Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide


  1. 1. Neonatal Sepsis Alicia Pacala, RN BSN Prepared for MSN 621 Advanced Pathophysiology (Spring 2006) Alverno College
  2. 2. Welcome !! Instructions on use of Tutorial: To start Tutorial: tutorial InstructionsInstructions Causes Symptoms Diagnosis Treatments Summary What is Neonatal Sepsis? Objectives
  3. 3. Instructions on how to navigate through tutorial: Click on to go to next slide. Click on to go back to previous slide. Click on to go to main menu. Click on to go back to submenu. (Note: This option will only be available on slides derived from submenus.) Roll mouse over highlighted words to receive definition. Whenever you see click on it to receive more information about that topic. When answering questions: If answer picked is incorrect there will only be one option to return to the question. Click on back button to try question again. When answer is correctly answered you will be able to continue through new content or go back to the question.
  4. 4. Tutorial Objectives Completing this tutorial will provide the learner with a better understanding of Neonatal Sepsis: * Pathology * Causes * Symptoms * Diagnosis * Treatments What will I learn?
  5. 5. What is Neonatal Sepsis? Neonatal Sepsis is a term used for a severe infection in newly born infants. It can cause death if not recognized and treated properly. Image used with permission and provided by
  6. 6. More facts about Neonatal Sepsis Neonatal Sepsis affects approximately 2 infants per 1000 births with a higher incidence in premature & low birth weight infants [2]. There are two types of Neonatal Sepsis: Early Onset Late Onset * This tutorial will focus primarily on Early Onset Sepsis
  7. 7. Causes of Neonatal Sepsis The primary causes of Neonatal Sepsis are bacteria, such as Staphylococcus and Group Beta Strep (GBS). 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
  8. 8. What makes a neonate’s immune system immature? 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]. Pathogen enters body Neutrophils move in Chemotaxis occurs Opsonization causes phagocytosis Monocytes kill pathogen
  9. 9. pathogens can enter a neonate’s body in many ways ! Pathogens can enter through the prenatal, perinatal, and postnatal periods [6]. Prenatal Maternal Substance Abuse Premature Rupture of Membranes (>18 Hours) Maternal Infection Perinatal Microbial Colonization at Birth Maternal Infection Vaginal Exam of Mother Postnatal Invasive Catheters Endotracheal Intubation Exposure to Nosocomial Microorganisms
  10. 10. neutrophils: an important cell in immunity against pathogens Neonatal neutrophils are deficient in their ability to adhere to vessel walls at site of infection [2&6]. Further release of neutrophils depletes a neonatal storage pool because the bone marrow storage of a neonate is only 20-30% of the pool in an adult [2&6]. Neonatal neutrophils have a decreased ability to “deform” & migrate into tissues [2&6]. Neutrophils Red Blood Cells Image provided with permission from
  11. 11. chemotaxis 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!! 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.
  12. 12. opsonization Opsonization is the coating of a pathogen with antibodies that makes it susceptible to phagocytosis [2&6]. Phagocytosis is the process of cells (phagocytes) engulfing, ingesting, & destroying pathogens [2&6]. Neonates have a decreased amount of opsonins (antibodies that promote opsonization) [2&6]. Opsonization Pathogen
  13. 13. monocytes: another important cell in the fight against pathogens Monocytes are a type of White Blood Cell that ingests pathogens. 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
  14. 14. What makes a neonate’s immune system susceptible to sepsis? OR Maturity Immaturity
  15. 15. You’re Right!!!! The immaturity of a neonate’s immune system makes them MORE SUSCEPTIBLE to sepsis.
  16. 16. Not Quite! Try Again
  17. 17. Genetic Predisposition to Sepsis Multiple factors play into a neonate’s response to infection and the possible development of sepsis. One of these factors is genetics. As science has moved into recognizing the human genome there have also been advances with finding genetic contributions to sepsis. The body’s first response to infection requires recognition of the presence of a pathogen. After recognition has occurred the body responds appropriately to resolve the problem [3&14]. Many polymorphisms have been recognized within both of these phases and they have been implicated in influencing the susceptibility to and/or outcome from sepsis [3&14]. Let’s look further into these two phases to see the effect polymorphisms have on neonatal sepsis: Recognition Phase Response Phase
  18. 18. Recognition Phase The body’s 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]. Let’s look into two of these: Mannose-Binding Lectine (MBL) Lipopolysaccharide (LPS)
  19. 19. 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. Let’s look into two of these : Tumor Necrosis Factor (TNF) Interleukin 10 (IL-10)
  20. 20. LPS, a major component of bacteria, is a powerful stimulator of the innate immune response [3]. LPS elicits it’s 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! Lipopolysaccharide (LPS)
  21. 21. Mannose-Binding Lectin (MBL) MBL has two primary immunodefensive roles [3]: – involved with opsonization – leads to activation of complement system, independent of antibodies. Polymorphisms cause deficiencies in MBL level [3]. This results in decreased levels of MBL. This deficiency is associated with increased susceptibility to infections!
  22. 22. Tumor Necrosis Factor (TNF) TNF is a proinflammatory cytokine that is responsible for the initial activation of the inflammatory response [3&14]. There are several polymorphisms associated with an increased secretion of TNF resulting in the susceptibility to sepsis[3].
  23. 23. 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].
  24. 24. What effect do polymorphisms have in Neonatal Sepsis? They make a neonate more susceptible to sepsis. They have no apparent effect. They make a neonate less susceptible to sepsis.
  25. 25. Not quite! Try again.
  26. 26. Great answer! You’re correct! 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.
  27. 27. This is not correct! Try again!
  28. 28. Symptoms of Neonatal Sepsis The symptoms of neonatal sepsis are not concrete and vary widely [9]. Tachypnea Heart Rate Changes Feeding difficulties Difficulty Breathing Temperature Instability Jaundice Irritability Why are symptoms so broad?
  29. 29. Symptoms Symptom variability occurs because of the metabolic and inflammatory processes that occur in neonatal sepsis. A neonate’s symptoms are rooted in these two processes. Let’s look more into these areas: Metabolism Inflammation
  30. 30. Metabolism in Neonatal Sepsis Sepsis can alter a neonate’s metabolism [11]. The Ebb & Flow Metabolic Response [11] best describes how a neonate’s metabolism is affected by sepsis. Flow Phase Ebb Phase
  31. 31. Ebb Flow This is the initial phase and last only 1-3 days. This is how a neonate’s 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
  32. 32. Flow Phase This is the phase that occurs after the initial Ebb Phase. If the body doesn’t 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
  33. 33. What metabolic phase causes a neonate’s body into “hyperdrive”? Hyper Phase Flow Phase Ebb Phase
  34. 34. This is not right!!
  35. 35. Wow! You’re so smart!! The flow phase DOES put the neonate’s body into hyperdrive. This phase leads to much of the mortality and morbidity in neonatal sepsis.
  36. 36. Not quite. Try again.
  37. 37. Inflammation in Neonatal Sepsis It is widely known that sepsis occurs because of an exaggerated systemic inflammatory response (SIR) [12]. Let’s find out how this is true Inflammatory Process
  38. 38. Inflammatory Process [12] 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
  39. 39. Inflammation Overall, the imbalance among inflammation, over coagulation, and decreased fibrinolysis are the cause for the majority of deaths in sepsis [12].
  40. 40. How is Neonatal Sepsis Diagnosed? There is no definite marker in neonatal sepsis, but there are determinants of infection. 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
  41. 41. Is there a diagnostic marker for neonatal sepsis? True False
  42. 42. Yeah!!! You are correct! There is NOT a specific diagnostic marker, only determinants of infection (labs, x-rays).
  43. 43. Are you sure? Try again!
  44. 44. Treatments for Neonatal Sepsis It is of vital importance that treatment is initiated as soon as sepsis is suspected, especially for those infants at risk. Broad Spectrum Antibiotics (Ampicillin & Gentamycin) are the first line of defense against neonatal sepsis [2]. Why???? What are other recommendations/options?
  45. 45. Why is it so important to start antibiotic treatment? If not treated as soon as sepsis is suspected a neonate is more likely to die from sepsis and it’s complications. 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+).
  46. 46. 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 neonate’s 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).
  47. 47. 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 neonate’s 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 neonate’s immune system [6]. The second factor is related to a possible genetic predisposition that is caused by polymorphisms [3&14]. A Neonate’s 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 neonate’s assessment. When sepsis is suspected a neonate will undergo a septic work up [2], which includes lab work and x- rays. 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
  48. 48. I hope you have enjoyed your experience and have learned some new information about neonatal sepsis. Contact Information:
  49. 49. References 1. Amaxa Biosystems. (n.d.). “Mission #3: Transfect human monocytes”. [Online image]. Retrieved March 22, 2006 from 2. Bellig, L.L. & Ohning, B.L. (2004). Neonatal Sepsis. Retrieved February 8, 2006, from emedicine: 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 5. LaRosa, S.P. (2002). Sepsis. Retrieved February 14,2006, from The Cleveland ClinicWebsite: 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 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.
  50. 50. References 9. Neonatal Handbook:Sepsis. (n.d.). Retrieved February 14, 2006, from 10. Oostdyk, R. (2005). “Neutrophil”. [Online image]. Retrieved April 20, 2006, from 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: 13. St. Elizabeth Hospital. (n.d.). “The newborn center at St. Elizabeth’s”. [Online image]. Retrieved March 22, 2006 from 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. End Show