Evaluation and management of febrile infants younger than 60 days of age.
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Biomedical subjects
Publications and source records attributed to K R Powell.
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Previously healthy infants younger than 2 months of age without evidence of soft tissue or musculoskeletal infection who had white blood cell counts between 5000 and 15,000/mm3, band form counts less than or equal to 1500/mm3, urinalysis less than or equal to 10 white blood cells/high power field (spun sediment) and stool less than or equal to 5 white blood cells/high power field (if diarrhea) were considered at low risk for a serious bacterial infection. Infants meeting these criteria whose parents were judged to be adequate observers and had a telephone and automobile were eligible for outpatient management. Infants were given ceftriaxone to cover the possibility that the low risk criteria might miss more infants with serious bacterial infections than was predicted. From Jan. 1, 1987 to May 31, 1989, 86 infants younger than 2 months were enrolled. There were no serious complications in these infants. Twelve had transient problems possibly related to the intramuscular ceftriaxone therapy. One low risk infant was hospitalized for Neisseria meningitidis bacteremia and five other infants were hospitalized for medical or social reasons. All six hospitalized infants had short admissions and did well. This study supports the continued use of the low risk criteria to distinguish infants unlikely to have a serious bacterial infection. Furthermore, in a selected group of low risk infants, outpatient management may be an acceptable alternative to inpatient therapy.
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A prospective study was conducted to determine the frequency and distribution of bacterial and viral pathogens in infants hospitalized with suspected sepsis and to evaluate the potential of virus detection for improving patient management. A causative organism was detected in 157 (67%) of 233 previously healthy infants less than 3 months of age, who had been hospitalized for suspected sepsis: 19 (8%) had bacterial infections, 135 (58%) had viral infections, and 3 (1%) had mixed viral-bacterial infections. Viral infections occurred in a seasonal pattern: enteroviruses were responsible for most of the hospitalizations during summer and fall (65/110; 63%) and respiratory syncytial and influenza A viruses were responsible for most of the infections during winter (44/81; 55%). In contrast, bacterial infections were not seasonally distributed. Virus was detected in 33% of the 138 infected infants within 24 hours, and in 64% within 3 days. We conclude that viral infections are prevalent among infants hospitalized for suspected sepsis, and most can be detected early enough to influence patient management.
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The down-regulation of beta adrenergic receptors by chronic imipramine treatment was investigated with high resolution autoradiography of [125I]pindolol binding to brain sections. Neuroanatomically selective down-regulation of [125I]pindolol binding was found after chronic imipramine treatment. Subdivisions of the amygdala and hippocampus and discrete cortical regions were differentially affected. In the hippocampus, reduction of [125I]pindolol binding was observed in imipramine-treated rats in the CA-1 stratum radiatum and dentate molecular layer, but not in the CA-3 stratum radiatum. In the amygdala, the basolateral nucleus exhibited reduced [125I]pindolol binding after imipramine treatment but the central and medial nuclei were not affected. Chronic imipramine treatment was also associated with reduced [125I]pindolol binding in layer 1 of the cingulate cortex and layer 3 of the piriform cortex. In contrast, no effect on [125I]pindolol binding was apparent in the ventrolateral thalamic nucleus, caudate-putamen, lateral hypothalamus or layers 2 and 3 of the somatosensory cortex. In order to determine if regional variation in binding sites for imipramine, or its pharmacologically active metabolite desipramine, was responsible for the observed neuroanatomically selective reduction in [125I]pindolol binding, the binding of [3H]imipramine and [3H]desipramine was investigated. In some brain regions that exhibited high densities of [3H]imipramine and [3H]desipramine binding sites, [125I]pindolol binding was reduced after chronic treatment with imipramine. However, other regions that contained high densities of binding sites for antidepressant drugs did not show a reduction in [125I]pindolol binding after chronic imipramine treatment. Thus, regional binding of [3H]imipramine or [3H]desipramine cannot fully explain the neuroanatomical specificity of imipramine-induced beta adrenergic receptor down-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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Medical records of 144 children hospitalized for 146 episodes of periorbital cellulitis were reviewed. During 44 episodes, systemically administered antibiotics were given before hospitalization. Bacterial pathogens were isolated in only two (5%) of 44 episodes in pretreated patients compared with 33 (32%) of 102 episodes in patients who were not pretreated. Thirty-one children who were not pretreated were bacteremic. Compared with nonbacteremic children who were not pretreated, bacteremic children were younger, more often had a history of upper respiratory tract infection and fever, had a higher white blood cell count and temperature at admission, and more often had a violaceous cellulitis. No difference between groups existed in the frequency of a history of trauma or a local lesion near the affected eye. Tear specimens from 13 of 89 children tested by countercurrent immunoelectrophoresis (CIE) to detect Haemophilus influenzae type b capsular polysaccharide were positive. Compared with positive blood culture results, tear CIE has a sensitivity of 50% and a specificity of 93%. Streptococcus pneumoniae infections were not detected by CIE.
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In the present investigation, experiments were performed in order to determine whether antidepressants are capable of inducing regionally specific adaptation of beta adrenergic and 5-hydroxytryptamine2 (5-HT2) receptors after chronic administration or when combined with the forced swim test. The drugs tested were imipramine, amitriptyline, pargyline and nomifensine. The regional pattern of beta adrenergic or 5-HT2 receptor binding changes induced after chronic treatment with these antidepressants was not uniform. All of the drugs reduced [3H]dihydroalprenolol binding to cortical membranes after chronic treatment but only two, imipramine and pargyline, did so in hippocampus. All of the antidepressants reduced cortical, but not hippocampal, beta adrenergic receptor binding after 2 days of treatment, indicating that the rate of antidepressant-induced neural adaptation is regionally specific. All of the drugs, except nomifensine, induced down regulation of both cortical and hippocampal 5-HT2 receptors after chronic treatment, as measured by [3H]ketanserin binding. The forced swim test accelerated the reduction of [3H] dihydroalprenolol binding in hippocampus induced by imipramine and pargyline while producing no further effect on cortical beta adrenergic receptors. The down-regulation of hippocampal, but not cortical 5-HT2 receptors by imipramine and pargyline was also facilitated in rats processed in the forced swim test. These results provide further support for the view that the forced swim antidepressant drug screen may be of heuristic value as a model of the adaptive neural mechanisms that accompany chronic antidepressant drug treatment. Furthermore, these data provide evidence that multiple neural mechanisms may be involved in the adaptive changes after antidepressant drug treatment.
Because infants hospitalized with respiratory syncytial virus (RSV) infection frequently receive antibiotics, our study was undertaken to determine what the actual risk of secondary bacterial infections in patients with RSV infection is and what effect antibiotic treatment might have on the course of illness. In a 9-year prospective study of 1706 children hospitalized with acute respiratory illnesses, 565 children had documented RSV infections. A subsequent bacterial infection rarely developed in those with RSV lower respiratory tract disease. The rate of subsequent bacterial infection was 1.2% in the total group of children infected with RSV, and 0.6% in the 352 children who received no antibiotics. A significantly greater proportion (4.5%) of subsequent bacterial infections occurred in infants who received parenteral antibiotics (p = 0.01), and especially in a subgroup who received parenteral antibiotics for 5 or more days (11%, p less than 0.001). We conclude that the risk of secondary bacterial infection appears to be low for most infants with RSV infection. In a few infants given parenteral broad-spectrum antibiotics the risk may be greater, but whether this is related to the antibiotic therapy or to other risk factors is not clear.
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From November 1, 1980, to December 31, 1985, 3959 infants were admitted to the neonatal intensive care unit and 2385 infants (60%) received 2791 courses of aminoglycoside therapy. Aminoglycoside use totaled 16,279 patient days of which 16,070 (98.7%) were with amikacin. From November 1, 1980, to January 31, 1983, 1017 pairs of pre- and posttreatment endotracheal or pharyngeal specimens yielded 318 Gram-negative bacteria isolates. From November 1, 1980, to December 31, 1985, Gram-negative bacteria were isolated from 381 clinical specimens. Of the 318 surveillance and 380 clinical isolates tested, 285 (90%) and 358 (94%), respectively, were susceptible to amikacin. Amikacin resistance did not increase during the study. Amikacin-resistant organisms were isolated more frequently from patients receiving multiple courses than those receiving single courses of amikacin and resistant organisms were not usually found before the administration of amikacin. None of the 15 amikacin-resistant isolates made 6'-N-aminoglycoside acetyltransferase and 3 isolates took up only small amounts of radiolabeled amikacin, suggesting that resistance was due to decreased permeability. The extensive use of amikacin in a neonatal intensive care unit for over 5 years did not result in an increase of amikacin-resistant Gram-negative bacteria.
The hospital records of 118 2-month-old to 3-year-old children who had been treated for bacterial meningitis were reviewed. Within 2 weeks after hospitalization, one fourth of the patients sought medical attention for an acute illness, but only one was treated for the possible relapse or recurrence of meningitis. Because only five of the 113 patients with available follow-up information required a diagnostic lumbar puncture procedure, it is not recommended that a lumbar puncture be performed following treatment of bacterial meningitis to provide end-of-treatment baseline information.