Staphylococcal scalded skin syndrome: a complication of circumcision.
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Biomedical subjects
Publications and source records attributed to E K Anday.
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The relative contribution of transfusions of adult blood to the development of retrolental fibroplasia (RLF) in very low-birth-weight infants was examined. Five years of experience with the expanded use of replacement and exchange transfusions in 90 infants with birth weight less than or equal to 1,250 gm was reviewed. Twenty percent of the infants developed cicatricial RLF. Exchange transfusion was not related to development of cicatricial RLF. The incidence of RLF in infants receiving greater or equal to 130 ml of packed red blood cells per kilogram of birth weight as replacement blood transfusion (RBT) was significantly higher (42.9%) than that in infants receiving 61 to 131 ml of packed red blood cells per kilogram (15.4%) and infants receiving less than or equal to 60 ml of packed red blood cells per kilogram (0%), P less than .001. The need for RBT, however, was strongly correlated (r = .85, P less than .001) with increasing duration of O2 therapy. When O2 therapy was controlled for, the association between RBT and RLF did not achieve statistical significance (P = .07). The association between RBT and RLF remained significant when adjusted for duration of therapy in fractional inspired oxygen (FIO2) greater than 0.4. Further detailed studies of large numbers of susceptible infants are warranted to assess the magnitude of the contribution of transfusions of adult blood to development of RLF.
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The growth and development of inborn very low birth weight infants was evaluated in 50 of 60 survivors from 132 babies weighing less than or equal to 1,250 gm born July 1974 to December 1977. Mean +/- SE birth weight and gestation was 1,066 +/- 19.3 gm and 29.5 +/- 0.3 weeks, respectively, with 13 infants small-for-gestational age. Of the survivors, 26% weighed less than or equal to 1,000 gm. Male to female ratio was 1:1.4. Apgar scores less than or equal to 5 at five minutes occurred in 16% of the infants. Respiratory distress syndrome occurred in 56%, but only 10% (5/50) required mechanical ventilation. At 1 year, 46% small for gestational age (SGA) and 8% appropriate for gestational age (AGA) infants were less than the third percentile for weight. Major neurologic abnormality occurred in three infants (6%), one of whom is also blind. Grade V retrolental fibroplasia occurred in two others. Severe developmental delay (development quotient < 80, Gesell) occurred in these five infants and two other neurologically normal babies. Of 15 infants weighing less than or equal to 1,000 gm, two had major handicaps. Eight percent of the AGA infants and 30% of the SGA infants had major handicaps. These data indicate that infants born and treated in a perinatal center have a decreased incidence of asphyxia and severe respiratory distress syndrome and that the incidence of major handicaps is reduced, especially in the appropriate for gestational age baby.
To examine why newborn infants frequently cannot maintain adequate levels of plasma glucose in the interval between delivery and the time they are first fed, circulating metabolic fuel and regulatory hormone concentrations were determined in 44 healthy infants at the end of an eight-hour postnatal fast. Plasma glucose fell below 40 mg/100 ml prior to eight hours in four of 24 term-appropriate-for-gestational-age (AGA), two of nine preterm-AGA, five of six term-small-for-gestational-age (SGA), and three of five preterm-SGA infants. Fuel and hormone patterns in the premature and SGA infants were not different from those found in term-AGA infants. Results in these neonates differed in two areas from the response to fasting seen later in life. In fasted term-AGA infants, ketones were low (beta-hydroxybutyrate 0.29 +/- 0.04 mM/liter) despite elevated concentrations of fatty acid precursors (1.4 +/- 0.07 mM/liter), and the group of infants studied failed to demonstrate the increase in plasma ketones with lower glucose levels (r = ".23, P = .07) which is found in older children. Levels of glucose precursors were two to three times higher in term-AGA infants (lactate 2.9 +/- 0.2 mM/liter; alanine 0.48 +/- 0.02 mM/liter) than levels found beyond the neonatal period and, in contrast to older children and adults, were not diminished in infants with lower plasma glucose (lactate, r = -.28, P less than .035; alanine, r = -33, P less than .02). These differences between the responses to postnatal fasting and those seen beyond the neonatal period suggest that the capacity for both hepatic ketone synthesis and gluconeogenesis is not fully developed at birth.
Sequential lung function was measured in 12 very low-birth weight infants (less than or equal to 1,250 g) within 14 hours of birth, and at daily intervals thereafter for the first week of life, using an esophageal balloon and pneumotachograph system. All infants were clinically free of respiratory distress syndrome and radiographically showed no evidence of atelectasis or pulmonary edema. The alveolar-arterial oxygen tension gradient was high at birth and remained elevated over the period during which arterial blood gases were monitored. Increases of lung compliance and tidal volume between the first day and the end of the first week of life were not significant. Day-to-day determinations of lung compliance revealed an individual and group variability without a definite pattern. Lung resistance measurements indicated no clear trend for the group as a whole, but inspiratory resistance was generally lower than expiratory resistance. Possible causes, in addition to technical factors, that may account for the variability in the pulmonary mechanics of these small infants include an instability of lung volume and uneven distribution of pleural pressure due to chest wall distortion, differences in sleep-state, and alteration in the distribution of body fluids, resulting in a change in lung water. Any or all of these mechanisms may result in an unstable lung, even in an apparently clinically stable very low-birth weight infant.
Pregnancy is associated with altered liver function, particularly in serum enzymes. Anabolic steroids are responsible to some degree in mediating the physiologic and biochemical changes that occur during an uncomplicated pregnancy. However, several liver disorders are unique to pregnancy and include intrahepatic cholestasis of pregnancy, acute fatty liver of pregnancy, and hepatic dysfunction associated with pre-eclampsia and eclampsia. It is imperative for the clinician to diagnose these liver disorders in a timely manner and to institute appropriate management as maternal and fetal outcome are affected in an adverse manner if these conditions are left untreated.
Based on a three year surveillance in the neonatal intensive and transitional care nurseries (NICU) at the Hospital of the University of Pennsylvania (HUP), an analysis of all cases of nosocomial bacteremia was made. From January 1982 to September 1984, a total of 57 nosocomial bacteremic episodes were identified. This gave a rate of 3.6 episodes per 100 NICU admissions or 6.5 per 1000 live hospital births. While coagulase-negative staphylococci (CNS) accounted for approximately 40 percent of all positive blood cultures, it was responsible for 73 and 66 percent of the nosocomial bacteremias in 1982 and 1983, respectively. In 1984, coagulase-negative staphylococcus was the responsible pathogen for 92 percent of all nosocomial bacteremic episodes. Of 139 infants weighing less than or equal to 1250 g at birth, 30 (22 percent) developed CNS bacteremia. The risk of coagulase-negative staphylococcus bacteremia was associated with low birth weight, respiratory distress, prolonged hyperalimentation, and multiple supportive measures. Infants were treated with vancomycin hydrochloride, as most of the CNS were resistant to methicillin and/or gentamicin. There were no deaths related to coagulase-negative staphylococcal septicemia.