Neonatal Sepsis (NS) PDF
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Dr. Amal Awad
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Summary
This presentation provides an overview of neonatal sepsis (NS), a life-threatening condition in newborns. It covers the common causative organisms, epidemiology, and pathogenesis of neonatal infections. The presentation also discusses clinical features, diagnosis, and treatment approaches.
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Neonatal sepsis (NS) DR. AMAL AWAD Neonatal sepsis (NS) is defined as clinical syndrome of bacteraemia with systemic signs and symptoms of infection in the first four weeks of life. ETIOLOGY Common organisms identified: 1. Escherichia coli. 2. Group B Streptococci. 3. Listeria...
Neonatal sepsis (NS) DR. AMAL AWAD Neonatal sepsis (NS) is defined as clinical syndrome of bacteraemia with systemic signs and symptoms of infection in the first four weeks of life. ETIOLOGY Common organisms identified: 1. Escherichia coli. 2. Group B Streptococci. 3. Listeria monocytogenes. 4.Others: Coagulase negative staphylococci. Streptococcus pneumoniae. Klebsiella pneumoniae. Acinetobacter species. Pseudomonas aeruginosa. Candida. EPIDEMIOLOGY Incidence: 1-8 cases per 1,000 live births. Mortality: 13-70% world wide. 13-15% of all neonatal deaths (USA) (8 th cause). Sex: Males > Females. Age: premature infants Pathogenesis Neonatal infections are unique in several ways: 1. Infectious agents can be transmitted from the mother to the fetus or newborn infant by diverse modes. 2. New-born infants are less capable of responding to infection because of 1 or more immunologic deficiencies. 3. Coexisting conditions often complicate the diagnosis and management of neonatal infections. 4. The clinical manifestations of newborn infections vary and include subclinical infection, mild to severe manifestations of focal or systemic infection, and, rarely, congenital syndromes resulting from in utero infection. The timing of exposure, inoculum size, immune status, and virulence of the etiologic agent influence the expression of disease. Pathogenesis 5. aternal infection that is the source of trans placental fetal infection is often undiagnosed during pregnancy because the mother was either asymptomatic or had nonspecific signs and symptoms at the time of acute infection. 6. A wide variety of etiologic agents infect the new-born, including bacteria, viruses, fungi, protozoa, and mycoplasmas. 7. Immature, very low birthweight (VLBW) newborns have improved survival but remain in the hospital for a long time in an environment that puts them at continuous risk for acquired infections. Classification Neonatal sepsis include the following: Congenital infection —major risk factor is maternal infection. Early-onset sepsis (birth to 7 days)—transplacental, ascending, or intrapartum, manifests as: 1. Pneumonia (Frequently) 2. Less commonly as: Septicemia. Meningitis. Late-onset sepsis (8 to 28 days)—acquired in hospital, home, or community, manifests as: 1.Septicemia. 2.hematogenous seeding may result in focal infections, such as meningitis (in 75% of cases), osteomyelitis (group B streptococci, S. aureus), arthritis (gonococcus, S. aureus, Candida albicans, gramnegative bacteria), and urinary tract infection (gramnegative bacteria). Early Versus Late Neonatal Sepsis CLINICAL FEATURES Manifestations of neonatal sepsis are usually VAGUE and demand A HIGH INDEX OF SUSPICION for early diagnosis. Most common manifestations include: 1. Respiratory distress in early onset NS. 2. Altered feeding behavior in a well established feeding newborn (aspiration, vomiting, etc). 3. Baby who was active, suddenly or gradually becomes lethargic, inactive or unresponsive and refuses to suckle. 4. Temperature instability: Hypo- or hyperthermia. 5. Skin: Poor peripheral perfusion, cyanosis, pallor, petechiae, rashes, or jaundice. 6. Metabolic:Hypo- or hyperglycemia or metabolic acidosis. Diagnosis A. Non-specific: White blood cell count and differential: Neutropenia can be a threatening sign (< 1,800/cmm). Immature to Total neutrophil (I:T) ratio ≥ 0.2 is predictive (Normal: ˂ 0.16). Acute phase reactants: C-Reactive Protein (CRP): rises early. ESR rises > 15 mm 1 st hr. Platelet count: Decreases, a late sign and nonspecific. Others: – Bilirubin, glucose, sodium. Diagnosis B. Definitive, specific: Cultures: Blood: Confirms sepsis. Urine: CSF: May be useful in clinically ill new-borns or those with positive blood cultures. C: Radiology Chest X-Ray: – For infants with respiratory symptoms. Renal ultrasound: – For infants with accompanying UTI. CT scan: – For infants with probable meningitis or seizures. Differential Diagnosis Respiratory distress syndrome (RDS). Metabolic diseases. Hematologic diseases. CNS diseases. Cardiac diseases. Other infections (e.g. ToRCH infections). TREATMENT 1. Antibiotics: Should be based on culture & sensitivity Antibiotics are used to suppress bacterial growth, allowing the infant's defense mechanisms time to respond. 2. Supportive therapy In addition, support measures, such as assisted ventilation and cardiovascular support, are equally important to the management of the infant. TREATMENT 1. Antibiotics: A combination of ampicillin and an aminoglycoside (usually gentamicin) for 10 to 14 days is effective treatment against most organisms responsible for early-onset sepsis. The combination of ampicillin and cefotaxime also is proposed as an alternative method of treatment. If meningitis is present, the treatment should be extended to 21 days or 14 days after a negative result from a CSF culture. TREATMENT 2. Supportive therapy: Respiratory: Oxygen and ventilation as necessary. Cardiovascular: Support blood pressure with volume expanders. Hematologic: Treat DIC. CNS: Treat seizures with phenobarbital. Metabolic: Correct hypo-/hyperglycemia and metabolic acidosis. PREVENTION Good antenatal care. Maternal infections diagnosed and treated early. Babies should be breastfed early. Infection control policies applied in the unit