Synthetic surfactants in infants with respiratory distress syndrome.
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Biomedical subjects
Publications and source records attributed to J M Perlman.
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OBJECTIVES: To determine the clinical and sonographic features of late-onset meningitis (after 7 days of life) in sick, very-low-birth-weight infants. DESIGN: Retrospective study of a patient series. SETTING: Neonatal intensive care nursery at Parkland Memorial Hospital in Dallas, Tex. PARTICIPANTS: Ten preterm infants with birth weights of more than 1750 g who developed late-onset meningitis during a 42-month study period. INTERVENTIONS: None. RESULTS: Ten preterm infants developed meningitis at a mean (+/- SD) postnatal age of 20 +/- 14 days. Eight of the infants survived. Initial clinical signs were nonspecific, eg, apnea and bradycardia (eight infants), abdominal distention (five infants), hyponatremia (serum sodium level, < 130 mmol/L), and a decrease in urine output with an increase in weight (three infants). Specific neurologic signs occurred in three infants (seizures [n = 2] and third-nerve palsy [n = 1]). Sonographic abnormalities noted in seven (70%) of the 10 infants included progressive ventriculomegaly (n = 6), thalamic echodensities (n = 3), ventriculitis (n = 4), and cystic leukomalacia (n = 1). The progressive ventriculomegaly developed from 1 to 2 weeks after diagnosis; permanent shunting was required in all six infants. The thalamic echodensities were linear or punctate and developed from 1 to 2 weeks after diagnosis in two infants. CONCLUSIONS: The data indicate the need for a high index of suspicion of meningitis in very-low-birth-weight infants suspected of having sepsis because of the nonspecific clinical presentation of meningitis. Because both progressive ventriculomegaly and thalamic echodensities are late and frequent findings, serial sonograms are essential for careful monitoring of sequelae of disease.
Fifteen premature infants with lethal congenital cytomegalovirus infection were studied to determine the clinical, neuroradiological, and neuropathological characteristics of the disease in this population. Nine infants were liveborn but died at a postnatal age of 18 +/- 21 days; 6 infants were stillborn. Clinical findings in liveborn infants included microcephaly (77%), seizures (55%), hypotonia (33%), and multiple contractures (18%). Ophthalmological findings included chorioretinitis, optic atrophy, and corneal opacities. Neuroradiological findings included the postnatal evolution of periventricular calcification in 1 infant, and cerebellar hypoplasia diagnosed by magnetic resonance imaging in 1 infant. Neuropathological findings included periventricular necrosis and calcification (12), associated diffuse calcification frequently involving the convexity of the gyri (6), cerebellar hypoplasia (5), periventricular leukomalacia (2), intraventricular hemorrhage (2), hydrocephalus (2), and porencephalic cyst (1). Intranuclear inclusion bodies within the brain were observed in 4 infants, whereas systemic inclusion bodies were present in all infants. These data indicate several atypical findings in preterm infants rarely reported in term infants, including hypotonia, multiple contractures, periventricular leukomalacia, and optic atrophy.
Catecholamine levels and associated cardiovascular responses were determined in 21 control and 30 term infants with meconium-stained amniotic fluid (MSAF). Cord arterial blood was obtained for determination for norepinephrine (NE) and epinephrine (EPI) levels; cardiovascular measurements included heart rate and systolic blood pressure at 30 min. Pregnancy was uncomplicated in all cases. The total length of labor 964 +/- 402 versus 555 +/- 312 min (P < 0.001) and active phase of labor 300 +/- 261 versus 135 +/- 104 min (P < 0.001) were significantly longer in MSAF infants when compared to controls. The 1 min Apgar score was < 7 (range 1-6) in 11 of 30 MSAF infants versus 0 of 21 control infants; these 11 infants required positive pressure ventilation for approximately 60 s secondary to transient respiratory depression (RD). The 5 min Apgar score was > 7 in 49 of the 51 infants. Infants with MSAF exhibited a higher PaCO2 (6.89 +/- 1.17 vs 6.24 +/- 1.17 mmHg; P < 0.02) and lower pH (7.25 +/- 0.06 vs 7.29 +/- 0.05; P < 0.02) compared to controls. Infants with transient RD demonstrated the most marked arterial blood gas differences, i.e., PCO2 7.41 +/- 1.30 mmHg (P < 0.001), pH 7.21 +/- 0.07 (P < 0.001) and base deficit -6 +/- 4 versus -3 +/- 2.8 (P < 0.001) when compared to controls. NE and EPI levels were significantly higher in MSAF versus control infants, i.e., 12600 +/- 3040 versus 3740 +/- 1000 pg/ml (SEM) (P < 0.02) and 1550 +/- 250 versus 620 +/- 130 pg/ml (P < 0.001) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral blood flow (CBF) was measured with positron emission tomography in 23 newborns following extracorporeal membrane oxygenation. In 9 newborns the common carotid artery was reanastomosed after extracorporeal membrane oxygenation and in 14 newborns the common carotid artery remained ligated. The ratio of right/left hemispheric CBF was not significantly different in the newborns with reanastomosed or occluded common carotid arteries (right/left CBF ratio was 0.98 in both groups). The maximum asymmetry was 8% and was observed in 2 newborns. All 9 newborns with reanastomosis of the carotid artery are normal at follow-up at 1 year or longer. Three newborns with ligation of the common carotid artery were lost to follow-up and 1 newborn died. Eight of 10 remaining newborns are normal at follow-up; the 2 other infants have developmental quotients of 60 and 64, respectively, and no other deficits. The data indicate (1) that hemispheric CBF is symmetric in newborns who have undergone extracorporeal membrane oxygenation and have no evidence of brain injury, and (2) that reanastomosis of the common carotid artery does not alter hemispheric CBF in the newborn period.
Two premature infants exhibited an acute cardiorespiratory collapse shortly after receiving a 50-fold overdose of amphotericin B (AmB). Despite aggressive intervention both infants died. Serum AmB levels were double the normal therapeutic range. We speculate that two less well-recognized toxic complications of AmB involving the cardiac and respiratory systems may have contributed to the fatal outcome.
This report describes the occurrence of rapid progression of hydrocephalus after discharge from the nursery in four of 48 infants who had had previous arrest of progression of post-hemorrhagic hydrocephalus, and at least partial resolution of ventriculomegaly. This later-onset hydrocephalus occurred at a mean age of seven months; the most consistent presenting clinical feature was rapid head growth. Three of the four infants required a ventriculo-peritoneal shunt and the fourth was treated with acetazolamide, with apparent resolution of the hydrocephalus. Newborn infants with post-hemorrhagic hydrocephalus should be followed carefully throughout the first year for prompt detection of later hydrocephalus.
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The systemic manifestations of "asphyxia" were evaluated prospectively in 35 consecutively intubated term newborn infants. The following systemic organ injuries were identified most often: (1) renal, ie, oliguria less than 1 mL/kg per hour for at lest 24 hours (40%), an elevated urinary beta-2-microglobulin concentration (57%), azotemia (11%), and an elevated serum creatinine level (17%); (2) central nervous system, ie, hypoxic-ischemic encephalopathy (including seizures) (31%) or an abnormal cranial ultrasound scan, ie, diffuse parenchymal echogenicity, slitlike ventricles, and poor visualization of the sulci, and/or intracranial hemorrhage (26%); (3) cardiovascular, ie, an abnormal echocardiogram (25%) or abnormal electrocardiogram (11%); (4) pulmonary complications, including persistent pulmonary hypertension (23%); and (5) gastrointestinal complications, which were rare. Traditional markers of fetal distress were not related to the frequency and/or distribution of systemic organ injury. An important implication of this study relates to the recognition of the extent and distribution of organ injury in the "asphyxiated" infant.
The occurrence of neurologic abnormalities is described in a series of nine infants with chronic hypertension, in whom antihypertensive therapy decreased BP markedly and for a prolonged period, although to levels often within the normal range. All infants had mean systolic BPs greater than 113 mm Hg and elevated renin values to a mean of 134 +/- 128 ng/mL/h. Antihypertensive therapy, such as captopril, an inhibitor of angiotensin I-converting enzyme, consistently lowered the systolic BP by 20% from baseline per dose. However, the nine infants exhibited a total of 17 episodes of striking decreases in systolic BP of greater than 40% from baseline; the markedly decreased systolic BP values were usually within the normal range for corrected age. Seven of the 17 episodes were characterized by marked decrease in systolic BP, ie, decreased by 57% +/- 10%, and were prolonged, ie, remained at the lower values for 17 +/- 6 hours despite therapeutic interventions. These seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/h) and neurologic abnormalities (ie, seizures). In the remaining ten episodes, the systolic BP decreased by 50% +/- 8%, but the decreases were relatively brief, ie, remained at the lower values for 2.8 +/- 2 hours. These briefer episodes were not accompanied by renal or neurologic signs. These data indicate a particular vulnerability of the cerebral and renal circulation in premature infants with chronic hypertension to decreases in systolic BP to levels that would otherwise be considered in the normal range. The findings suggest that adaptive responses in both cerebral and renal blood flow are altered by chronic hypertension in such infants.(ABSTRACT TRUNCATED AT 250 WORDS)
This article reviews renal, neurologic, cardiac, and pulmonary abnormalities in the term infant following perinatal asphyxia. The relationship of oliguria to central nervous system abnormalities is discussed, as well as the relationship of current measures of fetal hypoxia and long-term neurologic outcome.
A previously unrecognized, striking movement disorder has been observed in 10 premature infants with severe bronchopulmonary dysplasia. Chronic hypoxemia, hypercarbia, bronchospasm, and inadequate nutrition were present in all. The movement disorder developed from approximately the third postnatal month. The dominant movements involve the limbs, neck, trunk, and oral-buccal-lingual structures. The limb movements were most prominent distally and consisted of rapid, random, jerky movements (similar to chorea) and "restless" movements (similar to akathisia). Similar movements of the neck and face were observed; tongue movements had a "darting" quality. The oral-buccal-lingual movements were similar to the dyskinesia of older patients. Movements were exacerbated during episodes of respiratory failure and attenuated during sleep. All infants exhibited feeding disorders, largely due to tongue movements. In 3 infants treated with clonazepam, there was striking improvement in motor function, including feeding. The natural history was partial or complete resolution or a static course. Thus, of the 7 surviving infants, the movements were absent (without therapy) at 15, 18, and 30 months of age. In the remaining 4 infants (3 of whom receive clonazepam), the movements, though attenuated, persisted at 6, 12, 15 and 21 months of age, respectively. Neuropathologically, 1 infant showed neuronal loss with astrocytosis in caudate, putamen, globus pallidus, and thalamus. These data defined a previously unrecognized extrapyramidal movement disorder of infants with severe bronchopulmonary dysplasia; pathogenesis may be related to chronic hypoxemia.
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The clinical and radiographic features of five sick premature infants with idiopathic hypertrophic pyloric stenosis are presented. Clinical features were nonspecific, the common findings being recurrent nonbilious emesis, persistent abdominal distention, and the inability to place a nasojejunal feeding tube through the pylorus. Plain abdominal radiographs demonstrated persistent gastric dilatation in four of the infants. Idiopathic hypertrophic pyloric stenosis should be considered in the differential diagnosis of premature infants with upper gastrointestinal tract symptoms.
Six premature infants with congenital tracheal stenosis underwent diagnostic evaluation. Clinical features and chest roentgenograms were nonspecific; difficulty with intubation was the most common clinical finding and persistent lobar collapse the more common radiologic finding. The diagnosis was established by bronchoscopy in all infants. In the differential diagnosis of the sick premature infant, problems with airway patency must be considered because early intervention may reduce morbidity and mortality.
Measurements of regional cerebral blood flow (CBF) with positron emission tomography in adult humans with cerebrovascular disease have demonstrated consistently that values below 10 ml/(100 gm.min) occur only in infarcted brain. Although experimental data suggest that the newborn brain may be more resistant to ischemic injury than the adult brain, the minimum CBF necessary to sustain neuronal viability in newborn infants is unknown. We have measured CBF with positron emission tomography in 16 preterm and 14 term newborn infants and have determined the relationship between CBF and subsequent brain function as assessed by neurological examination and developmental assessment. The range of mean CBF in the preterm infants was 4.9 to 23 ml/(100 gm.min) and the range of mean CBF in the term infants was 9.0 to 73 ml/(100 gm.min). Five preterm infants and one term infant with mean CBF less than 10 ml/(100 gm.min) survived. Three of these 5 preterm infants, with mean CBF of 4.9, 5.2, and 9.3 ml/(100 gm.min), respectively, have normal neurological examinations and Bayley Scales of 80 or greater at 6, 6, and 24 months of age, respectively. One (mean CBF 6.9) has normal cognitive development (Bayley 103) and a mild spastic diplegia at age 19 months, and one infant (mean CBF 6.2) has a left hemiparesis and a Binet IQ score of 70 at age 33 months. The term infant, with a mean CBF of 9.0 ml/(100 gm.min), was developing normally when he died of sepsis at age 5 months.(ABSTRACT TRUNCATED AT 250 WORDS)
A young infant is presented with a mass partially obstructing the distal stomach. Sonography demonstrated the superficial origin of the lobulated lesion which proved to be focal foveolar hyperplasia, the most common cause of a gastric polypoid mass in adults but rare in children.