Mean platelet volume during coagulase-negative staphylococcal sepsis in neonates.

Coagulase-negative staphylococci are the most common cause of late-onset septicemia in neonates in intensive care nurseries. Clinical and laboratory diagnosis of infection with coagulase-negative staphylococci can be difficult. The authors reviewed serial mean platelet volumes of 18 infants in whom coagulase-negative staphylococci sepsis developed and found a significant increase in the mean platelet volume at the time of diagnosis and a return to baseline after resolution of the infection. The increase in mean platelet volume occurred although thrombocytopenia developed in only two of the infants and no difference was found in the mean platelet counts before and at the time of diagnosis of the infection. This finding may be a useful adjunct to the current laboratory tests used to diagnose coagulase-negative staphylococci sepsis in neonates.

Cocaine detection in neonatal gastric aspirate samples.

We prospectively analyzed the feasibility and sensitivity of gastric fluid detection of cocaine compared with standard meconium analysis. Cocaine was detected in nearly half (45.5%) of gastric aspirate samples tested from infants in whom meconium was positive for cocaine. The time to sample acquisition was substantially shorter for gastric aspirate sampling versus meconium analysis. The possible ramifications of the presence of cocaine in amniotic fluid are discussed.

Cytologic detection of urothelial cancer and other abnormalities in a cohort of workers exposed to aromatic amines.

A total of 541 members of a cohort at increased risk for occupational bladder cancer underwent a 33-month program of screening with urine cytology. Selected workers received further urologic study with cystoscopy and bladder biopsies. Eight workers had positive or suspicious cytologic findings. Only one of the eight had a prior history of bladder cancer. Biopsies showed invasive carcinoma and/or nonpapillary carcinoma in situ in five workers in this group, severe atypia in one, and no significant abnormality in two. Of 56 workers who had atypical cytologic findings, 16 had bladder biopsies, which showed atypia of flat urothelium in 11, nonpapillary carcinoma in situ in one, noninfiltrating papillary carcinoma in one, and no significant abnormality in three. The cytologic detection of urothelial abnormalities often required more than a single specimen. Since the cohort in this study may develop more bladder cancers with the passage of time, continued follow-up is indicated.

Salt supplementation, growth, and nephrocalcinosis in the furosemide-treated weanling rat.

OBJECTIVE: Furosemide treatment in the human neonate is associated with sodium depletion, growth retardation, hypercalciuria and nephrocalcinosis. Dietary sodium intake is known to directly influence urinary calcium excretion. The objectives of this study were to create a rat model of furosemide-induced nephrocalcinosis and to test the effects of dietary sodium supplementation on growth, electrolyte balance, calciuria, and renal calcifications. METHODS: Initially, 18 weanling Sprague-Dawley rats were randomly divided into three groups. Groups A (control) and B were fed a basal diet. Group C was fed a sodium-enriched diet. Groups B and C received furosemide (40 mg/kg) intraperitoneally daily for 28 days. At the end of the study, serum, urine, and kidney samples were obtained for biochemical and histologic analyses. The three groups were then compared for differences in growth, electrolyte homeostasis, calcium excretion and nephrocalcinosis. Subsequently an additional 15 rats were studied to confirm our findings regarding urinary calcium excretion and kidney calcifications. RESULTS: Treatment with furosemide without sodium supplementation (group B) resulted in decreased weight gain compared with group A (137.5 +/- 12.9 vs 154.0 +/- 10.6 g; p < 0.05), hypokalemia (3.7 +/- 0.1 vs. 4.4 +/- 0.4 mEq/l; p < 0.05), and nephrocalcinosis (187.1 +/- 155 vs. 18.8 +/- 6.9 micrograms Ca/g dry kidney; p < 0.05). Sodium supplementation (group C) normalized weight gain and corrected electrolyte abnormalities without increasing calciuria or nephrocalcinosis. CONCLUSIONS: We conclude that in this animal model, chronic furosemide treatment results in growth failure and development of nephrocalcinosis. Sodium supplementation protects against the deleterious effects of furosemide on weight gain and electrolyte homeostasis with no adverse effect on nephrocalcinosis.