Neonatal Sepsis Clinical Presentation
- Author: Ann L Anderson-Berry, MD, PhD; Chief Editor: Ted Rosenkrantz, MD more...
An awareness of the many risk factors associated with neonatal sepsis prepares the clinician for early identification and effective treatment, thereby reducing mortality and morbidity. Among these risk factors are the following:
Maternal group B Streptococcus (GBS) status
Premature rupture of membranes (PROM)
Maternal GBS status
The most common cause of neonatal bacterial sepsis is GBS. There are 9 serotypes, each of which is related to the polysaccharide capsule of the organism. Types I, II, and III are commonly associated with neonatal GBS infection. The type III strain has been shown to be most highly associated with central nervous system (CNS) involvement in early-onset infection, whereas types I and V have been associated with early-onset disease without CNS involvement.
The GBS organism colonizes the maternal gastrointestinal (GI) tract and birth canal. Approximately 25% of women have asymptomatic GBS colonization during pregnancy. GBS is responsible for approximately 50,000 maternal infections per year in women, but only 0.36-2 neonates per 1000 live births are infected.
Women with heavy GBS colonization and chronically positive GBS culture results have the highest risk of perinatal transmission. Also, heavy colonization at 23-26 weeks’ gestation is associated with prematurity and low birth weight. Colonization at delivery is associated with neonatal infection.
Intrapartum chemoprophylaxis for women with positive culture results for GBS has been shown to decrease the transmission of the organism to the neonate during delivery. Mothers may have a negative prenatal culture for GBS but a positive one at the time of labor.
Premature rupture of membranes
PROM may occur in response to an untreated urinary tract infection (UTI) or birth canal infection. Other risk factors are previous preterm delivery, uterine bleeding in pregnancy, and heavy cigarette smoking during pregnancy. Rupture of membranes without other complications for more than 24 hours before delivery is associated with a 1% increase in the incidence of neonatal sepsis; however, when chorioamnionitis accompanies the rupture of membranes, the incidence of neonatal infection is quadrupled.
A multicenter study demonstrated that clinical chorioamnionitis and maternal colonization with GBS are the most important predictors of subsequent neonatal infection after PROM. Seaward et al found that more than 6 vaginal digital examinations, which may be carried out as part of the evaluation for PROM, were associated with neonatal infection even when considered separately from the presence of chorioamnionitis.
When membranes have ruptured prematurely before 37 weeks’ gestation, a longer latent period precedes vaginal delivery, increasing the likelihood that the infant will be infected. The duration of membrane rupture before delivery and the likelihood of neonatal infection are inversely related to gestational age. Thus, the more premature an infant is, the longer the delay between rupture of membranes and delivery and the higher the likelihood of neonatal sepsis.
In addition to the relation between preterm PROM and neonatal sepsis, there are other associations between prematurity and neonatal sepsis that increase the risk for premature infants.
Preterm infants are more likely to require invasive procedures, such as umbilical catheterization and intubation. Prematurity is associated with infection from cytomegalovirus (CMV), herpes simplex virus (HSV), hepatitis B virus (HBV), Toxoplasma,Mycobacterium tuberculosis, Campylobacter fetus, and Listeria species. Intrauterine growth retardation and low birth weight are also observed in CMV infection and toxoplasmosis.
Premature infants have less immunologic ability to resist and combat infection. Consequently, they are more susceptible to infection caused by common organisms such as coagulase-negative Staphylococcus— an organism usually not associated with severe sepsis.
The relationship between chorioamnionitis and other risk variables is strong. Suspect chorioamnionitis in the presence of fetal tachycardia, uterine tenderness, purulent amniotic fluid, an elevated maternal white blood cell (WBC) count, and an unexplained maternal temperature higher than 100.4°F (38°C).
The clinical signs of neonatal sepsis are nonspecific and are associated with the characteristics of the causative organism and the body’s response to the invasion. These nonspecific clinical signs of early sepsis are also associated with other neonatal diseases, such as respiratory distress syndrome (RDS), metabolic disorders, intracranial hemorrhage, and a traumatic delivery. In view of the nonspecificity of these signs, it is prudent to provide treatment for suspected neonatal sepsis while excluding other disease processes.
To obtain the most information from the examination, systematic physical assessment of the infant is best performed in a series that should include observation, auscultation, and palpation, in that order. Changes in findings from one examination to the next provide important information about the presence and evolution of sepsis.
Congenital pneumonia and intrauterine infection
Inflammatory lesions are observed post mortem in the lungs of infants with congenital and intrauterine pneumonia. They may result not from the action of the microorganisms themselves but, rather, from aspiration of amniotic fluid containing maternal leukocytes and cellular debris. Tachypnea, irregular respirations, moderate retraction, apnea, cyanosis, and grunting may be observed.
Neonates with intrauterine pneumonia may also be critically ill at birth and require high levels of ventilatory support. The chest radiograph may depict bilateral consolidation or pleural effusions.
Congenital pneumonia and intrapartum infection
Neonates who are infected during the birth process may acquire pneumonia through aspiration of microorganisms during delivery. Klebsiella species and S aureus are especially likely to generate severe lung damage, producing microabscesses and empyema. Early-onset GBS pneumonia has a particularly fulminant course, with significant mortality in the first 48 hours of life.
Intrapartum aspiration may lead to infection with pulmonary changes, infiltration, and destruction of bronchopulmonary tissue. This damage is partly due to the granulocytes’ release of prostaglandins and leukotrienes. Fibrinous exudation into the alveoli leads to inhibition of pulmonary surfactant function and respiratory failure, with a presentation similar to that of RDS. Vascular congestion, hemorrhage, and necrosis may occur. Infectious pneumonia is also characterized by pneumatoceles within the pulmonary tissue.
Coughing, grunting, costal and sternal retractions, nasal flaring, tachypnea or irregular respiration, rales, decreased breath sounds, and cyanosis may be observed. Radiographic evaluation may demonstrate segmental or lobar atelectasis or a diffuse reticulogranular pattern, much like what is observed in RDS. Pleural effusions may be observed in advanced disease.
Postnatally acquired pneumonia may occur at any age. Because these infectious agents exist in the environment, the likely cause depends heavily on the infant’s recent environment. If the infant has remained hospitalized in a neonatal intensive care unit (NICU), especially with endotracheal intubation and mechanical ventilation, the organisms may include Staphylococcus or Pseudomonas species.
Additionally, these hospital-acquired organisms frequently demonstrate multiple antibiotic resistances. Therefore, the choice of antibiotic agents in such cases requires knowledge of the likely causative organisms and the local antibiotic-resistance patterns.
In overwhelming sepsis, an initial early phase characterized by pulmonary hypertension, decreased cardiac output, and hypoxemia may occur. This phase is followed by further progressive decreases in cardiac output with bradycardia and systemic hypotension. The infant manifests overt shock with pallor, poor capillary perfusion, and edema. These late signs of shock are indicative of severe compromise and are strongly associated with mortality.
Hypoglycemia, hyperglycemia, metabolic acidosis, and jaundice are all metabolic signs that commonly accompany neonatal sepsis. The infant has an increased glucose requirement as a result of the septic state. The infant may also be malnourished as a consequence of diminished energy intake. Hypoglycemia accompanied by hypotension may be secondary to an inadequate response from the adrenal gland and may be associated with a low cortisol level.
Metabolic acidosis is due to a conversion to anaerobic metabolism with the production of lactic acid. When infants are hypothermic or are not kept in a neutral thermal environment, efforts to regulate body temperature can cause metabolic acidosis. Jaundice occurs in response to decreased hepatic glucuronidation caused by both hepatic dysfunction and increased erythrocyte destruction.
Meningitis is the common manifestation of CNS infection. Acute and chronic histologic features are associated with specific organisms.
Meningitis due to early-onset neonatal sepsis usually occurs within 24-48 hours and is dominated by nonneurologic signs. Neurologic signs may include stupor and irritability. Overt signs of meningitis occur in only 30% of cases. Even culture-proven meningitis may not demonstrate white blood cell (WBC) changes in the cerebrospinal fluid (CSF).
Meningitis due to late-onset disease is more likely to demonstrate neurologic signs (80-90%); however, many of these physical examination findings are subtle or inapparent. Neurologic signs include the following:
Impairment of consciousness (ie, stupor with or without irritability)
Bulging anterior fontanelle
Focal cerebral signs
Cranial nerve signs
Temperature instability is observed with neonatal sepsis and meningitis, either in response to pyrogens secreted by the bacterial organisms or from sympathetic nervous system instability. The neonate is most likely to be hypothermic. The infant may also have decreased tone, lethargy, and poor feeding. Signs of neurologic hyperactivity are more likely when late-onset meningitis occurs.
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