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a. Congenital infection: Congenital infection is thought to occur during the pregnancy, either across the placenta or via ascent up the birth canal. The principal organisms that account for congenital infection leading to neonatal sepsis include syphilis, human immunodeficiency virus (HIV), Toxoplasma, and cytomegalovirus. Risk factors for the development of congenital infection include a maternal infection with these organisms (which then leads to infection of the fetus), or prolonged rupture of membranes (leading to ascending infection). b. Early-onset infection: Early onset infection is thought to occur during passage of the fetus through the birth canal. The principal organisms that account for early-onset infection include predominantly group B streptococcus (GBS), as well as Escherichia coli (E. coli) in the remainder. Since early-onset infection is thought to occur during parturition, it is not surprising that the major risk factor for this phase of neonatal sepsis is the asymptomatic colonization of the maternal gastrointestinal or genitourinary tracts. The maternal GI or GU tracts are colonized by GBS in up to 30% of pregnant women. Risk factors for higher colonization rates include African American descent and diabetes. Additional risk factors for early-onset infection include prolonged rupture of membranes, prematurity, male gender, low birth weight, maternal infection, and poor prenatal care.As will be discussed below, treatment of the mother with antibiotics against GBS has resulted in a decreased incidence of GBS-induced neonatal sepsis, and a corresponding increase in sepsis from other organisms, in particular Gram-negative organism including E. coli and Klebsiella species. c. Late-onset infection: Late-onset infection is thought to occur well beyond the early delivery phase, and as such reflects organism that may be acquired in the hospital setting or at home. As such, infants with late-onset neonatal sepsis develop infections from common hospital pathogens, including bacteria (coagulase negative staphylococcal species), viruses, and fungi (Candida species). Patients that are on antibiotics for any length of time are at increased risk for the development of late-onset infection, as are those infants that have any centrally placed intravenous catheter. Such lines may include a Broviac or percutaneously-inserted central catheter (PICC-line), an umbilical arterial line, or an umbilical venous line. Indeed, neonates that are on ventilators for reasons other than sepsis may acquire an infection in the hospital, a so-called nosocomial infection. Late-onset neonatal sepsis can also occur in infants after they leave the hospital. In these cases, organisms that are similar to those causing early-onset sepsis i.e., GBS, E. coli and other Gram-negative species predominate.
Why are neonates at particularly increased risk for the development of sepsis?
There are several key features of neonates that place them at increased risk for the development of sepsis. Neonates have a relatively immature immune system, and the effects on the immune system are more pronounced in more premature neonates. Such defects include a loss of protective maternal antibodies, as well as non-specific alterations in macrophage phagocytosis and clearance of invading pathogens, impaired T-cell and B-cell responses, and altered production of complement and antibodies. In addition, the newborn infant particularly the preterm infant has relatively permeable mucosal surfaces that allow for the trans-epithelial passage of bacteria and other pathogens. The frequency with which preterm neonates undergo invasive procedures, that themselves result in the introduction of potential pathogens, also increases the specific risk to the neonate of the development of sepsis. The presence of co-morbidities, such as impaired cardiac function, anatomic defects of the gastro-intestinal or urinary tract, and abnormalities in glucose metabolism worsen the neonate s ability to withstand infection, and lead to an increased risk for the development of neonatal sepsis.
Baseline data Name: Baby Boy X Address: Canaan East, Rizal Age: NB Birthplace: ELJ Memorial Hospital Gender: Male Religion: R/C Nationality: Filipino Father s Name: J.J. Mother s Name: S.B.G. Date Admission: June 15, 2011 Time of Admission: 1:17am Admitting Diagnosis: Live bb. Boy delivered to 2* LCCS 37-38 weeks, birth wt. 2.7kg SGA, AS 8/9 Principal Diagnosis: To consider neonatal sepsis Admitting Physician: Dr. Wy Health History 44y.o. G1P0 Meconium Stained PROM by 10*
a. Physical examination On physical examination, a head-to-toe evaluation is necessary in order for the diagnosis of sepsis to be established. After obtaining vital signs (temperature, heart rate, respiratory rate), the infant is examined first to assess the extent of hydration the fontanelle is examined for evidence of dehydration (sunken) or bulging (occasionally seen in meningitis). Nasal flaring is assessed, as is the presence of sunken or bulging orbits (evidence of dehydration vs. meningitis). The skin is carefully palpated, and evidence of petechiae are noted, as are signs of poor perfusion, including mottling, pallor, and coolness to the extremities. The lungs are auscultated, and evidence of pneumonia (asymmetrical breath sounds) or crackles (evidence of fluid leakage) is noted. The heart tones are examined for evidence of murmur (patent ductus arteriosus), and the heart rate and strength of the heart tones are noted (decreased with pericardial effusion). Examination of the abdomen will detect evidence of distention, tenderness, or erythema, as may be seen in the setting of ileus (which may accompany neonatal sepsis) or necrotizing enterocolitis (discussed in another Knol). Evidence of peripheral edema (seen in more advanced sepsis) and other signs of skin infection (redness, warmth) should also be noted. Although the physical findings do not point to a specific etiology, they should raise the suspicion for sepsis, and lead to the acquisition of additional tests. b. Laboratory tests The laboratory work-up of septic neonates begins with a complete blood count, including leukocyte count with differential, and platelet count. Evidence of decreased circulating white blood cells may be noted (leucopenia), as may signs of increased white blood cells (leukocytosis). Leucopenia is probably more common than leukocytosis in cases of neonatal sepsis. Neonatal sepsis may also be associated with an increase in the release of immature white blood cells into the circulation, as manifest by an increase in circulating band forms. A decrease in platelet count may also be noted, a manifestation of the formation of small blood clots within the tissue or impaired production in the bone marrow 16. Additional tests of note include abnormalities in serum electrolytes, including increased or decreased sodium concentrations, both of which are evidence of the free water imbalance that accompanies sepsis. Septic infants may also manifest hyper- or hypo-glycemia. Obtaining accurate cultures of all body fluids is the most important step in establishing the diagnosis of sepsis. This includes a blood culture, as well as a culture of the urine and the cerebrospinal fluid. When obtaining a blood culture, it is important to avoid drawing blood from intravenous catheters or central lines. It is particularly important to be able to recognize the presence of common contaminants in blood cultures, especially coagulase-negative staphylococcus or viridans streptococci. The practice of obtaining cultures from two clean sites facilitates this task. It is noteworthy that neonatal endotracheal cultures are often not very helpful in establishing the diagnosis of neonatal sepsis, given the frequency and speed with which endotracheal tubes become colonized with microbes.
In certain cases, a viral etiology will be suspected, particularly in cases of congenital neonatal sepsis. Rapid viral testing may be available, especially in cases in which herpes simplex virus infection is suspected.There is not an individual x-ray that will reliably diagnose neonatal sepsis, although many tests may provide supportive information. For instance, the chest x-ray may illustrate evidence of diffuse infiltrates and poor overall aeration (Figure 2). Pneumonia may also be seen. There is great interest in the use of markers of systemic inflammation to diagnose systemic sepsis in neonates. Such markers include C-reactive protein, tumor necrosis factor, interleukin-1, and interleukin-6. Initial results with these markers show some promise in selected patients
Diagnostic Procedure
Test Hemoglobin Hematocrit WBC count Segmenters Lymphocytes Blood Type Normal Values M: 120-190mg/dL F: 120-150mg/dL M: 0.40-0.54g/L F: 0.37-0.47g/L M/F: 5.10x10L 0.40-0.60 0.20-0.40 Result 234 0.69 14.2 0.84 0.16 B
b. Antimicrobial therapy
In addition to the maintenance of systemic vital signs, treatment of neonatal sepsis requires specific antimicrobial therapy. The specific antimicrobial agent is influenced by the particular phase of neonatal sepsis, as characterized in Figure 1. For instance, early-onset neonatal sepsis is treated with a combination of agents that treat group B streptococcus as well as Gram-negative species. Useful agents include ampicillin and gentamicin, or ampicillin plus cefotaxime. These agents in combination cover a broad spectrum of the most common pathogens in early-onset sepsis, and have excellent penetration into the central nervous system. There is evidence to support the use of ampicillin and gentamicin in the treatment of early-onset neonatal sepsis. When gentamicin is used, close monitoring of renal function is required. It is important to note that the pharmacy of an individual nursery will greatly facilitate the choice of antibiotics, based upon the prevailing antibiotic sensitivity spectra against these and other known antibiotics. For late-onset sepsis, the choice of antibiotic therapy should be based, in part, on the prevailing flora of the individual NICU, and the infection history of a particular infant. In general, the same empiric treatment as for early-onset sepsis may be used (i.e., ampicillin and gentamicin), unless micro-organisms with resistance to these agents are identified. In instances in which a central line is present, treatment should be instituted to cover S. aureus and coagulase-negative staphylococci.
There is increasing incidence of methicillin-resistant S. aureus or MRSA in infants with line infections. In view of this, a reasonable first-line antimicrobial choice is vancomycin, in addition to an aminoglycoside such as gentamicin, for empiric coverage of Gram-negative bacilli while awaiting the results of cultures. Persistent bacteremia, or evidence of progressive sepsis despite adequate antimicrobial coverage, necessitates the urgent removal of the infected line. Similarly, the presence of fungemia in the setting of an infected central line necessitates line removal. In neonates who are admitted to the NICU from the community, antibiotic selection should include treatment of meningitis. Empiric choices include a third-generation cephalosporin (i.e., cefotaxime or ceftriaxone) plus ampicillin.
However, despite advances in neonatal care overall, there is still a significant mortality rate. Specifically, the mortality rate for early-onset infection is estimated to be 5% to 10% and for late-onset disease from 2% to 6%. Infants that develop meningitis are at greater risk for the development of long term sequelae, including issues of global mental retardation, motor anomalies (i.e., spastic quadriplegia), seizures, cortical blindness, and deafness. The outcome of patients with late-onset neonatal sepsis may be influenced, in part, by the presence of associated anomalies to a greater extent than the septic episode itself. There is also the possibility of recurrent neonatal sepsis in both earlyand late- onset varieties, likely due to persistent mucosal colonization with pathogens such as GBS. Death from neonatal sepsis is somewhat more likely for early-onset disease and for infants born prematurely. Mortality from early-onset GBS disease has fallen from 55% in the 1970s to 10% to 15% in the 1980s, to a current rate of 3% to 5%. Mortality from late-onset GBS is approximately 5% to 7%.