Neonatal sepsis (sepsis on new born) with case presentation

Newborn sepsis is a severe infection in an infant younger than 28 days old. A newborn may become infected before, during, or after birth. Newborn sepsis can be hard to diagnose. Early diagnosis and treatment are the best ways to stop sepsis.

1. Submitted by Joel Rajan u Neonatal sepsis (sepsis on new born) & case presentation

2. Neonatal sepsis  is a type of  neonatal infection and specifically refers to the presence in a  new born baby of a bacterial  bloodstream infection  (BSI) (such as  meningitis ,  pneumonia ,  pyelonephritis , or  gastroenteritis ) in the setting of fever INTRODUCTION

3. 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 ETIOLOGY

4. 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: Septicaemia , 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, gram negative bacteria), and urinary tract infection (gram negative bacteria). Classification

5. • Respiratory distress syndrome (RDS). • Metabolic diseases. • Hematologic diseases. • CNS diseases. • Cardiac diseases. • Other infections (e.g. TORCH infections). Differential Diagnosis

6. Respiratory distress in early onset NS. Altered feeding behaviour in a well established feeding new-born (aspiration, vomiting, etc). Baby who was active, suddenly or gradually becomes lethargic, inactive or unresponsive and refuses to suckle. Temperature instability : Hypo- or hyperthermia. Skin : Poor peripheral perfusion, cyanosis, pallor, petechiae, rashes, or jaundice. Metabolic : Hypo- or hyperglycaemia or metabolic acidosis CLINICAL FEATURES

7. Diagnosis  B. Definitive, specific: Cultures: • Blood : Confirms sepsis. • Urine : • CSF : May be useful in clinically ill newborns 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.  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,

8. • 1. Antibiotics:  Should be based on culture & sensitivity  Antibiotics are used to suppress bacterial growth, allowing the infant's defence mechanisms time to respond. • 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  In addition, support measures, such as assisted ventilation and cardiovascular support, are equally important to the management of the infant. 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-/hyperglycaemia and metabolic acidosis.

9. Case Presentation

10. A 19-year-old woman, gravida 2, delivered vaginally, a 1.95 kg girl at 34 weeks gestation. She had 6 prenatal consultations and the pregnancy was uneventful. No intrapartum antibiotics were given. Membranes ruptured spontaneously six hours before delivery, and there was no maternal fever. The infant was born vigorous with Apgar scores of 8 at one minute and 9 at five minutes. Case Report

11. Mild tachypnoea was noted ( The tachypnoea was transient and lasted only three hours)  She was pink , active and with good peripheral perfusion At 18 hours of age the infant had severe apnoea , mottled skin and delayed capillary refill time Symptoms

12. The clinical course was fulminant, with respiratory failure , severe metabolic acidosis and profound arterial hypotension unresponsive to aggressive fluid resuscitation , and high doses of dopamine and dobutamine Clinical features

13. A cell blood count showed leukopenia (2,100 × mm 3 ), neutropenia (1,400 × mm 3 ) normal platelet count of 265,000 × mm 3   normal C- reactive protein (4 mg/dL). A chest radiograph showed a reticulogranular pattern in both lung fields, which was suggestive of pneumonia . Laboratory Diagnosis

14. Neonatal  Streptococcus Pneumoniae  sepsis [The infant was pronounced dead at 23 hours of postnatal age] Diagnosis

15.  The blood culture grew penicillin-sensitive  Streptococcus Pneumoniae  28 A serotype. Mother’s vaginal swab was also positive for the same bacteria and serotype. Bacteriological test

16. She was quickly intubated, and placed on mechanical ventilation. Umbilical artery and umbilical vein catheters were placed. Ampicillin and gentamicin were begun after a blood culture was obtained. Lumbar puncture was not done due to the critical condition of the infant. Treatment

17. Neonatal  Streptococcus Pneumoniae  sepsis is uncommon high mortality Rate more recent reports have shown that most cases occurred during the first week of life, predominantly within the first 48 hours. Early onset infections can be acquired through a colonized birth canal or rarely, by hematogenous transplacental transmission, secondary to maternal bacteraemia  In our case the mother’s genital tract was colonized, so most likely, the infant acquired the infection, through the birth canal Note: Streptococcus Pneumoniae  is not normally present in the vagina, colonization of the lower genital tract can occur through orogenital contact with a nasopharyngeal carrier or with a person suffering from acute upper respiratory tract pneumococcal infection. Conclusion

18. In conclusion, strategies to prevent early- onset NSPS are evolving. Some interventions we think are mandatory, these include treatment for all pregnant women with a positive vaginal culture to  Streptococcus Pneumoniae , and clinicians’ increased awareness of SPNS and prompt aggressive antibiotic treatment of affected neonates. Further surveillance studies, assessment of risk factors for SPNS, as well as evaluation of other strategies such as vaccination during pregnancy, aiming to protect these infants are needed

19. Good antenatal care. Maternal infections diagnosed and treated early. Babies should be breastfeed early. Infection control policies applied in the unit PREVENTION

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