Timing.

A retrospective review was taken of 150 newborns with seizures evaluated at the same medical center and by the same investigator(s) from 1982 to 1987. The aims of the study were to determine in this current population the distribution of clinical seizure types, the distribution of causative etiologies, and the relation of etiology to the timing of onset of the seizures. Seizures were classified as subtle, multifocal clonic, generalized tonic, focal clonic, and myoclonic. Subtle (65% of total) and multifocal clonic seizures (54% of total) were the most common seizure types. Subtle seizures usually occurred in combination with other seizure types. Only one seizure type was related to gestational age, i.e., focal clonic seizures in the term infant. Hypoxic-ischemic encephalopathy (65% of total) was by far the most common etiology in both preterm and term infants. Seizures with hypoxic-ischemic encephalopathy occurred characteristically early in the neonatal period, i.e., 90 percent in the first 2 days of life. Moreover, 80 percent of all seizures in the first 2 days of life were related to hypoxic-ischemic encephalopathy.

Cerebral Hemorrhage↗
PubMed1988

Renal injury in sick newborn infants: a prospective evaluation using urinary beta 2-microglobulin concentrations.

Urinary concentrations of beta 2-microglobulin and creatinine were measured serially in 140 sick infants, of whom 109 were asphyxiated, and in 35 healthy preterm and term infants. First voided urines and samples from days 3 and 7 postpartum were studied. Urinary beta 2-microglobulin concentrations in healthy infants averaged 1.34 +/- 1.34 mg/L (mean +/- SD) in first voided specimens and 1.32 +/- 0.98 mg/L in day 3 samples; the calculated upper limit of normal (95% confidence limit) was 4.00 mg/L. Elevated values (those exceeding the 95% confidence limit) occurred most often in the sick asphyxiated patients (56%); the first voided sample value in these patients was 10.0 +/- 10.4 mg/L. The equivalent value in the sick nonasphyxiated infants was 8.32 +/- 7.27 mg/L. Values were significantly and persistently elevated in the sick infants on days 3 and 7. Factoring beta 2-microglobulin levels by urinary creatinine concentration did not affect the significance of the findings. The increased urinary beta 2-microglobulin levels were not (1) related to gestational age; low beta 2-microglobulin values occurred at all gestational ages for both healthy and sick infants; (2) a consequence of urine flow rate; urinary beta 2-microglobulin did not correlate with urinary creatinine concentration or with urine to plasma creatinine ratio; and (3) a consequence of increased production of beta 2-microglobulin; urinary and serum beta 2-microglobulin values did not correlate (r = .03). Thus, we propose that the elevated levels of urinary beta 2-microglobulin in the sick infants were the consequence of tubular injury. This was associated with hematuria but not with a high incidence of azotemia or oliguria.(ABSTRACT TRUNCATED AT 250 WORDS)

Asphyxia Neonatorum↗
PubMed1987

Binding of C-terminal segments of neuropeptide Y to chicken brain.

The C-terminal pentapeptide amide segment of neuropeptide Y (NPY) binds specifically to chicken brain membrane preparations. The contribution of each residue of the C-terminus to this binding has been investigated through the synthesis and evaluation of a series of pentapeptide analogs. The binding of these molecules is strongly dependent on the presence of certain functional groups, in particular the guanidinium group of Arg-35 and the C-terminal aromatic amide function. The significance of these results for the binding to chicken brain tissue of NPY, pancreatic polypeptide and other potentially related neuropeptides is discussed.

Amino Acid Sequence↗
PubMed1987

Recognition of neuropeptides FMRFamide and LPLRFamide by chicken cerebellum avian pancreatic polypeptide binding sites.

Binding isotherms were constructed for the binding of synthetic tetrapeptide and pentapeptide fragments to membranes prepared from chicken cerebellar tissue. Both the tetrapeptide (FMRFamide), which was originally isolated from ganglia of mollusks, and the pentapeptide (LPLRFamide) previously isolated from chicken brain are known to increase blood pressure and modulate brain neurons in rats. The C-terminal dipeptide sequences of the two peptides are identical and both show similarity to the dipeptide sequence established for the pancreatic polypeptide (PP) family. Specific high-affinity binding sites exist for the latter peptide, sites which are competed for (though with less affinity) by neuropeptide Y (NPY). Affinity for cerebellar membranes was virtually equivalent for the synthetic peptide LPLRFamide and FRMFamide; the binding affinities (IC50) of all fragments tested (C-terminal pentapeptides of avian PP and NPY, and FMRFamide and LPLRFamide) fell in the same approximate range. Since the N-terminal residues of FMRFamide and LPLRFamide are not homologous with equivalent residues of APP or NPY, our results indicate that only Arg-Tyr-NH2 or Arg-Phe-NH2 sequences are necessary for binding of the carboxy terminus peptides of the PP family. In this respect, these sequences are functionally equivalent.

Amino Acid Sequence↗
PubMed1987

Are venous circulatory abnormalities important in the pathogenesis of hemorrhagic and/or ischemic cerebral injury?

The venous circulatory changes in 12 intubated premature infants with fluctuations or elevations in arterial BP were studied. The objectives of the study were to determine whether important alterations in venous pressure occur in infants with fluctuations in arterial BP or with elevations in arterial BP associated with suctioning. Venous and arterial catheters were present in all infants. Perfusion pressure was derived from the difference between mean arterial BP and venous pressure. At rest, minimal change in arterial BP, venous pressure, and perfusion pressure was observed. Elevations in arterial BP were accompanied by pronounced changes in venous pressure. However, because the magnitude and the direction of the changes in venous pressure were not consistent, pronounced changes in perfusion pressure resulted. Fluctuations in arterial BP were associated with fluctuations in venous pressure, which also resulted in pronounced and continuous alterations in perfusion pressure. Induced muscle paralysis in two infants obliterated the changes in arterial BP, venous pressure, and perfusion pressure associated with suctioning. These data demonstrate that marked venous circulatory changes accompany common arterial circulatory abnormalities; such alterations on the venous side of the circulation may be important in the pathogenesis of neonatal hemorrhagic and/or ischemic injury.

Blood Pressure↗
PubMed1986

Intraventricular hemorrhage in extremely small premature infants.

The incidence, timing, severity, and outcome of intraventricular hemorrhage (IVH) were studied in extremely small premature infants with birth weights (BWs) between 500 and 700 g; 366 infants with BWs between 701 and 1500 g, admitted during the same period, served as a comparison group. Intraventricular hemorrhage occurred in 34 (62%) of 55 infants with BWs less than 700 g vs 91 (25%) of the 366 comparison infants. In the group with BWs less than 700 g, IVH occurred in the first 18 hours, from 19 to 72 hours, and after 72 hours of life in 62%, 20%, and 18% of the infants, respectively. In the comparison group, the occurrence for these periods was 13%, 82%, and 5%, respectively. The severity of IVH in infants with BWs less than 700 g was grade III (with or without intraparenchymal hemorrhage) in 97% of the lesions, but in the comparison group such severe IVH accounted for only 32% of the lesions. Intraventricular hemorrhage was a common contributor to death in the infants with BWs less than 700 g. Thus, in 24 infants who died before 72 hours of life, 21 infants (88%) had severe IVH. In addition, intracranial hemorrhage (four infants with IVH and two infants with intracerebellar hemorrhage) occurred late (days 8 to 25) and contributed to death in six of the infants with BWs less than 700 g. These data indicate that in comparison with larger premature infants, infants with BWs less than 700 g exhibit a higher incidence of IVH, which is more severe, occurs earlier, and is associated more often with a fatal outcome. In addition, late and lethal intracranial hemorrhage is also more likely to occur in these smaller infants.

Birth Weight↗
PubMed1986

Is chloride depletion an important contributing cause of death in infants with bronchopulmonary dysplasia?

A retrospective analysis of infants with bronchopulmonary dysplasia requiring prolonged hospitalization (greater than 100 days) was carried out to determine those factors associated with fatal outcome. Twenty-three infants made up the study population. Eleven infants died and 12 survived (survivors). No differences were noted between the groups regarding ventilator requirement, radiographic changes, and medication use (digoxin, aldactazide), except for furosemide which was used twice as frequently in the group of infants who died v the group of infants who survived (P less than .001). Differences noted between the groups included moderate hypochloremia (chloride less than 80 mEq/L) in all 11 infants who died v six of 12 survivors, severe hypochloremia (chloride less than 70 mEq/L) in the nine of 11 infants who died v two of 12 survivors, metabolic alkalosis (pH greater than 7.45) in nine of 11 infants who died v three of 12 survivors, hypertension (systolic BP greater than 113 mm Hg) in eight of 11 infants who died v one of 12 survivors, decrease in head growth in ten of the 11 infants who died v one of the 12 survivors; these differences were all significant (P less than .001). The metabolic alkalosis and head growth changes appear to be related to the hypochloremia. The data suggest that chloride deficiency may be an important contributing factor in the genesis of poor outcome in infants with bronchopulmonary dysplasia and that close attention to chloride supplementation might influence outcome.

Acid-Base Imbalance↗
PubMed1986

Periventricular intraparenchymal echodensities in the premature newborn: critical determinant of neurologic outcome.

Controversy exists concerning the degree of importance of periventricular intraparenchymal echodensities (IPE) observed on neonatal ultrasound scans in the determination of subsequent neurologic disability in premature infants. In this report, IPE was studied in 75 infants weighing less than 2,000 g at birth to determine the basic characteristics of the lesion, the likely pathogenesis, the outcome, and the aspects of the ultrasonographic appearance in the acute period of neonatal illness that are important for prediction of outcome. IPE was defined as any periventricular echodensity greater than 1 cm in at least one dimension. IPE was strikingly associated with large areas of intraventricular hemorrhage (IVH) (81% of cases). IPE was distinctly asymmetric. Thus, the lesion was either exclusively unilateral (67%) or bilateral with marked predominance on one side. The associated IVH was asymmetric in approximately 80% of cases, and in all 50 cases of large asymmetric IVH, IPE occurred on the same side as the larger amount of intraventricular blood. Moreover, more than 50% of such cases of IPE associated with large asymmetric IVH were progressive. Neuropathologic correlation showed that IPE represented hemorrhagic necrosis of periventricular tissue. Concerning pathogenesis, these data raise the possibility that large asymmetric IVH is related etiologically to IPE. Outcome varied with the severity of the IPE. Thus, the mortality rate among the 38 infants with extensive IPE was 79%. Of the survivors with extensive IPE, all had subsequent major motor deficits and all but one exhibited cognitive function less than 80% of normal. Among the 37 infants with localized IPE, the mortality rate was 38%. Of the survivors, although 79% had major motor deficits, 43% had cognitive function greater than 80% of normal. Thus, the findings demonstrate that with extensive IPE there is little or no chance for survival with normal neurologic and cognitive outcome, but with localized IPE, although major motor deficits are common, an appreciable proportion of infants have cognitive function in the normal range. Careful, quantitative assessment of the ultrasonographic features of IPE in the acute period of illness in the premature infant is of major value in estimating outcome.

Brain↗
PubMed1985

Reduction in intraventricular hemorrhage by elimination of fluctuating cerebral blood-flow velocity in preterm infants with respiratory distress syndrome.

In a previous study of preterm infants requiring mechanical ventilation for the respiratory distress syndrome, we demonstrated a striking association of fluctuating cerebral blood-flow velocity in the first day of life with the subsequent occurrence of intraventricular hemorrhage. Because this fluctuating pattern could be eliminated by muscle paralysis, we conducted a prospective study of preterm infants receiving mechanical ventilation for the respiratory distress syndrome in which we evaluated the effect of paralysis and this flow-velocity pattern on the incidence and severity of intraventricular hemorrhage. Twenty-four infants with the fluctuating pattern in the first hours of life were identified and randomly selected to serve as controls (10) or to be subjected to muscle paralysis (14). Intraventricular hemorrhage developed in all 10 control infants but in only 5 of the 14 infants subjected to muscle paralysis. Moreover, in 4 of the 5 paralyzed infants in whom hemorrhage developed, it did so after cessation of the paralysis. Seven of the 10 control infants had Grade III hemorrhage, the most severe variety of intraventricular hemorrhage, whereas none of the paralyzed infants had Grade III hemorrhage. We conclude that elimination of fluctuating cerebral blood-flow velocity in preterm infants with respiratory distress syndrome markedly reduces the incidence and severity of intraventricular hemorrhage.

Blood Flow Velocity↗
PubMed1985

Positron emission tomography in the asphyxiated term newborn: parasagittal impairment of cerebral blood flow.

Hypoxic-ischemic encephalopathy secondary to perinatal asphyxia in the term newborn is the most common recognized cause of the subsequent motor deficits often grouped under the rubric "cerebral palsy." In order to provide insight into the basic nature and pathogenesis of the brain injury in such infants, we studied regional cerebral blood flow (CBF) by positron emission tomography (PET) in 17 asphyxiated term infants during the acute period of illness. A consistent and apparently unifying abnormality was observed, namely, a relative decrease in CBF to parasagittal regions, generally symmetrical and more marked posteriorly than anteriorly. Thus, parasagittal values for CBF were generally 25 to 50% lower than those for the sylvian cortex; in the normal or near normal infant, parasagittal values are only approximately 10% lower than those for the sylvian cortex. (Additional normal findings for regional CBF were 50% higher flows to the cerebral cortex than to the cerebral white matter and flows to the basal ganglia and thalamus at least as high as those to the cerebral cortex). That the relative deficit in CBF to parasagittal regions reflects tissue injury was indicated by the close topographic correlation on technetium brain scans in 3 patients of increased tissue uptake of radionuclide and the CBF abnormality. Moreover, the single patient studied at postmortem examination exhibited parasagittal ischemic cerebral injury that correlated well with the PET abnormality of regional CBF. The topography of the PET abnormality, i.e., the cerebrovascular watershed regions, suggests that the brain injury is basically ischemic and that the pathogenesis relates to impaired cerebral perfusion, perhaps secondary to systemic hypotension occurring in association with the perinatal asphyxia. Experimental data support this formulation.

Asphyxia Neonatorum↗
PubMed1985

Positron emission tomography in the newborn: effect of seizure on regional cerebral blood flow in an asphyxiated infant.

Regional cerebral blood flow (CBF) was measured by positron emission tomography (PET) with 15O-labeled water in an asphyxiated infant during a seizure. After intrauterine asphyxia, the infant had a syndrome characteristic of hypoxic-ischemic encephalopathy. During a PET scan on the second postnatal day, the infant had a focal seizure with deviation of eyes to the right and clonic jerking of the right arm. Regional blood flow was highest, about 80 ml/100 g/min, in the left temporal-parietal frontal region of the left hemisphere, the site of origin of the seizure; blood flow in the same region on the other side was about 57 ml/100 g/min. These observations extend to the newborn previous demonstrations in older patients of a focal increase of CBF at the cerebral site of origin of a focal seizure.

Asphyxia Neonatorum↗
PubMed1985

Intestinal perforations by tube feedings in small infants: clinical and experimental studies.

The clinical and radiographic findings of eight low-birth-weight neonates (mean, 900 g) with perforations of the duodenum or jejunum associated with transpyloric feedings are reported. In four patients, the perforations occurred distal to any known tube position. In experimental studies in young rabbits, Silastic or polyvinyl chloride tubes were sewn in place with the tube tips in the proximal duodenum or proximal jejunum, and either normal oral feedings or feedings through the tubes were given. Perforations and gross or microscopic abnormalities of the bowel mucosa in the area of the tubes and beyond were more frequent in rabbits with tube feedings than those given normal oral feedings. It appears that tube feedings induce some degree of mucosal damage and contribute to bowel perforation.

Animals↗
PubMed1985

Neonatal cerebral blood flow velocity measurement.

This article discusses the background, methodology, previous clinical studies, and the clinical role and limitations of the noninvasive Doppler technique in the assessment of the cerebral circulation of the newborn infant.

Blood Pressure↗
PubMed1985

Urinary beta 2-microglobulin in full-term newborns: evidence for proximal tubular dysfunction in infants with meconium-stained amniotic fluid.

Urinary concentrations of beta 2-microglobulin (beta 2M) and creatinine were measured in normal term infants and in those born with meconium-stained amniotic fluid. None of the infants or their mothers had conditions known to modify beta 2M excretion. Measurements of beta 2M were made on urines collected by bagging; urines obtained from diapers were not satisfactory. Urinary beta 2M concentrations increased significantly (P less than .02) in the normal infants from the first day (0.36 +/- 0.29 mg/L: n = 29) to the third day (0.60 +/- 0.43 mg/L: n = 21) postpartum. Compared with the normal infants, values for the infants with meconium-stained amniotic fluid were increased significantly on days 1 (1.64 +/- 2.16 mg/L: n = 25: P less than .005) and 3 (2.12 +/- 2.04 mg/L: n = 23: P less than .005). Levels exceeded two standard deviations above the normal mean in 12 of the 26 infants with meconium-stained amniotic fluid on postpartum day 1, and 12 of the 23 infants with meconium-stained amniotic fluid on day 3. Urinary creatinine levels were similar in both the normal infants and those with meconium-stained amniotic fluid. All infants with meconium-stained amniotic fluid with a one-minute Apgar score of 6 or less had an elevated urinary beta 2M concentration. The elevated levels of urinary beta 2M in infants with meconium-stained amniotic fluid indicate the existence of tubular dysfunction, probably mild acute tubular necrosis secondary to hypoxia.

Amniotic Fluid↗