Neonatal Infections



Neonatal Infections


Samir S. Shah



NEONATAL SEPSIS


Overview

The most common classification of neonatal sepsis is by age at onset.



  • Early-onset infection. Clinical manifestations of early-onset infection occur within the first 7 days of life (95% present within the first 72 hours). Frequently, maternal complications of labor or delivery lead to these infections. Organisms from the maternal genital tract during the intrapartum period colonize the infant’s skin and gastrointestinal and respiratory tracts. The reasons for progression from colonization to infection are not well understood. The most common organisms causing early-onset infection are group B streptococci (GBS), Escherichia coli, and, occasionally, Listeria monocytogenes.


  • Late-onset infection. Clinical manifestations of late-onset infection occur between 7 and 30 days of life. Infection may be the result of colonization during birth or during hospitalization in the intensive care unit. Although most infants do not become ill as a result of this colonization, necessary invasive procedures put them at increased risk for infection. The most common organisms causing late-onset infection are coagulase-negative staphylococci, Staphylococcus aureus, Enterococcus spp., GBS, E. coli, Klebsiella pneumoniae, and Candida spp.


  • Late, late-onset infection. The improved survival rate of very low-birth-weight infants (<1,500 g) has prompted the addition of this third category: late, lateonset infection (generally between 31 and 90 days of life). Although these infants are no longer neonates, their “corrected” gestational age (usually 28 to 34 weeks) and continued need for hospitalization because of complications of prematurity accord them “newborn” status. A quarter of all very low birthweight infants who survive beyond 3 days of life have at least one episode of late-onset or late, lateonset sepsis. These infants usually have central venous catheters or endotracheal tubes in place. Infection in this group is nosocomially acquired and often caused by coagulase-negative staphylococci, Pseudomonas aeruginosa, Enterobacter spp., Klebsiella spp., Serratia marcescens, and Candida spp.


Common Pathogens


Group B Streptococcus Infection

The maternal colonization rate for GBS is 15% to 30%, and 50% of these women deliver infants who are colonized at birth; 1% of colonized infants develop invasive
GBS infection. Women with prenatal colonization are 25 times more likely to deliver an infant with early-onset GBS disease. Table 56-1 shows other risk factors for infection. The most common clinical manifestations for early-onset infection are sepsis, pneumonia, and, less often, meningitis (5% to 10% of earlyonset GBS cases). Early-onset GBS infection has a fulminant presentation; 50% of infected infants are symptomatic at birth. Initial manifestations include respiratory distress, hypoxia, and shock. The mortality rate of early-onset GBS infection is 5% to 10%. Late-onset infections typically occur within the first month of life, but a small subset of infants develops GBS infection 3 to 6 months after birth. Late-onset infections include sepsis, meningitis (30% to 40% of late-onset GBS cases), and, occasionally, skin or soft tissue infections, osteomyelitis, or septic arthritis. The mortality rate of late-onset GBS infection is 2% to 6%. Permanent neurologic sequelae occur in ˜50% of patients with meningitis caused by GBS infection.








TABLE 56-1 Select Risk Factors for Group B Streptococcal Infection

















Maternal Risk Factors


Prior infant with group B streptococcal sepsis


Group B streptococcal bacteriuria


Prolonged rupture of membranes (≥18 hr)


Premature rupture of membranes (<37 wk of gestation)


Preterm labor (<37 wk of gestation)


Intrapartum fever >100.4°F (37.9°C)


The use of intrapartum antibiotics to treat GBS colonized women has decreased the incidence of early-onset GBS infection in neonates by about 30%; the incidence of late-onset disease remains unchanged because intrapartum antibiotic administration does not effectively eradicate neonatal colonization. Currently, half of all cases of invasive GBS disease are late onset. American Academy of Pediatrics (AAP) and American College of Obstetrics and Gynecology recommendations include vaginal and rectal GBS screening of all pregnant women at 35 to 37 weeks of gestation. Intrapartum penicillin is administered in the following situations: previous infant with GBS; GBS bacteriuria; positive GBS screening culture; and unknown GBS status if there is preterm labor, membrane rupture >18 hours, or intrapartum temperature >100.4°F (38°C). Cefazolin, clindamycin, erythromycin, or vancomycin may be given to penicillin-allergic women based on results of GBS isolate susceptibility testing. Other factors that increase the risk of neonatal sepsis include a multiple gestation pregnancy and maternal chorioamnionitis.


E. coli Infection

E. coli, like GBS, is passed from mother to infant, and the ratio of infected to colonized babies is similar. Early-onset and late-onset infections occur. Organisms that have the K1 surface antigen are more apt to cause infection, especially meningitis.



Coagulase-Negative Staphylococcal Infection

Coagulase-negative staphylococci (primarily S. epidermidis) are most commonly associated with nosocomial infection. Risk factors include prematurity and the use of indwelling catheters. The organism produces a slime coating that allows it to adhere to the surfaces of synthetic polymers used to make central venous catheters and also enables it to evade the immune system. Clinical manifestations of staphylococcal sepsis are often subtle, and a high index of suspicion is needed to diagnose the infection early.


Fungal Infection

Candida albicans has been the most common cause of neonatal fungal infection; however, C. parapsilosis and other non-albicans Candida species (C. tropicalis, C. glabrata) are becoming more prevalent. Risk factors for fungal infection include gestational age <32 weeks, indwelling intravascular catheter, endotracheal intubation >7 days, receipt of intralipids or parenteral nutrition, and broad-spectrum antibiotic use, especially third-generation cephalosporins. Systemic infection occurs after hematogenous dissemination. Infants with persistently positive blood cultures for Candida spp. (>3 days) with a central venous catheter in place are three times more likely to have disseminated disease. The most commonly involved sites are the heart (15%), retina (6%), kidneys (5%), and liver (3%). Malassezia furfur bloodstream infection is associated with intralipid infusion.


DIFFERENTIAL DIAGNOSIS

Neonatal sepsis may present with a variety of clinical presentations. These same presentations can have a variety of other causes simulating or accompanying sepsis. Table 56-2 summarizes the differential diagnosis for sepsis.


Evaluation of Sepsis

All infants with suspected sepsis should receive antibiotics while awaiting blood culture results. The remainder of the evaluation, including lumbar puncture (LP), can be completed once the infant is stabilized.


Patient History



  • Are there maternal factors that place the infant at risk for sepsis (see Table 56-1)?


  • Is there a family history of infection or other diseases (e.g., galactosemia) in newborns?


  • Does the infant have poor feeding, feeding intolerance (e.g., vomiting, abdominal distention), decreased activity, lethargy, or irritability?


Physical Examination

Signs of infection in the newborn infant are nonspecific and include the following disturbances:



  • Temperature—fever (>100.2°F [37.9°C]) or hypothermia (<96.8°F [36.0°C])


  • Neurologic— bulging fontanel, lethargy, irritability, weak suck or cry, hypotonia, hypertonia










TABLE 56-2 Differential Diagnosis of Sepsis
















































































Category

Disorder

Associated Symptoms and Signs

Differentiating Features


Metabolic

Hypoglycemia

Respiratory distress, jitteriness, lethargy, seizures

Hypoglycemia can occur with sepsis; check blood glucose in sick infants; especially common in infants of diabetic mothers and small for gestational age infants.

Hypocalcemia

Respiratory distress, jitteriness, seizures

Check calcium; especially common in infants of diabetic mothers and preterm infants.

Inborn error of metabolism

Lethargy, vomiting, seizures, tachypnea

Urea cycle defects and organic acidemias often present after the first few feedings.


Pulmonary

Respiratory distress syndrome

Respiratory distress in preterm infant

CXR shows hazy, “ground-glass” appearance; often indistinguishable from bacterial pneumonia.

Meconium aspiration

Respiratory distress in term infant Classic

CXR shows diffuse, patchy interstitial infiltrates with hyperinflation; may have severe cyanosis from pulmonary hypertension and right-to-left shunting.

Transient tachypnea of the newborn

Tachypnea without significant respiratory distress

CXR clear or with fluid in fissures; usually minimal supplemental oxygen requirement; usually seen after cesarean section delivery.


Cardiac

Cyanotic congenital heart disease: tetralogy of Fallot, TGA, tricuspid atresia, truncus arteriosus, TAPVR

Tachypnea, cyanosis unresponsive to oxygen, cardiac murmur, extra heart sounds, or abnormal S2

CXR without infiltrates but with abnormal pulmonary vasculature or cardiac silhouette; difference in pre- and postductal pulse oximetry; lack of response to hyperoxia test (PaO2, 100 mm Hg breathing 100% O2).

Congestive heart failure (VSD, patent ductus arteriosus, myocarditis, AVM—especially hepatic or cerebral)

Poor feeding, tachypnea, poor perfusion, hepatomegaly, S2

Congestive heart failure from a left-to-right shunt is unusual in the immediate newborn period when the pulmonary vascular resistance is high; onset is gradual.

Ductal-dependent lesions (aortic coarctation, hypoplastic left heart, critical pulmonic stenosis)

Poor perfusion, tachypnea, metabolic acidosis, cyanosis

Often sudden in onset, from hours to weeks after birth; check arterial blood gas, four-extremity blood pressures, and preand postductal pulse oximetry.


Neurologic

Hemorrhage

Pallor, hypotonia, tachycardia, hypotension

Especially common in preterm infants and following traumatic vaginal delivery.

Cerebral infarct

Seizures

May be associated with polycythemia or cocaine exposure; often idiopathic.


Gastrointestinal

Necrotizing enterocolitis

Feeding intolerance, abdominal distention, bloody stools

Usually associated with prematurity; abdominal radiograph may show pneumatosis, portal venous air, or free air; associated laboratory findings may include metabolic acidosis and thrombocytopenia.

Malrotation, volvulus

Bilious emesis, abdominal distention, bloody stools, and shock

All newborns with bilious emesis should be evaluated for GI obstruction; volvulus is a surgical emergency.


Hematologic

Profound anemia

Pallor, tachycardia, jaundice (if caused by hemolysis)

Hemolysis, perinatal bleeding (vasa previa, placental abruption), or postnatal hemorrhage.


AVM, arteriovenous malformation; CXR, chest radiograph; GI, gastrointestinal; PaO2, arterial oxygen tension; S2, second heart sound; S3, third heart sound; TAPVR, total anomalous pulmonary venous return; TGA, transposition of the great arteries; VSD, ventricular septal defect.










TABLE 56-3 Standard Sepsis Workup















Complete blood count with differential


Blood culture


Lumbar puncture (LP) and cerebrospinal fluid (CSF) analysisa


Urinalysis and urine cultureb


Chest radiographc


a If the infant is clinically stable and has a platelet count >50,000/mm3, an LP can be performed to obtain CSF for analysis of cell count, protein level, and glucose level, and for Gram stain and culture.



b If infant is <72 hr of life.



c If respiratory symptoms are present.




  • Respiratory—tachypnea (respiratory rate >60/minute), grunting, nasal flaring, retractions, hypoxemia, apnea


  • Cardiovascular—tachycardia, bradycardia, hypotension (systolic blood pressure <60 mm Hg in term infants), delayed capillary refill (<2 seconds)


  • Cutaneous—jaundice, mottled skin, cyanosis, or petechiae


  • Skeletal—focal bone tenderness


Laboratory Studies

Table 56-3 lists the studies included in a standard sepsis workup.

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Sep 14, 2016 | Posted by in PEDIATRICS | Comments Off on Neonatal Infections

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