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List of references.

Astana Medical University.

V.G.Korpachev Department of pathological physiology.

IWS

Theme:“Sepsis in neonates”.

 

 

Prepared by:Yessenbekkyzy N.

General Medicine faculty,

2nd course, 226 – group.

Faculty member:Kalizatova A.S.

2013.

 

Contents.

1. Introduction…………………………………………………………….....….3

2. Literature review

2.1. Etiology.………………………………………………………......4-5

2.2. Pathogenesis…………………………………………………........5-6

2.3. Treatment.........................................................................................6-7

3.Conclusion………………………………………………………..........8

4.List of references…………………………………………..............9

 

 


Introduction

Neonatal sepsis occurs in 1 to 8 per 1000 live births with the highest incidence occurring among infants of very low birth weight and gestation. It is mandatory to have a high index of suspicion for the possibility of sepsis, as well as a low threshold for commencing antibiotic treatment. While more babies are treated than are infected the consequences of untreated sepsis are devastating.Neonatal sepsis is invasive infection, usually bacterial, occurring during the neonatal period. Signs are multiple and include diminished spontaneous activity, less vigorous sucking, apnea, bradycardia, temperature instability, respiratory distress, vomiting, diarrhea, abdominal distention, jitteriness, seizures, and jaundice. Diagnosis is clinical and based on culture results. Treatment is initially with ampicillin plus either gentamicin or cefotaxime, narrowed to organism-specific drugs as soon as possible.

Early onset sepsis (within the first 48 hours of life)

· often manifests with pneumonia and/or septicaemia

· equal male and female incidence

· characterised by high risk of mortality (10 to 30%)

· predominantly due to organisms acquired from the birth canal

· occasionally intrapartum haematogenous spread occurs eg Listeria

· over 80% of cases are due to GBS and gram negative bacteria

Late onset sepsis (after the first 48 hours)

· due to organisms acquired either around the time of birth or in hospital eg Coagulase Negative Staphylococcus during hospitalisation in the NICU

· male predominance

· infants < 1000gms are particularly at risk

· mortality rate approximately 5%

· > 70% due to Coagulase Negative Staphylococcus and Staphylococcus aureus, 10 - 15% due to Gram negatives. Candida is an important pathogen, particularly among extremely low birth weight infants

· gram negatives and GBS predominate among infections acquired outside the NICU setting

 

Literature review.

Etiology.

Neonatal sepsis can be early onset (within 7 days of birth) or late onset (after 7 days). Early onset: Early-onset sepsis usually results from organisms acquired intrapartum. Most infants have symptoms within 6 h of birth, and almost all cases occur within 72 h. Group B streptococcus (GBS) and gram-negative enteric organisms (predominantly Escherichia coli) account for most cases of early-onset sepsis. Vaginal or rectal cultures of women at term may show GBS colonization rates of up to 30%. At least 35% of their infants also become colonized. The density of infant colonization determines the risk of early-onset invasive disease, which is 40 times higher with heavy colonization. Although only 1/100 of infants colonized develop invasive disease due to GBS, > 50% of those present within the first 6 h of life. Nontypeable Haemophilus influenzae sepsis has been increasingly identified in neonates, especially premature neonates.



Other gram-negative enteric bacilli (eg, Klebsiella sp) and gram-positive organisms—Listeria monocytogenes, enterococci (eg, Enterococcus faecalis, Enterococcus faecium), group D streptococci (eg, Streptococcus bovis), α-hemolytic streptococci, and staphylococci—account for most other cases. Streptococcus pneumoniae, H. influenzae type b, and, less commonly, Neisseria meningitidis have been isolated. Asymptomatic gonorrhea occurs occasionally in pregnancy, so Neisseria gonorrhoeae may be a pathogen.

Late onset: Late-onset sepsis is usually acquired from the environment . Staphylococci account for 30 to 60% of late-onset cases and are most frequently due to intravascular devices (particularly umbilical artery or vein catheters). E. coli is also becoming increasingly recognized as a significant cause of late-onset sepsis, especially in very LBW infants. Isolation of Enterobacter cloacae or E. sakazakii from blood or CSF suggests contaminated feedings. Contaminated respiratory equipment is suspected in outbreaks of hospital-acquired Pseudomonas aeruginosa pneumonia or sepsis. Although universal screening and intrapartum antibiotic prophylaxis for GBS have significantly decreased the rate of early-onset disease due to this organism, the rate of late-onset GBS sepsis has remained unchanged, which is consistent with the hypothesis that late-onset disease is usually acquired from the environment.

The role of anaerobes (particularly Bacteroides fragilis) in late-onset sepsis remains unclear, although deaths have been attributed to Bacteroides bacteremia. Anaerobes may account for some culture-negative cases in which autopsy findings indicate sepsis.

Candida sp are increasingly important causes of late-onset sepsis, occurring in 12 to 13% of very LBW infants.

Early and late onset: Certain viral infections (eg, disseminated herpes simplex, enterovirus, adenovirus, respiratory syncytial virus) may manifest as early-onset or late-onset sepsis.

Pathogenesis.

Early onset: Certain maternal perinatal and obstetric factors increase risk, particularly of early-onset sepsis, such as the following:

· Premature rupture of membranes occurring ≥ 18 h before birth

· Maternal bleeding (eg, placenta previa, abruptio placentae)

· Preeclampsia

· Precipitous delivery

· Maternal infection (particularly of the urinary tract or endometrium, most commonly manifests as maternal fever shortly before or during delivery)

· Heavy colonization with GBS

· Preterm delivery

Hematogenous and transplacental dissemination of maternal infection occurs in the transmission of certain viral (eg, rubella, cytomegalovirus), protozoal (eg, Toxoplasma gondii), and treponemal (eg, Treponema pallidum) pathogens. A few bacterial pathogens (eg, L. monocytogenes, Mycobacterium tuberculosis) may reach the fetus transplacentally, but most are acquired by the ascending route in utero or as the fetus passes through the colonized birth canal.

Though the intensity of maternal colonization is directly related to risk of invasive disease in the neonate, many mothers with low-density colonization give birth to infants with high-density colonization who are therefore at risk. Amniotic fluid contaminated with meconium or vernix caseosa promotes growth of GBS and E. coli. Hence, the few organisms in the vaginal vault are able to proliferate rapidly after PROM, possibly contributing to this paradox. Organisms usually reach the bloodstream by fetal aspiration or swallowing of contaminated amniotic fluid, leading to bacteremia. The ascending route of infection helps to explain such phenomena as the high incidence of PROM in neonatal infections, the significance of adnexal inflammation (amnionitis is more commonly associated with neonatal sepsis than is central placentitis), the increased risk of infection in the twin closer to the birth canal, and the bacteriologic characteristics of neonatal sepsis, which reflect the flora of the maternal vaginal vault.

Late onset: The most important risk factor in late-onset sepsis is preterm delivery. Others include

· Prolonged use of intravascular catheters

· Associated illnesses (which may, however, be only a marker for the use of invasive procedures)

· Exposure to antibiotics (which selects resistant bacterial strains)

· Prolonged hospitalization

· Contaminated equipment or IV or enteral solutions

Gram-positive organisms (eg, coagulase-negative staphylococci and Staphylococcus aureus) may be introduced from the environment or the patient's skin. Gram-negative enteric bacteria are usually derived from the patient's endogenous flora, which may have been altered by antecedent antibiotic therapy or populated by resistant organisms transferred from the hands of personnel (the major means of spread) or contaminated equipment. Therefore, situations that increase exposure to these bacteria (eg, crowding, inadequate nurse staffing or provider hand washing) result in higher rates of hospital-acquired infection. Risk factors for Candida sp sepsis include prolonged (> 10 days) use of central IV catheters, hyperalimentation, use of antecedent antibiotics, necrotizing enterocolitis or other abdominal pathology, and previous surgery.

Initial foci of infection can be in the urinary tract, paranasal sinuses, middle ear, lungs, or GI tract, and may later disseminate to meninges, kidneys, bones, joints, peritoneum, and skin.

Treatment

· Antibiotic therapy

· Supportive therapy

Because sepsis may manifest with nonspecific clinical signs and its effects may be devastating, rapid empiric antibiotic therapy is recommended (see Bacteria and Antibacterial Drugs: Selection and Use of Antibiotics); drugs are later adjusted according to sensitivities and the site of infection. If bacterial cultures show no growth by 48 h (although some pathogens may require 72 h) and the neonate appears well, antibiotics are stopped.

General supportive measures, including respiratory and hemodynamic management, are combined with antibiotic treatment.

Antimicrobials: In early-onset sepsis, initial therapy should include ampicillin or penicillin G plus an aminoglycoside. Cefotaxime may be added to or substituted for the aminoglycoside if meningitis is suspected. If foul-smelling amniotic fluid is present at birth, therapy for anaerobes (eg, clindamycin , metronidazole) should be added. Antibiotics may be changed as soon as an organism is identified. Previously well infants admitted from the community with presumed late-onset sepsis should also receive therapy with ampicillin plus gentamicin or ampicillin plus cefotaxime. If gram-negative meningitis is suspected, ampicillin, cefotaxime, and an aminoglycoside may be used. In late-onset hospital-acquired sepsis, initial therapy should include vancomycin (active against methicillin-resistant S. aureus) plus an aminoglycoside. If P. aeruginosa is prevalent in the nursery, ceftazidime may be used instead of an aminoglycoside. For neonates previously treated with a full 7- to 14-day aminoglycoside course who need retreatment, a different aminoglycoside or a 3rd-generation cephalosporin should be considered. If coagulase-negative staphylococci are suspected (eg, an indwelling catheter has been in place for > 72 h) or are isolated from blood or other normally sterile fluid and considered a pathogen, initial therapy for late-onset sepsis should include vancomycin. However, if the organism is sensitive to nafcillin, cefazolin or nafcillin should replace vancomycin. Removal of the presumptive source of the organism (usually an indwelling intravascular catheter) may be necessary to cure the infection because coagulase-negative staphylococci may be protected by a biofilm (a covering that encourages adherence of organisms to the catheter).

Because Candida may take 2 to 3 days to grow in blood culture, initiation of amphotericin B therapy and removal of the infected catheter without positive blood or CSF cultures may be life saving.

Other treatment: Exchange transfusions have been used for severely ill (particularly hypotensive and metabolically acidotic) neonates. Their purported value is to increase levels of circulating immunoglobulins, decrease circulating endotoxin, increase Hb levels (with higher 2,3-diphosphoglycerate levels), and improve perfusion. However, no controlled prospective studies of their use have been conducted.

Fresh frozen plasma may help reverse the heat-stable and heat-labile opsonin deficiencies that occur in LBW neonates, but controlled studies of its use are unavailable, and transfusion-associated risks must be considered.

Granulocyte transfusions have been used in septic and granulocytopenic neonates but have not convincingly improved outcome.

Recombinant colony-stimulating factors (granulocyte colony-stimulating factor [G-CSF] and granulocyte-macrophage colony-stimulating factor [GM-CSF]) have increased neutrophil number and function in neonates with presumed sepsis but do not seem to be of routine benefit in neonates with severe neutropenia; further study is required.

 

Conclusion.

The pathological basis of sepsis is initially an excessive inflammatory response against invading pathogens, leading to systemic inflammatory response syndrome (SIRS). Evidence reveals that a variety of inflammatory mediators orchestrate the intense inflammation through complicated cellular interactions. More recent data indicate that most septic patients survive this stage and then subjected to an immunoparalysis phase, termed compensatory anti-inflammatory response syndrome (CARS), which is more fatal than the initial phase. Sepsis is a complicated clinical syndrome with multiple physiologic and immunologic abnormalities.

A major shift has occurred in the way investigators view the problem of sepsis. Sepsis may not be attributable solely to an “immune system gone haywire” but may indicate an immune system that is severely compromised and unable to eradicate pathogens. Mechanisms of organ failure and death in patients with sepsis remain unknown, and autopsy studies do not reveal widespread necrosis. Future therapy may be directed at enhancing or inhibiting the patient’s immune response, depending on genetic polymorphisms, the duration of disease, and the characteristics of the particular pathogen.

At present, in order to obtain better prognosis, quick and accurate diagnosis in an early stage of sepsis is above all important. An initial therapy with prompt speed and appropriateness is essential. New therapeutic options based on the scientific evidence may pave the way for the treatment of sepsis and septic shock in the new era. However, recent clinical trials aimed at modulating inflammatory response have failed or shown only modest clinical benefit. Recently, there is a growing consensus that the general strategy of research on

sepsis needs to be reconsidered.

 

 

List of references.

1. American Academy of Pediatrics. Red Book 2003. 26th ed. 2003;117-123, 237-43, 561-73,584-91.

2. Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A. Prevention of perinatal group B streptococcal disease. Revised guidelines from CDC. MMWR Recomm Rep. Aug 16 2002;51(RR-11):1-22.

3. Adams-Chapman I, Stoll BJ. Neonatal infection and long-term neurodevelopmental outcome in the preterm infant. Curr Opin Infect Dis. Jun 2006;19(3):290-7.

4. Davis KL, Shah SS, Frank G, Eppes SC. Why are young infants tested for herpes simplex virus?. Pediatr Emerg Care. Oct 2008;24(10):673-8.

5. Enomoto M, Morioka I, Morisawa T, Yokoyama N, Matsuo M. A novel diagnostic tool for detecting neonatal infections using multiplex polymerase chain reaction. Neonatology. 2009;96(2):102-8.

6. Garges HP, Moody MA, Cotten CM. Neonatal meningitis: what is the correlation among cerebrospinal fluid cultures, blood cultures, and cerebrospinal fluid parameters?. Pediatrics. Apr 2006;117(4):1094-100.

7. Kermorvant-Duchemin E, Laborie S, Rabilloud M, Lapillonne A, Claris O. Outcome and prognostic factors in neonates with septic shock. Pediatr Crit Care Med. Mar 2008;9(2):186-91.

8. Khashu M, Osiovich H, Henry D. Persistent bacteremia and severe thrombocytopenia caused by coagulase-negative Staphylococcus in a neonatal intensive care unit. Pediatrics. Feb 2006;117(2):340-8.

9. Klinger G, Levy I, Sirota L, Boyko V, Reichman B, Lerner-Geva L. Epidemiology and risk factors for early onset sepsis among very-low-birthweight infants. Am J Obstet Gynecol. Jul 2009;201(1):38.e1-6.

10. Ng PC, Li K, Leung TF. Early prediction of sepsis-induced disseminated intravascular coagulation with interleukin-10, interleukin-6, and RANTES in preterm infants. Clin Chem. Jun 2006;52(6):1181-9.

11. Sarkar S, Bhagat I, DeCristofaro JD. A study of the role of multiple site blood cultures in the evaluation of neonatal sepsis. J Perinatol. Jan 1 2006;26(1):18-22. .

12. Van den Hoogen A, Gerards LJ, Verboon-Maciolek MA, Fleer A, Krediet TG. Long-Term Trends in the Epidemiology of Neonatal Sepsis and Antibiotic Susceptibility of Causative Agents. Neonatology. Jul 2 2009;97(1):22-28.


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