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Instructions on use of Tutorial:
Instructions What is Neonatal Sepsis? Objectives Causes Symptoms
To start Tutorial:
Diagnosis tutorial Treatments Summary
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Tutorial Objectives
Completing this tutorial will provide the learner with a better understanding of Neonatal Sepsis: * Pathology * Causes What will I learn? * Symptoms * Diagnosis * Treatments
There are two types of Neonatal Sepsis: Early Onset Late Onset
* This tutorial will focus primarily on Early Onset Sepsis
Bacteria may be the cause of neonatal sepsis, but neonates are more susceptible to these bacteria for two reasons [3&6]:
Immature immune response
Genetic predisposition
Neutrophils move in
Normally an immune system responds to a pathogen in a specific manner, but if there are problems with any element the immune system is unable to function properly [3&6].
Chemotaxis occurs
Perinatal
Postnatal
Neutrophils
Image provided with permission from http://en.wikipedia.org/wiki/Image:Segmented_neutrophils.jpg
Chemotaxis
Neonatal neutrophils have decreased chemotaxis due to decreased chemoattractant Production [2&6]. Chemoattractants attract neutrophils to the site of infection [2&6]. Neonatal neutrophils therefore cannot reach the site of infection because of the chemotaxis deficiency caused by decreased chemoattractant production.
Imagine: Being in a dark tunnel without any direction or a way out. Finally you see light. You move towards the light and get out of the tunnel. Well this is like chemotaxis. The sun is the chemoattractant attracting you out to the world!!
Opsonization
Opsonization is the coating of a pathogen with antibodies that makes it susceptible to phagocytosis [2&6].
Opsonization
Phagocytosis is the process of cells (phagocytes) engulfing, ingesting, & destroying pathogens [2&6].
Pathogen
Neonates have a decreased amount of opsonins (antibodies that promote opsonization) [2&6].
Neonates have a sufficient amount of monocytes and full capability to kill organisms [2], but because of a neonates deficiencies previously discussed very few monocytes get to the site of infection.
Image provided with permission and copyrighted by amaxa GmbH at www.amaxa.com/mission3.html
Maturity
OR
Immaturity
Youre Right!!!!
The immaturity of a neonates immune system makes them MORE SUSCEPTIBLE to sepsis.
Lets look further into these two phases to see the effect polymorphisms have on neonatal sepsis:
Recognition Phase Response Phase
Recognition Phase
The bodys initial response to infection requires recognition of the presence of a pathogen [3].
Polymorphisms in genes coding for proteins involved in the recognition of pathogens can influence the susceptibility to and/or outcome of neonatal sepsis [3].
Lipopolysaccharide (LPS)
Response Phase
After the initial recognition of a pathogen occurs the body responds by releasing elevated levels of proinflammatory cytokines followed by a release of anti-inflammatory cytokines [3]. This dual release of opposite cytokines helps the cytokines return to a baseline level and that enables the start of tissue repair to start [3]. It is generally accepted that an imbalance between proinflammatory and anti-inflammatory cytokines result in clinical manifestations of sepsis [3]. This Imbalance is due to polymorphisms in various proteins involved in the response to pathogens.
Lipopolysaccharide (LPS)
LPS, a major component of bacteria, is a powerful stimulator of the innate immune response [3]. LPS elicits its response by binding to a cell surface receptor that is compromised of 3 proteins [3]. One of these proteins is TLR4. TLR4 is required for LPS to respond.
When there are polymorphisms in TLR4 there is a reduced response to LPS and that enhances the susceptibility to infection!
Polymorphisms cause deficiencies in MBL level [3]. This results in decreased levels of MBL. This deficiency is associated with increased susceptibility to infections!
There are several polymorphisms associated with an increased secretion of TNF resulting in the susceptibility to sepsis[3].
Interleukin 10 (IL-10)
IL-10 is an anti-inflammatory cytokine produced by primarily monocytes [3]. IL-10 helps regulate the over expression of proinflammatory cytokines.
There are three polymorphisms noted that result in an over expression of IL-10. This over expression is proposed to induce immunosuppression in bacterial sepsis and therefore increasing mortality by inhibiting bacterial clearance [3].
Polymorphisms cause either an over expression or under expression of proteins and/or genes that have significant roles in the immune response to infection. This alters their ability to properly function which makes a neonate more susceptible to sepsis.
Tachypnea Heart Rate Changes Feeding difficulties Difficulty Breathing Temperature Instability Jaundice Irritability
Why are symptoms so broad?
Symptoms
Symptom variability occurs because of the metabolic and inflammatory processes that occur in neonatal sepsis.
Metabolism
Inflammation
Ebb Phase
Flow Phase
Ebb Flow
This is the initial phase and last only 1-3 days. This is how a neonates body initially tries to compensate for losses that occur during sepsis. The body slows things down in order to let the body recover.
The Ebb Phase consists of several clinical manifestations [11]: Hypometabolism Decreased energy expenditure Decreased cardiac output Lowered oxygen consumption Vasoconstriction
Flow Phase
This is the phase that occurs after the initial Ebb Phase. If the body doesnt recover it goes into hyperdrive. This is partly due to the exaggerated inflammatory response (further discussion in inflammatory process section). This phase leads to much of the mortality and morbidity related to neonatal sepsis [11].
The Flow Phase consists of several clinical manifestations [11]: Hypermetabolism Increased energy expenditure Increased cardiac output High oxygen consumption
Hyper Phase
Flow Phase
Ebb Phase
The flow phase DOES put the neonates body into hyperdrive. This phase leads to much of the mortality and morbidity in neonatal sepsis.
Inflammatory Process
Inflammatory Process
Pathogen enters body Inflammatory mediators released (cytokines) Injury to endothelium Tissue factors released Production of thrombin Coagulation promotes clot formation Increased activity of fibrinolysis inhibitors Decreased fibrinolysis [12]
Inflammation
Overall, the imbalance among inflammation, over coagulation, and decreased fibrinolysis are the cause for the majority of deaths in sepsis [12].
When a neonate presents with sepsis symptoms a septic work-up is completed [2]. What is included in a septic work up? * Complete Blood Count (CBC) * Blood & Urine cultures * Lumbar Puncture (LP) * Chest X-Ray * Line cultures
True
False
There is NOT a specific diagnostic marker, only determinants of infection (labs, x-rays).
Broad Spectrum Antibiotics (Ampicillin & Gentamycin) are the first line of defense against neonatal sepsis [2].
What are other recommendations/options?
For this reason it is of vital importance that healthcare workers (nurses and physicians) notice and act upon even the most subtle changes in a neonates assessment, particularly those infants at risk (GBS+).
Treatment Recommendations
Antibiotics should be initiated after all cultures and lab work is completed to ensure proper diagnosis. All neonates will remain on IV antibiotics until blood/urine culture results come back in approximately 2-3 days. Further therapy will depend on lab work results and the neonates response to treatment.
* Every hospital/organization has an antibiotic protocol specific to their site.
Although antibiotic therapy is vital, it is just as important to continue the overall support of the neonate (i.e. respiratory & cardiac).
Summary
Neonatal Sepsis is a severe infection in neonates that has the ability to cause death if not recognized and treated appropriately. The primary causes of sepsis are pathogens, such as Staphylococcus and Group Beta Strep [2&6]. These pathogens can enter a neonates body during the prenatal, perinatal, and postnatal period [6]. Although pathogens are the culprit in sepsis, neonates have factors that make them more susceptible to sepsis. One of these factors is the immaturity of the neonates immune system [6]. The second factor is related to a possible genetic predisposition that is caused by polymorphisms [3&14]. A Neonates symptoms in sepsis are broad and vary [9]. This is due in part to the metabolic and inflammatory processes that occur in neonatal sepsis. Because symptoms are broad and not very concrete, it is of vital importance that the healthcare professional notice even the most subtle changes in a neonates assessment. When sepsis is suspected a neonate will undergo a septic work up [2], which includes lab work and xrays. After lab work is completed intravenous antibiotics are initiated immediately and will continue until lab work demonstrates no infection and the neonate shows no further symptoms.
Print
I hope you have enjoyed your experience and have learned some new information about neonatal sepsis.
Contact Information:
pacalaay@alverno.edu
References
1. Amaxa Biosystems. (n.d.). Mission #3: Transfect human monocytes. [Online image]. Retrieved March 22, 2006 from www.amaxa.com/mission3.html 2. Bellig, L.L. & Ohning, B.L. (2004). Neonatal Sepsis. Retrieved February 8, 2006, from emedicine:http://wwwemedicine.com/ped/topic2630.htm 3. Dahmer, M.K., Randolph, A., Vitali, S., & Quasney, M.W. (2005). Genetic polymorphisms in sepsis. Pediatric Critical Care Medicine, 6(3), 61-73. Retrieved February 23, 2006 from PubMed database. 4. Farlex Inc. (n.d.). The Free Dictionary. Retrieved March 30, 2006, from www.thefreedictionary.com 5. LaRosa, S.P. (2002). Sepsis. Retrieved February 14,2006, from The Cleveland ClinicWebsite: http://www.clevelandclinicmeded.com/diseasemanagement/infectiousdisease/sepsis.htm 6. McKenney, W.M. (2001). Neonatal nursing: Understanding the neonatal immune system: High risk for infection. Crtitical Care Nurse, 21(6), 35-58. Retrieved February 14, 2006, from ProQuest database. 7. Microsoft Corp. (2006). Microsoft Clip Art. Retrieved March 30, 2006, from www.microsoftclipart.com 8. Mrozek, J.D., Georgieff, M.K., Blazer, B.R., Mammel, M.C., & Schwarzenburg, S.J. (2000). Effect of sepsis syndrome on neonatal protein and energy metabolism. [Electronic version] Journal of Perinatology, 2, 96-100.
References
9. Neonatal Handbook:Sepsis. (n.d.). Retrieved February 14, 2006, from http://www.netsvic.org.au/nets/handbook/index.cfm?doc_id=898 10. Oostdyk, R. (2005). Neutrophil. [Online image]. Retrieved April 20, 2006, from http://en.wikipedia.org/wiki/Image:Segmented_neutrophils.jpg 11. Orr, P.A., Case, K.O., & Stevenson, J.J. (2002). Metabolic response and parenteral nutrition in trauma sepsis and burns. Journal of Infusion Nursing, 25(1), 45-53. Retrieved March 7, 2006 from Ovid database. 12. Sharma, S. & Mink, S. (2004). Septic shock. Retrieved February 14, 2006, from emedicine: http://www.emedicine.com/MED/topic2101.htm 13. St. Elizabeth Hospital. (n.d.). The newborn center at St. Elizabeths. [Online image]. Retrieved March 22, 2006 from www.steliz.org/newborn_center.htm 14. Villar, J., Maca-Meyer, N., Perez-Mendez, L., & Flores, C. (2204). Bench to bedside review: Understanding genetic predisposition to sepsis. Critical Care, 8(3), 180-189. Retrieved February 23, 2006, from PubMed database.
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