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Neonatal Sepsis - Science topic

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I am an early career faculty member at the Federal University Oye-Ekiti, Nigeria. I am into infectious diseases (bacterial) research cum alternative medicine (medicinal plants).
I am currently working on group B streptococci causing neonatal sepsis leading to mortality and also searching for medicinal plants that can solve the problem of antibacterial resistance among the maternal and child healthcare.
Herewith attached is my CV.
Ojo, S.K.S (PhD)
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Explore: what you know, enjoy doing. where, when, whom with, what else do you need to know about you.
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I want to conduct a parallel trial study in which 3 care bundles will be implemented aimed to decrease neonatal sepsis.How is sample size calculated?
Data to be collected from patients will be clinical signs of sepsis and blood samples for culture to determine the presence of infection. The outcome variable will be incidence of neonatal sepsis among participants.The study aims to evaluate the impact of the intervention on incidence of sepsis. What will be the best method to analyze this data
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Hi
For sample size calculation you will need what is the current incidence of sepsis and what amount of changes you are expecting from the intervention. You can go for both randomized and non-randomized design. In the sample size calculation, you have decide how much absolute precision (1-alfa) and power (1-beta) you want. Usually, absolute precision of 5% and power of 80% is acceptable lower limit. If your trial is non-randomized, it is better to put a design effect. You can use online free statistical site www.openepi.com for this.
For analysis, it depends on the data. but from your objective, it appears that you will require unpaired t-test, Fisher's exact/Chi-square test. You can also calculate the sensitivity and specificity if the intervention is diagnostic and calculate the area under the curve for all interventions. For this you have to have one gold standard (these tests will be required if intervention is diagnostic only). At present statistical software also prompts what tests are appropriate provided you enter the data type correctly.
Hope this helps you
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Previously, the master key of antibiotic therapy was to hit hard and strong to reduce development of antibiotic resistance. Newer studies show that the development of resistance isn't only reduced by minimizing the frequency of antibiotic donations but also by shortening the duration of the therapy. (e.g. Ehl et al. 1997 - C-reactive protein is a useful marker for guiding duration of antibiotic therapy in suspected neonatal bacterial infection; Yusuf et al. 2017 -  Emergence of antimicrobial resistance to Pseudomonas aeruginosa in the intensive care unit: association with the duration of antibiotic exposure and mode of administration.)
Do you maybe know some more studies showing this trend? (Maybe also in connection with neonatal sepsis?)
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Do literature review thoroughly, hope you can get the answers.
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I've collected around 100 cleft lip/palate samples from a region in Brazil with high incidence of clefting. I would like to do some studies on those samples in collaboaration.
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if they are non syndromic then if you have parents too you can do TDT and the easiest start is to see if that group replicated the now 20 or so confirmed GWAS hits. then altho 100 is small for GWAS you could try that IF you have parents or other good controls. then as ieda says if its a population isolate of any kind all the genetic association (and even whole exome/genome seq could work)
ieda will be a terrific partner for this
jeff
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I read about hypoglycemic neonatal epilepsy with occipital lobe origin, hypoglycemia-dependent occipital edema and Willis circle variants.
However, it is my understanding that these are all incidental or occasional causes of occipital lesions, am I mistaken? Are there different energy requirements across neonatal brain regions? 
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Hi Jeeva,
Thank you very much for the answer and the useful reference.
It does clarify my query, in particular I am intrigued by the "significant reduction in regional glucose uptake in the occipital WM" and the concept of regional Cerebral Glucose Utilization, as defined in an article (http://ajpheart.physiology.org/content/256/6/H1659 ) in the references of the one you kindly suggested me. Despite the particular condition of hypothermia studied in the article, I find interesting that regional glucose uptake in the occipital regions is particularly reduced. This, along with the previous insight on cerebral circulation, helps a lot, thanks!
Best regards,
Luigi
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My name is Jeremy, I am a senior staff nurse working in a general medical and surgical ICU in the UK.
With recently reading some work on Immunomodulatory Effect of Continuous Venovenous Hemofiltration during Sepsis: Preliminary Data.
As such I would like to ask for the readers help and advice.
With some of our septic patients experiencing acute renal failure needing CVVHDF, I have posed the question, that as yet I can find no answer to.
With 'normal' patients in ARF on CVVHDF, they would become hypothermic to a temperature of 35 Degrees or below. Hence needing active warming through a Bear Hugger and filter heater aids.
With septic patients on CVVHDF, I have seen temperatures of 36-37 Degrees with no heater elements to aid this.
If this is the case, should we not then be complementing them with heater elements to achieve an active temperature of 38-38.5 Degrees? As you may see in the normal immune response to increase an individuals temperature.
Patients are not actively given antipyretic's due to the researched based evidence of increased mortality.
If we are placing septic patients on CVVHDF, then we are actively cooling them! As such, are we not increasing the patients chances of mortality and morbidity?
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Fabulous question. I thought one of the reasons we avoid administering pharmocological antipyretics was their anti-inflammatory effects not necessarily the effect of reducing core temperature. CVVHDF cools by convection so the effect of cooling is confined to the reduction in temperature rather than the effect on of reduced cytokine release on the inflammatory response. 
I will continue to follow this question with interest. 
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in low income countries we can use this parameter to diagnose neonatal sepsis
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It may help if the sepsis complicated with disseminated intravascular coagulation.
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I am looking for fast sepsis diagnosis. Normally serum is used for the analysis  which most often takes a (too) long time. The goal is to accelerate the diagnosis e.g. by continuous non invasive measuring lactate.
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Unless there is such continuous measurement system otherwise it will be hard to do. The turnaround time for lactate measurement usually will take hours even in level 3 hospitals. It will be hard to use it for monitoring sepsis.
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Serum procalcitonin is often used as biomarker to diagnosed presymptomatic or probable neonatal sepsis.
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I know there are several biomarkers such as procalcitonin, SSA, CRP, IL-8, etc. They are all very good but still not a gold standard. Most of us still go by the culture results, clinical judgement, and personal preference.
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Severe Sepsis is often caused by germs that release LPS or ß-glucans, that are toxic for blood monocytes. Monocyte fragments generate systemically circulating thrombin.
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Thomas,
Pablo is making an important point that most often it is the gram negative bacteria responsible for the causation of acute sepsis, the LPS component of the cell wall of these bacteria trigger the Toll-Like receptor response activating the inflammatory cascade.  In my opinion Pablo is right that this is the acute septic response rather than chronic sepsis.  If Pablo can come up with some test to detect that acute response you may have the answer to your original question.  Thanks to Pablo and Thomas for a good dialogue on this important subject.
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I am currently reviewing data of umbilical venous catheter related extravastion injuries in our unit. The retrospective analysis lead to identifying large number of cases. Put together, it could easily become one of the largest published cohort of UVC extravasation injuries, till date. But still the total number of cases will be in single digit. We are specifically looking to study the possible associated factors, clinical manifestations, complications and outcome. More like a descriptive study. I wanted to have your opinion regarding what would be the best category of paper under which such research could be published?
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It would depend upon the available evidence in the literature and what you wish to study. I think it could be a Case Series providing information about the possible associated factors, clinical manifestations, complications and outcome. Alternatively, you could study the associated factors using a case-control study design. This might help answer a question why some develop this complication while the others do not!
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Rational use of antibiotics is necessary for optimal results in the care of newborns with sepsis. Clear guidelines are often not available in many a center in developing countries. Due consideration needs to given to various issues before settling on certain antibiotics in initiating treatment for neonatal sepsis. What are some of these issues?
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It depends on the most common pathogens in your area. In the first two months ampicillin with gentamicin have the best coverage for most area in the world. I am not familiar with the pathogens in your area so can not guarantee this will be the best comnination for empirical treatment. Some hospital prefer ampicilloin and cefotaxime due to the fact no pharmacokinetics need to be considered.