Risks and burdens of third-generation cephalosporin resistant Enterobacteriaceae in neonatal sepsis.

Third-generation cephalosporin resistant Enterobacteriaceae (TCRE) is a global concern especially in neonatal sepsis. We performed a secondary data analysis in a Thai neonatal intensive care unit to identify the risk factors for acquisition of TCRE sepsis and mortality of Enterobacteriaceae sepsis between 1991 and 2017. Multivariate logistic and Cox proportional regression were used for analysis. Numbers of neonates with TCRE and nonTCRE sepsis were 100 and 41 patients, respectively. Medians (interquartile ranges) of gestational age, birthweight, onset of sepsis and total hospital stay of neonates with Enterobacteriaceae sepsis were 32 (28, 38) weeks, 1670 (1025, 2750) grams, 11 (6, 25) days and 41 (22, 74) days, respectively. Univariate and multivariate analysis, neonates with TCRE sepsis were more likely to have birth asphyxia (adjusted odds ratio [aOR] = 2.6; 95% confidence interval [CI] 1.1-6.0; p = 0.02) and history of aminoglycoside exposure (aOR = 2.9; 95% CI 1.3- 6.7; p = 0.01). In-hospital case fatality rate from Enterobacteriaceae sepsis was 26% (36/141). In Cox regression, neonates with TCRE sepsis was not an independent risk of non-survivors, but septic shock (adjusted hazard ratio = 9.9; 95% CI 5.0-19.7, p < 0.001) increased 30-day mortality in the final model. Asphyxia and previous aminoglycoside consumption were risks of acquisition for neonatal TCRE sepsis while the burden was not a significant difference. Infection prevention and control must be strictly implemented in high multidrug-resistant area.

Risks and burdens of third-generation cephalosporin resistant Enterobacteriaceae in neonatal sepsis

@#Third-generation cephalosporin resistant Enterobacteriaceae (TCRE) is a global concern especially in neonatal sepsis. We performed a secondary data analysis in a Thai neonatal intensive care unit to identify the risk factors for acquisition of TCRE sepsis and mortality of Enterobacteriaceae sepsis between 1991 and 2017. Multivariate logistic and Cox proportional regression were used for analysis. Numbers of neonates with TCRE and nonTCRE sepsis were 100 and 41 patients, respectively. Medians (interquartile ranges) of gestational age, birthweight, onset of sepsis and total hospital stay of neonates with Enterobacteriaceae sepsis were 32 (28, 38) weeks, 1670 (1025, 2750) grams, 11 (6, 25) days and 41 (22, 74) days, respectively. Univariate and multivariate analysis, neonates with TCRE sepsis were more likely to have birth asphyxia (adjusted odds ratio [aOR] = 2.6; 95% confidence interval [CI] 1.1-6.0; p = 0.02) and history of aminoglycoside exposure (aOR = 2.9; 95% CI 1.36.7; p = 0.01). In-hospital case fatality rate from Enterobacteriaceae sepsis was 26% (36/141). In Cox regression, neonates with TCRE sepsis was not an independent risk of non-survivors, but septic shock (adjusted hazard ratio = 9.9; 95% CI 5.0-19.7, p < 0.001) increased 30-day mortality in the final model. Asphyxia and previous aminoglycoside consumption were risks of acquisition for neonatal TCRE sepsis while the burden was not a significant difference. Infection prevention and control must be strictly implemented in high multidrug-resistant area.

Clinics in diagnostic imaging (112). Perinatal lethal hypophosphatasia (PLH).

A two-hour-old female infant presented with respiratory distress and short limbs. Neonatal radiographs showed micromelic dwarfism and generalised demineralisation, especially at the ribs, long bones of both forearms and both fibulae. The spine showed a flattened shape. All long bones showed metaphyseal irregularities and flaring. Normal serum calcium and elevated serum phosphorus were found, while serum alkaline phosphatase was markedly reduced. A diagnosis of perinatal lethal hypophosphatasia was made. The aetiology, clinical manifestations, radiographical findings, laboratory assays, prenatal diagnosis and treatment of hypophosphatasia are discussed.

Early neonatal mortality at Songklanagarind Hospital from 1987 to 1997.

During the 11 year period (1987-1997), there were 23,584 livebirths at Songklanagarind Hospital. The average incidence of low birth weight was 8.17 per cent, it has increased slightly during the last 6 year period (8.53 per cent) compared to the first 5 year period (7.59 per cent). There has been little decrease in the early neonatal mortality rate (ENMR) during the last 6 years (3.94 per 1000 livebirths) compared to the first 5 years (4.71 per 1000 livebirths). ENMR was markedly reduced when we compared ENMR of the first year (6.73 per 1000 livebirths in 1987) to the last year (1.52 per 1000 livebirths in 1997). During the last 6 year period, early neonatal mortality (ENM) of neonates less than 1000 g and 1000-1499 g has greatly reduced from 57.14 per cent to 16.67 per cent and from 50 per cent to 6.25 per cent respectively. The major cause of ENM was congenital anomalies in the first 5 year and the last 6 year period and all birth weight groups except the group less than 1000 g of which the leading cause of death was respiratory distress syndrome.

Neonatal hyperbilirubinemia associated with Southeast Asian ovalocytosis.

We report, herein, an infant who is twin A of a dizygotic twin, with premature birth and both twins having hemoglobin (Hb) E heterozygosity. Twin A who had Southeast Asian ovalocytosis (SAO) developed neonatal jaundice at the age of 2 days and needed phototherapy at the age of 3 days. The microbilirubin level was rapidly rising up to 535.2 micromol/L (31.3 mg/dl) with the hematocrit value of 38% at the age of 4 days prior to exchange blood transfusion. Exchange blood transfusion was done by 220 ml of O, Rh positive packed red blood cell reconstituted with 180 ml of O, Rh positive fresh plasma to lower the bilirubin level. Twin A received phototherapy from about 8 hr prior to exchange blood transfusion until 3 days later. Twin B, who did not have SAO, developed neonatal hyperbilirubinemia and needed only phototherapy. Twin A received a deletion of 27 basepairs in the erythroid band 3 gene and Hb E heterozygosity from his father.