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Sepsis Neonatorum

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Definition

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Symptoms

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Diagnosis

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Prognosis and Treatment

Sepsis

in a newborn (

sepsis neonatorum

) is an infection that spreads throughout the baby’s body.Sepsis occurs in less than 1 percent of newborns (1 out of every 100), but accounts for up to 30percent of deaths in the first few weeks of life. Infection is 5-10 times more common in prematurenewborns and in babies weighing less than 5½ pounds than in normal-weight, full-term newborns.Complications experienced during birth, such as premature or prolonged rupture of the membranes orinfection in the mother, put the newborn at increased risk of infection.

Symptoms

The onset of what is called early-onset neonatal sepsis is within six hours of birth in over half the casesand within 72 hours in the great majority of cases. Sepsis that begins four or more days after birth iscalled late-onest sepsis, and is probably an infection acquired in the hospital nursery (a nosocomialinfection). In both types of neonatal sepsis, the infection may be only in the bloodstream, or mayspread to the lungs (pneumonia), brain (meningitis), bone (osteomyelitis), joints, or other organs in thebody. Typical symptoms of a newborn with sepsis include:

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listlessness (a very sleepy baby)

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feeding problems

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a high OR low temperatureOther symptoms include:

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difficulty breathing, rapid breathing, or apnea (when the baby stops breathing)

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seizures

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excessive jitteriness

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repeated vomiting or diarrhea

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a swollen abdomen

Diagnosis

The organism that is causing the infection may be identified by taking cultures of the blood as well asfrom other sites of the body. Urine samples are often cultured for bacteria to look for an infection inthe urinary tract. Because only small samples of blood and other body fluids are taken, sometimes noorganism is found. However, the infant may still be treated if other laboratory studies or the infant’sclinical appearance strongly suggest an infection.Other laboratory studies that doctors use to detect an infection include the following:

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White Blood Cell Count and Differential:

When an infant is fighting an infection, theirwhite blood cell count may either go up, as the infant’s body produces more infection-fightingcells, or it might also go down if the infant has used up all of their white blood cells fightingthe infection and can no longer keep up with their production of white cells. Another changethat is seen when an infant is fighting an infection is an increase in the percentage of immature white cells. This is due to the increased production rate of white blood cells, suchthat more immature white blood cells are being released into the blood stream. This higherpercentage of immature white cells is sometimes referred to as a “left-shift,” and is one of thethings that can tell the doctors that the infant has an infection.

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C-Reactive Protein (CRP):

This is a laboratory test that measures a protein that is a non-specific marker for inflammation and therefore infection. If the infant has two normal CRPlevels measured 24 hours apart, then there is a 99% chance that the infant does not have aninfection. Therefore, this test is most useful in ruling out an infection.

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Lumbar Puncture:

If the doctor suspects meningitis, which is more common if something hasgrown in the baby’s blood culture, a spinal tap, or lumbar puncture will be performed. Lumbarpunctures allow the doctor to obtain a small amount of cerebrospinal fluid (CSF), which is theprotective fluid that surrounds the brain and the spinal cord. The CSF can then be cultured todetermine if the bacteria has spread to the nervous system. The doctor, nurse practitioner, or physician’s assistant will very carefully insert a special spinalneedle between two vertebrae, or backbones, in the baby’s back at a level below where theactual spinal cord ends, so there is no danger that the needle will come into contact with thebaby’s spinal cord. After a very small amount of fluid is removed, the needle is taken out, anda band-aid placed on the baby’s back.

The spinal needle is inserted (left) below where the spinal cord ends (right.)

Prognosis and Treatment

Sepsis in a newborn is treated with antibiotics given intravenously. Antibiotics are often started evenbefore laboratory and culture results are available. The doctor may then switch to a different antibioticthat is more specific to the baby’s infection once the results of laboratory tests are back. The length of antibiotic treatment varies depending on the infant’s clinical status, laboratory test results, and kind of infection. If blood cultures and other laboratory tests are all negative, antibiotics may be stopped after48 hours of treatment. If the infant’s cultures are positive, or if the laboratory tests and clinical statusare suggestive of infection, the infant will be treated with antibiotics, usually anywhere from 7-14 days.When appropriately treated with antibiotics and cared for in the intensive care unit, the great majorityof newborns with sepsis live without any long-term problems.

Pathophysiology of neonatal sepsis

: The infectious agents associated with neonatal sepsis havechanged over the past 50 years. S aureus and E coli were the most common infectious hazards forneonates in the 1950s in the United States. GBS then replaced S aureus as the most common gram-positive agent, causing early-onset sepsis during the next decades. During the 1990s, GBS and E colicontinued to be associated with neonatal infection; however, coagulase-negative S aureus is nowobserved more frequently. Additional organisms, such as L monocytogenes, Chlamydia pneumonia,Haemophilus influenzae, Enterobacter aerogenes, and species of Bacteroides and Clostridium havealso been identified in neonatal sepsis.Meningoencephalitis and neonatal sepsis syndrome can also be caused by infection with adenovirus,enterovirus, or coxsackievirus. Additionally, sexually transmitted diseases and viral diseases, such asgonorrhea, syphilis, herpes simplex virus (HSV), cytomegalovirus (CMV), hepatitis, HIV, rubella,toxoplasmosis, Trichomonas vaginalis, and Candida species, have all been implicated in neonatal

infection. Bacterial organisms with increased antibiotic resistance have also emerged and have furthercomplicated the management of neonatal sepsis. The colonization patterns in nurseries and personnelare reflected in the organisms currently associated with nosocomial infection. Infants with lower birthweight and infants who are less mature in today's neonatal intensive care units (NICUs) have increasedsusceptibility to these organisms.Staphylococcus epidermidis, or coagulase-negative Staphylococcus is increasingly seen as a cause of nosocomial or late-onset sepsis, especially in the premature infant. It is considered the leading causeof late-onset infections for this population. Its prevalence is related to its preference for the plasticmediums found in cannulas and shunts, which increases its introduction via umbilical catheters andother indwelling lines. The bacterial capsule polysaccharide adheres well to the plastic polymers of thecatheters. The adherence creates a capsule between microbe and catheter, which prevents C3deposition and phagocytosis. Also, proteins found in the organism [AtlE and SSP-1] enhanceattachment to the surface of the catheter.Biofilms are formed at the site from the aggregation of organisms that have multiplied with theprotection provided by the adherence to the catheter. Slimes are produced at the site from theextracellular material formed by the organism, which provides a barrier to the host defense, as well asantibiotic action. Therefore, it can be seen that slime production increases the difficulty to treatcoagulase-negative staphylococcal septicemia. The toxins formed by this organism have beenassociated with necrotizing enterocolitis. Coagulase-negative Staphylococcus is a frequentcontaminate of blood and cerebrospinal fluid (CSF) cultures; therefore, it can be a false indicator of coagulase-negative staphylococcal septicemia. The neonate is unable to respond effectively to infectious hazards because of deficits in thephysiological response to infectious agents. The neonatal neutrophil or polymorphonuclear (PMN) cell,which is vital for effective killing of bacteria, is defective in chemotaxis and killing capacity. Decreasedadherence to the endothelial lining of blood vessels reduces their ability to marginate and leave theintravascular area to migrate into the tissues. Once in the tissues, they may fail to deaggregate inresponse to chemotactic factors. Also, neonatal PMNs are less deformable; therefore, they are lessable to move through the extracellular matrix of tissues to reach the site of inflammation andinfection. The limited ability of neonatal PMNs for phagocytosis and killing of bacteria is impaired whenthe infant is clinically ill. Lastly, neutrophil reserves are depleted easily because of the diminishedresponse of the bone marrow, especially in the premature infant.Neonatal monocyte concentration and function are at adult levels; however, macrophage chemotaxisis impaired and continues to exhibit decreased function into early childhood. Macrophages aredecreased in the lungs and probably also in the liver and spleen. The chemotactic and bacteriocidalactivity and the antigen presentation by these cells are not fully competent. Cytokine production bymacrophages is decreased, which may be associated with a corresponding decrease in T-cellproduction. T cells are found in early gestation in fetal circulation and increase in number from birth to about age 6months; however, these cells represent an immature transitory population. Neonates are deficient in Tcells with the memory cell surface phenotype; however, the number of these T cells increases withmaturity as the neonate is exposed to antigenic stimuli. These antigenically naive cells do notproliferate as readily as adult T cells when activated. Also, neonatal T cells do not effectively producethe cytokines that assist with B-cell stimulation and differentiation and with bone marrow stimulation