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עמוד בית
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November 2011
D.E. Carney, K. Matsushima and H.L. Frankel

Since the Surviving Sepsis Campaign Guideline (SSG) was published in 2004, critical care physicians can readily access the evidence and current recommendations regarding management of patients with severe sepsis and septic shock. However, several issues including a potential conflict of interest in developing the guidelines were disclosed. There have also been dramatic changes in the management of sepsis, supported by high levels of evidence. SSG[1] 2008 was developed to update the evidence using a new grading system. We reviewed select topics, routinely addressed by intensivists in the surgical intensive care unit, that have changed between SSG 2004 and SSG 2008: namely, glucose control, and administration of steroids, recombinant human activated protein C (rhAPC) and total parenteral nutrition.






[1] SSG = Surviving Sepsis Campaign Guideline


June 2011
August 2009
G. Faris, M. Nashashibi, B. Friedman, A. Stein, Y. Sova and Y. Mecz
March 2009
A. Maayan-Metzger, A. Barzilai, N. Keller and J. Kuint

Background: Early-onset neonatal sepsis is a major cause of morbidity and mortality among newborn infants.

Objectives: To determine the incidence, type of pathogens and resistance to antibiotics among newborns with early-onset neonatal sepsis, and to identify the risk factors predisposing infants to resistant pathogens in order to reevaluate antibiotic regimens appropriate for resistant bacteria in these high risk neonates.

Methods: We retrospectively studied maternal and neonatal variables of 73 term and near-term infants and 30 preterm infants, born over a period of 10.5 years and exhibiting early-onset neonatal sepsis (positive blood cultures in the first 72 hours of life).

Results: Predominant pathogens in term and near-term infants were gram-positive compared with gram-negative organisms (mostly Escherichia coli) in preterm infants. Mothers of infants with antibiotic-resistant organisms were more likely to have prolonged rupture of membranes and prolonged hospitalization before delivery and to be treated with antibiotics. No trends towards more resistant strains of pathogens were recorded over the 10.5 years of the study period.

Conclusions: Early-onset neonatal sepsis in term infants differs in bacterial species from that in preterm infants, with predominantly gram-positive organisms in term and near-term infants and gram-negative organisms in preterms. Rates of bacterial resistance to the combination of ampicillin and gentamicin, though higher among infants born to mothers with prolonged hospitalization who had been treated with antibiotics, still remained very low in our department. Thus, it seems that our classic antibiotic regimen is still appropriate for both term and preterm newborns.
 

January 2009
I.R. Makhoul, H. Sprecher, R. Sawaid, P. Jakobi, T. Smolkin, P. Sujov, I. Kassis and S. Blazer

Background: According to the U.S. Centers for Disease Control guidelines, prolonged rupture of membranes mandates intrapartum antimicrobial prophylaxis for group B Streptococcus whenever maternal GBS[1] status is unknown.

Objectives: To evaluate the local incidence, early detection and outcome of early-onset GBS sepsis in 35–42 week old neonates born after PROM[2] to women with unknown GBS status who were not given intrapartum antimicrobial prophylaxis.

Methods: During a 1 year period, we studied all neonates born beyond 35 weeks gestation with maternal PROM ≥ 18 hours, unknown maternal GBS status and without prior administration of IAP[3]. Complete blood count, C-reactive protein, blood culture and polymerase chain reaction amplification of bacterial 16S rRNA gene were performed in blood samples collected immediately after birth. Unfavorable outcome was defined by one or more of the following: GBS bacteremia, clinical signs of sepsis, or positive PCR[4].

Results:  Of the 3616 liveborns 212 (5.9%) met the inclusion criteria. Only 12 (5.7%) of these neonates presented signs suggestive of sepsis. PCR was negative in all cases. Fifty-eight neonates (27.4%) had CRP[5] > 1.0 mg/dl and/or complete blood count abnormalities, but these were not significantly associated with unfavorable outcome. Early-onset GBS sepsis occurred in one neonate in this high risk group (1/212 = 0.47%, 95% CI 0.012–2.6). 

Conclusions: In this single-institution study, the incidence of early-onset GBS sepsis in neonates born after PROM of ≥ 18 hours, unknown maternal GBS status and no intrapartum antimicrobial prophylaxis was 0.47%.

 






[1] GBS = Group B Streptococcus



[2] PROM = prolonged rupture of membranes



[3] IAP = intrapartum antimicrobial prophylaxis



[4] PCR = polymerase chain reaction



[5] CRP = C-reactive protein



 
October 2006
V.H. Eisenberg, D. Raveh, Y. Meislish, B. Rudensky, Y. Ezra, A. Samueloff, A.I. Eidelman and M.S. Schimmel
 Background: Previous assessments of maternal group B Streptococcus carrier rates in women delivering at Shaare Zedek Medical Center ranged between 3.5 and 11% with neonatal sepsis rates of 0.2–0.9/1000 live births. Because of low colonization and disease rates, routine prenatal cultures of GBS[1] were not recommended, and intrapartum prophylaxis was mainly based on maternal risk factors.

Objectives: To determine whether this policy is still applicable. 

Methods: We performed prospective sampling and follow-up of women admitted for labor and delivery between February 2002 and July 2002. Vaginal and rectal cultures were obtained before the first pelvic examination. GBS isolation was performed using selective broth medium, and identified by latex agglutination and serotyping. Demographic data were collected by means of a standardized questionnaire. Data on the newborns were collected throughout 2002.

Results: Of the 629 sampled women, 86 had a positive culture and a carrier rate of 13.7%. A borderline significantly higher carriage rate was observed among mothers of North American origin (21% vs. 13.1%, P = 0.048), and a higher attack rate in their infants (3.8/1000 compared with 0.5/1000 live births in our general maternal population, P = 0.002). Eight newborns had early-onset neonatal GBS sepsis (a rate of 0.8/1000 live births), but none of them benefited from intrapartum antibiotic prophylaxis.

Conclusions: An increased neonatal disease rate was observed in a population with a higher colonization rate than previously seen. In lieu of the higher carrier rates, we now recommend routine prenatal screening for GBS in our perinatal population.


 





[1] GBS = group B Streptococcus


November 2003
N. Tweezer-Zaks, E. Shiloach, A. Spivak, M. Rapoport, B. Novis and P. Langevitz
July 2003
R. Satran and Y. Almog

Sepsis is an infection-induced inflammatory syndrome that results in a complex network of adaptive and maladaptive alterations in homeostatic mechanisms. Severe sepsis, defined as sepsis associated with acute organ failure, is a serious disease with a mortality rate of 30–50%. The coagulation system, through complex interactions, has an important role in the final outcome of the sepsis-induced inflammatory cascade. A fine and delicate balance that normally exists between anticoagulant mechanisms and the procoagulant response is altered in sepsis. Activated protein C, an endogenous vitamin K-dependent anticoagulant, plays a major role in the down-regulation of the procoagulant arm. It also possesses anti-inflammatory properties. Endothelial damage during sepsis impairs the endothelium-dependent activation of protein C, thus shifting the balance towards thrombosis. This shift may contribute to the development of sepsis-related multi-organ failure. Evidence suggesting that activation of the coagulation system may contribute to sepsis-related morbidity and mortality has led to extensive research attempting to correct the hemostatic defects seen in septic patients. Indeed, a recent randomized controlled trial demonstrated a reduction in overall mortality in patients with severe sepsis treated with APC[1]. In this review we discuss the pathogenesis of the coagulopathy of sepsis, as well as the new therapeutic approaches aimed at correcting the defects in the coagulation system.






[1] APC = activated protein C


January 2003
V. Klaitman and Y. Almog

Sepsis is an inflammatory syndrome caused by infection. Consequently, anti-inflammatory therapies in sepsis have been a subject of extensive research and corticosteroids have been used for years in the therapy of severe infections. However, studies conducted in the 1980s failed to demonstrate any beneficial effects of high dose, short-term steroid therapy in sepsis and this therapy was therefore abandoned during the last decade. Recently, a new concept has emerged with more promising results - low dose, long-term hydrocortisone therapy – and this approach is now being evaluated in the treatment of septic shock. It is supported by the observation that many sepsis patients have relative adrenal insufficiency. Moreover, the anti-inflammatory effects of steroids and their ability to improve reactivity to catecholamines further contribute to their effects in sepsis. Large randomized clinical trials will be required to determine the exact role of corticosteroids in septic shock.

May 2002
Alik Kornecki, MD, Riva Tauman, MD, Ronit Lubetzky, MD and Yakov Sivan, MD

Background: The role of continuous renal replacement therapy in patients with acute renal failure is well recognized. CRRT[1] has also become an important modality of treatment in various acute situations without renal failure.

Objectives: To describe our experience with CRRT in acutely ill infants and children without renal failure.

Methods: We analyzed all infants and children who underwent CRRT during the years 1998-2000 in the pediatric intensive care unit and we focus our report on those who were treated for non-renal indications.

Results: Fourteen children underwent 16 sessions of CRRT. The indications for CRRT were non-renal in 7 patients (age range 8 days to 16 years, median = 6.5). Three children were comatose from maple syrup urine disease, three were in intractable circulatory failure secondary to septic shock or systemic inflammatory response, and one had sepsis with persistent lactic acidosis and hypernatremia. Three children underwent continuous hemodiafiltration and four had continuous hemofiltration. The mean length of the procedure was 35 ± 24 hours. All patients responded to treatment within a short period (2–4 hours). No significant complications were observed. Two patients experienced mild hypothermia (34°C), one had transient hypotension and one had an occlusion of the cannula requiring replacement.

Conclusion: Our findings suggest that CRRT is a safe and simple procedure with a potential major therapeutic value for treating acute non-renal diseases in the intensive care setting.






[1] CRRT = continuous renal replacement therapy


June 2001
Philipp von Landenberg, MD and Yehuda Shoenfeld, MD

In diagnosing sepsis the rapid identification of bacteremia at an early stage of the disease is critical for a favorable outcome. Furthermore, it is important that exact information on the stage of the disease be obtained rapidly in order to choose and initiate the appropriate therapy. In recent years many new techniques have been added to the diagnostic tools. In this review we will focus on three new methods for the early diagnosis of sepsis. These are: polymerase chain reaction, which offers the possibility to attain detailed information about the involved bacterial (or viral) species, and the laboratory markers procalcitonin and hypophosphatemia, which are indicators of the presence of infection with gram-negative bacteria. The approaches reviewed here were developed to expedite the diagnosis of especially early sepsis and might be a further step towards the improvement of therapy for sepsis.

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