Microbes causing severe neonatal septicemia in a tertiary neonatal intensive care unit

Neonatal sepsis is the most challenging neonatal disease in developing countries despite the progress in the neonatal management. The aim of the study is to demonstrate the most common organisms causing severe neonatal sepsis in a tertiary neonatal intensive care unit. The study conducted in the neonatal intensive care unit (ICU) unit of pediatric department in Suez Canal University Hospital in the period from December 2013 to November 2014.Blood cultures showed the growth of Escherichia coli (40 %), Staphylococcus aureus (27 %), Klebsiella (20 %), and Pseudomonas (13 %). Escherichia coli is the most common quarantine in a tertiary neonatal intensive care unit. [Med-Science 2016; 5(4.000): 999-1001

Cortisol and other adrenal steroids in critical neonatal disease associated with shock

Abstract Circulatory collapse associated with refractory hypotension is a frequent complication seen in neonatal intensive care units that treat ill neonates especially in middle-income countries. The timely and effective management of neonatal hypotension is crucial. Volume substitution by both crystalloid or blood products and administration of inotropes are the therapies of choice. However, according to the current knowledge, many newborn infants continue to suffer from circulatory collapse despite both volume expansion and maximum doses of inotrope therapy. I aimed to elucidate whether a life-threatening circulatory shock in neonates is a potential consequence of inadequate cortisol production in the adrenal glands and whether it could contribute to serious disease. Prospective, case-control studies were performed to compare seriously ill neonates with circulatory collapse to those with normal circulation. The further aim was to analyze the blood levels of cortisol and other steroids that serve as cortisol precursors as well as the level of dehydroepiandrosterone (DHEA) in neonates who either responded or did not respond to conventional treatments that included volume expansion and inotrope therapy. All of the recruited neonates were born at term or late preterm. Their clinical histories were taken, and they underwent complete clinical examinations. The prospective laboratory investigation included determination of baseline serum cortisol concentrations. Cortisol and the other steroids were analyzed using liquid chromatography–tandem mass spectrometry. I found that serum concentrations of cortisol were not statistically different between neonates who had refractory hypotension and those who responded to the conventional treatment. This result was unexpected because the critically ill neonates were presumed to have higher cortisol concentrations during extreme stress. However, the increase in steroids proximal to the 3β-hydroxysteroid dehydrogenase activity was higher in neonates with apparent cortisol insufficiency, suggesting that this enzyme may be rate limiting. I found that the serum cortisol concentrations did not increase in the critically ill neonates with circulatory collapse. However, these neonates responded favorably to hydrocortisone treatment and their clinical signs and symptoms related to adrenal insufficiency improved. Thus, circulatory collapse in term or late preterm neonates with life-threatening illnesses and refractory hypotension may possibly be a consequence of the insufficient synthesis of cortisol during excessive stress.Tiivistelmä Matalaan verenpaineeseen eli hypotensioon voi erityisesti vastasyntyneellä liittyä verenkierron kollapsi eli shokki. Tämä ongelma on yleinen erityisesti keskituloisissa maissa. Vastasyntyneen uhkaavan shokin nopea ja tehokas hoito on ratkaisevan tärkeää. Sekä kristalloidien että erityisesti verituotteiden antaminen matalan verivolyymin hoidoksi sekä inotrooppien käyttö kuuluvat käypään hoitoon. Monet vastasyntyneet voivat kuitenkin saada shokkioireita huolimatta asianmukaisista nestetäytöistä ja inotrooppihoidosta. Tämän tutkimuksen tavoitteena oli selvittää, voiko vastasyntyneen henkeä-uhkaavaan shokkiin liittyä riittämätön lisämunuaisten kortisolituotanto ja voivatko vakavat oireet suorastaan johtua riittämättömästä endogeenisestä kortisolituotannosta. Tässä tutkimuksessa suoritettiin prospektiivisia, tapaus-kontrollitutkimuksia vakavasti sairailla vastasyntyneillä (sepsis tai hypoksis-iskeeminen enkefalopatia), joilla todettiin joko hoitoresistentti tai tavanomaiselle hoidolle vastaava hypotensio. Tavanomaiseen hoitoon kuului hypovolemian hoito ja inotrooppien käyttö. Edelleen tavoitteena oli analysoida näiden potilaiden verestä kortisolin ja kortisolin esituotteiden pitoisuuksia. Kaikki rekrytoidut vastasyntyneet olivat täysiaikaisia tai lähes täysiaikaisia. Vastasyntyneet tutkittiin ja kliininen historia selvitettiin. Seerumin kortisoli tutkittiin prospektiivisesti. Kortisoli, useita kortisolin esiasteita sekä dehydroepiandrosteroni (DHEA) analysoitiin tandem-massaspektrometrillä. Tutkimuksessa havaittiin, että vastasyntyneillä, joilla oli matala verenpaine, seerumin kortisolipitoisuudet eivät eronneet tilastollisesti konservatiivisesti hoidettujen vastasyntyneiden ja hoitoresistenttiin shokkiin joutuneiden vastasyntyneiden välillä. Tämä tulos oli odottamaton, koska kriittisesti sairailla vastasyntyneillä oletettiin olevan korkeampia kortisolin pitoisuuksia. Edelleen näillä hoitoresistenteillä vastasyntyneillä, joilla oli mahdollisesti lisämunuaisen riittämätön stressivaste, kortisolin esiastepitoisuudet olivat korkeampia tasoltaan kuin hoitoon vastaavilla potilailla. Nämä pitoisuudeltaan lisääntyneet steroidiyhdisteet sijaitsivat proksimaalisesti reaktiotiestä, jota katalysoi 3β-hydroksisteroididehydrogenaasientsyymi. Tämä viittaa siihen, että näillä hoitoresistenttiin shokkiin altistuneilla lapsilla tämä reaktiotien kohta saattoi rajoittaa kortisolin muodostumista. Näillä vastasyntyneillä oli lisäksi suotuisa kliininen vaste hydrokortisonihoitoon. Tämä viittaa siihen, että lisämunuaisen stressivasteen vajaatoiminnalla, joka esiintyi hoitoresistenteillä potilailla, oli vaikutusta vakaviin kliinisiin oireisiin. Niinpä nestetäyttöihin ja inotrooppihoitoon reagoimaton shokki jopa täysaikaisilla tai lähes täysaikaisilla vastasyntyneillä, joilla on primaarisairauteen liittyvä hypotensio, saattaa olla seurausta kortisolin riittämättömästä synteesistä ja erittymisestä vereen

Hyperdehydroepiandrosterone in neonates with hypoxic ischemic encephalopathy and circulatory collapse

Abstract Background: Circulatory collapse is a very common complication of the critical illnesses in neonates including neonates with hypoxic ischemic encephalopathy; it can be the end result and cause of death of several conditions. Often, despite treatment with fluid resuscitation and vasopressor agents, circulatory collapse persist, and blood pressure can remain critically low, compromising adequate blood flow to vital organs and brain. Low blood pressure has been associated with increased mortality. Method: To investigate adrenal function in newborn infants who suffer from circulatory collapse during hypoxic ischemic encephalopathy. A total of 30 infants were analyzed in the study: 15 neonates in group A (neonates had hypoxic ischemic encephalopathy with vasopressor resistant hypotension) and 15 neonates in group B (neonates with hypoxic ischemic encephalopathy without vasopressor resistant hypotension). All the studied patients were subjected to history, examinations and laboratory investigation including serum cortisol concentrations and cortisol precursor’s levels. Results: The cortisol concentrations did not differ significantly between the two groups: (12.9 ± 4.3) μg/dL and (12.1 ± 2.4) μg/dL in group A and group B, respectively. There are highly significant differences between groups A and B regarding Dehydroepiandrosterone (342.1 ± 101.3) μg/dL, (33.4 ± 16.5) μg/dL, respectively. Conclusion: In this study, we noticed that cortisol concentrations did not differ between both groups in contrast to the expectation that neonates with critical illnesses should have higher cortisol concentrations than normal neonates. However, the marked increase in dehydroepiandrosterone DHEA may cause decrease cortisol function, so those neonates having accumulation of dehydroepiandrosterone may suffer from manifestation of adrenal insufficiency and vasopressor resistant hypotension in spite of normal cortisol level

Fecal Calprotectin Level in Neonates with Necrotizing Enterocolitis

Background: Necrotizing enterocolitis (NEC) is a disease with high mortality. It is more present in premature infants and can also happen in term and late preterm neonates. It may affect any segment of the small intestine or colon. However, most commonly influences the terminal ileum and proximal ascending colon. This disease might damage the entire bowel, which can be irreversible. Intestinal mucosal defects cause the migration of large numbers of inflammatory cells into the gut lumen. Extensive mucosal affection results in increased calprotectin levels. This study aimed to investigate the role of fecal calprotectin as a non-invasive marker in the diagnosis of NEC for the better management of infants with NEC. Methods: This case-control cross-sectional study was performed in two groups. Group 1 was the case group consisting of the neonates admitted at Suez Canal University Hospital, Neonatal Intensive Care Unit with a clinical diagnosis of NEC. All cases were evaluated by Bell's staging criteria. Group 2 included control subjects. All the studied subjects had complete medical history, full physical examination, and laboratory investigations, including complete blood count, stool analysis, and C-reactive protein. Radiological examination entailed chest X-ray and erect abdomen X-ray, abdominal ultrasonography, and the measurement of stool calprotectin. Results: Fecal calprotectin level showed a positive strong correlation with NEC stages and this was statistically significant. Regarding the sequels of NEC, our study showed a positive correlation between NEC stage and fecal calprotectin level with r of 0.911 and P-value of < 0.001. The mean level of calprotectin in stage Ιa was 226.9 µg/g with the maximum in patients affected with stage ΙΙb (875 µg/g). Conclusion: According to the findings of this study, fecal calprotectin can be used as a marker in the diagnosis of NEC and has a strong positive correlation with the severity of NEC

Antenatal Corticosteroids and Respiratory Distresses Outcome in Preterm Neonates

Background: The value of antenatal corticosteroid regimen in lessening respiratory distress risk in preterm neonates has been well known, and accordingly, antenatal corticosteroid therapy was recommended for any pregnant woman likely to deliver between 24 and 34 weeks of gestation. Therefore, this study aimed to assess the association between the administration of antenatal corticosteroids within the ideal interval of one week before birth and the outcomes of preterm neonates. Methods: This prospective cohort study included 80 preterm neonates admitted to the neonatal intensive care unit with gestational age from 32 to 37 complete weeks at Suez Canal University Hospitals, Ismailia, Egypt. The newborns were then divided into groups A (did not receive antenatal corticosteroids; n=40) and B (received antenatal corticosteroids; n=40). Results: Severe respiratory distress syndrome was significantly less frequent in group B  (P<0.05) with lower levels of need for oxygen supplementation (P<0.05). Conclusion: Neonates who received antenatal corticosteroids developed less severe respiratory distress, compared to neonates who did not receive this medication. The results favored the use of antenatal corticosteroids to prevent respiratory distress when administrated within the ideal interval of one week before birth

Fecal calprotectin levels in preterm infants with and without feeding intolerance

Abstract Objectives: To assess the level of fecal calprotectin in preterm neonates with feeding intolerance, as well as to evaluate it as a marker of feeding intolerance and to determine a cut-off level of fecal calprotectin in feeding intolerance. Methods: Analytical, multicenter, case-control study, which was carried out in neonatal intensive care units in Egypt, in a period from August 1, 2014 to March 1, 2015 on 52 preterm neonates. Neonates were classified into two groups; a study group including 26 neonates who met inclusion criteria and a control group including 26 neonates for comparison. Results: Fecal calprotectin levels ranged from 3.9 µg/g to 971.8 µg/g, and there was a significant increase in fecal calprotectin in the study group when compared to the control group (334.3 ± 236.6 µg/g vs. 42.0 ± 38.2 µg/g, respectively) with moderate inverse significant correlation between fecal calprotectin and birth weight. Furthermore, there was moderate, significant correlation between fecal calprotectin and duration of breastfeeding range. On the other hand, there was no correlation between fecal calprotectin and post-natal age, gestational age, or volume of feeding. A cut-off at the 67.0 µg/g level, with 100.0% sensitivity and 76.9% specificity, was considered. Conclusion: Fecal calprotectin level increased significantly in neonates with feeding intolerance; it can be used to detect early cases with necrotizing enterocolitis in neonates, but this subject still needs more investigations on more patients

Causes of Neonatal Acute Renal Injury during Critical Illnesses

The aim of the study was to assess acute kidney injury (AKI) and its contributing risk factors among neonates to reduce morbidity and mortality. The study included 310 neonates who were admitted to the neonatal intensive care unit (NICU). Serum creatinine (SCr) was elevated at admission, after 48 h, and before discharge or death. AKI was defined by either an acute rise in SCr of at least 0.3 mg/dL within 48 h or an increasing or persistently high level of SCr >1.5 mg/dL after 48–72 h of life. The patients who developed AKI were studied regarding the most common risk factors and outcomes. The prevalence of AKI in these neonates was 11.9%. Nephrotoxic drugs were the highest risk factor among patients with AKI, but this was not statistically significant different from patients without AKI. Perinatal asphyxia (59.5%), respiratory distress syndrome (48.6%), shock (43.2%), prematurity (40.5%), and sepsis (37.8%) were the main risk factors of AKI following the nephrotoxic drugs (64.9%). The mortality rate for cases with AKI was 62.1%, with a statistically significant difference from non-AKI neonates. The death rate was higher among neonates born before 36 weeks' gestation. There was no statistical difference between oliguric and non-oliguric neonates with AKI regarding the outcome. The overall incidence of AKI in sick neonates admitted to the NICU was 11.9%. Nephrotoxic drugs, perinatal asphyxia, shock, and prematurity were the main risk factors for developing AKI

Fecal calprotectin levels in preterm infants with and without feeding intolerance

Abstract Objectives: To assess the level of fecal calprotectin in preterm neonates with feeding intolerance, as well as to evaluate it as a marker of feeding intolerance and to determine a cut-off level of fecal calprotectin in feeding intolerance. Methods: Analytical, multicenter, case-control study, which was carried out in neonatal intensive care units in Egypt, in a period from August 1, 2014 to March 1, 2015 on 52 preterm neonates. Neonates were classified into two groups; a study group including 26 neonates who met inclusion criteria and a control group including 26 neonates for comparison. Results: Fecal calprotectin levels ranged from 3.9 µg/g to 971.8 µg/g, and there was a significant increase in fecal calprotectin in the study group when compared to the control group (334.3 ± 236.6 µg/g vs. 42.0 ± 38.2 µg/g, respectively) with moderate inverse significant correlation between fecal calprotectin and birth weight. Furthermore, there was moderate, significant correlation between fecal calprotectin and duration of breastfeeding range. On the other hand, there was no correlation between fecal calprotectin and post-natal age, gestational age, or volume of feeding. A cut-off at the 67.0 µg/g level, with 100.0% sensitivity and 76.9% specificity, was considered. Conclusion: Fecal calprotectin level increased significantly in neonates with feeding intolerance; it can be used to detect early cases with necrotizing enterocolitis in neonates, but this subject still needs more investigations on more patients

Cortisol intermediates and hydrocortisone responsiveness in critical neonatal disease

<p><i>Objective</i>: Therapy-resistant hypotension complicates diseases in neonates. Our objective was to investigate whether lack of therapeutic response to plasma expanders and inotropes associates with serum levels of cortisol and its precursors.</p> <p><i>Methods</i>: We investigated 96 infants with hypotension and critical neonatal disease for cortisol metabolism and are divided into responders and non-responders to plasma expanders and inotropes. Serum concentrations of steroids were analysed soon after the onset of volume expansion and inotrope treatment for shock. The 48 non-responders were treated with intravenous hydrocortisone (HC) and serum cortisol concentrations were monitored a week later.</p> <p><i>Results</i>: The mean cortisol concentrations did not differ between the responders and non-responders: 13.6 ± 2.5 and 12.5 ± 4.5 μg/dL, respectively. Dehydroepiandrosterone (37.3 ± 19.5 versus 324.0 ± 106.3; <i>p </i>< 0.0001) and 17-hydroxy-pregnenolone concentrations were lower in responders than in non-responders. Dehydroepiandrosterone levels in non-responders were inversely associated with postnatal age (<i>r</i> = 0.50, <i>p </i>< 0.0001). There were no differences in 17-hydroxy-progesterone, 11-deoxy-cortisol and cortisone between the responders and non-responders. Hydrocortisone administration acutely increased blood pressure. Six non-responders who died despite HC administration had low levels of cortisol. The responders had normal serum cortisol after HC treatment.</p> <p><i>Conclusion</i>: Precursors of cortisol, proximal to the 3β-hydroxysteroid dehydrogenase activity, accumulated in neonates with hypotension, responding to HC treatment.</p

Serum cystatin C as an earlier predictor of acute kidney injury than serum creatinine in preterm neonates with respiratory distress syndrome

In this study, we aimed to evaluate serum cystatin C (sCysC) as an early predictor of acute kidney injury (AKI) in preterm neonates with respiratory distress syndrome (RDS). Sixty preterm neonates diagnosed with RDS and 40 healthy controls (28–36 weeks) admitted to the neonatal Intensive Care Unit were investigated. AKI was defined on the 3rd day of life (DOL-3) as an increase in serum creatinine (sCr) of >0.3 mg/dL from baseline (the lowest previous sCr). sCysC levels were measured on DOL-1, -3 and -7. Of the 60 neonates with RDS, 24 (40%) developed AKI. Five patients (79.17%) were classified as AKI Network (AKIN-1) and 19 patients (20.83%), as AKIN-2. At DOL-3, the mean sCysC values were significantly higher among neonates with RDS and AKI (1.68 ± 0.37) compared with controls (0.79 ± 0.83) and those with RDS and no AKI (0.85 ± 0.20) (P <0.001). sCysC levels significantly increased among neonates with AKI from DOL-3 to DOL-7 (P = 0.002). The sCr values showed no significant difference between those with RDS with AKI, RDS, and no AKI or control groups at DOL-1 and -3. Only as late as DOL-7, the mean values of sCr were higher among neonates with AKI compared with no AKI and controls (P <0.001). The receiver operating characteristic curves area under the curve was 0.97 for predicting the development of AKI within 72 h (P = 0.001). With the best cutoff value of ≥1.28 mg/L, the sensitivity and specificity of sCysC for detecting AKI within 72 h were 100 and 83.3%, respectively. In conclusion, sCysC is an early marker for AKI in neonates with RDS