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Neonatal sepsis kinara

Date post: 18-Feb-2017
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• Clinical syndrome of systemic illness accompanied by blood infection in infant younger than 90 days old.

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• Single most important cause of death in community….. Accounts for over half.

• Can be treated with antibiotics if discovered early.

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• Frequently bacterial, may also be viral (enterovirus, adenovirus, HSV) fungal (Candida spp), parasitic (TORCHES, malaria) or as a result of toxins produced by these microorganisms.

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The largest East African study – 242 positive blood cultures

Age < 7 days Age 7 – 59 days

1 E. coli 19% 1 Group A Streptococci 15%

2 Acinetobacter 12% 2 Group B Streptococci 13%

3 Klebsiella 10% 3 Strep. Pneumoniae 12%

4 Group B Streptococci 9% 4 Staph.

aureus 12%

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• Occurs in 0.5-8.0 in 1000 live births• Developing countries; 6-23 in 1000 live births• Highest rates n low birth weight infants,

premature infants, ill infants, those with RDS and those with maternal perinatal predisposing factors

• High mortality rate (13-25%)

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Risk Factors

1. Maternal; Chorioamnionitis, prolonged/preterm rupture of membranes, maternal bleeding, toxemia, precipitous delivery, maternal infection (UTIs), maternal GBS colonisation, >6 DVEs during labor in PROM, poor/no ANC, poor nutrition, difficult delivery.

2. Neonatal; prematurity, twinning(especially 2nd twin), galactosemia, IM administration of iron, face presentation, low apgar, aspiration, fetal distress,

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3. Environmental; overcrowding, understaffed units, improper sanitation, sick staff around neonates as well as poor delivery techniques.• Intravascular cannulas (S.epidermidis, S.

aureus), intravenous feeding, prolonged endotracheal intubation.

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1. Early onset; Occurs rapidly. 85% within 24hr, 5% within 24-48hr and rest within 48-72hr.

• Associated with acquisition of microorganisms from mother during passage through birth canal. Commonly pneumonia

• Microorganisms commonly associated with early onset; GBS, E. coli, coagulase neg Staph, H. influenza and L. monocytogenes.

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2. Late onset; at 4-90 days of life. Organism first colonises then invades, causing sepsis. Commonly meningitisAcquired from caregiving environment. Organisms implicated; coagulase negative Staphylococcus, S. aureus, E. coli, Klebsiella, Pseudomonas, Enterobacter, Candida, GBS, Serratia and AcinetobacterTrends in late onset sepsis show an increase in coagulase negative streptococcal sepsis, susceptible to first generation cephalosprorins.

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Portals of entry

• The infant’s skin, umbilicus, resp tract, GI tract, conjuctiva may be colonised from environment creating an entry point for invasive organisms that cause late onset sepsis.

• Vectors for such may be vascular or urinary catheters, other indwelling lines or contact with caregivers who have bacterial colonisation.

• Pneumonia is more common in early onset sepsis while meningitis and bacteremia are more common in late onset.

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Reasons for increased susceptibility in preterm infants

1. Immunological; ↓ IgG transplacental transfer, immaturity of immune systems

2. Poor surface defences; thin skin, easily traumatised

3. Invasive procedures; ET tube, IV catheters4. ↑risk of conditions predisposing to sepsis;

prolonged artificial ventilation, IV feeding5. ↑postnatal exposure; other babies in neonatal


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• Spectrum of sepsis ranges from microbial invasion of the bloodstream or intoxication with early signs of circulatory compromise (tachycardia, tachypnea, peripheral vasodilation and fever or hypothermia) to full-blown circulatory collapse with multiple organ dysfunction syndrome (MODS) and death.

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• In utero (transplacental)• Intrapartum (ascending); due to disruption of

membranes and during passage along birth canal.

• Postpartum (nosocomial/community acquired)

• Inflammatory cytokines most commonly produced in NNS; IL-6, 8 & TNFα.

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• The bacterial capsule polysaccharide adheres well to the plastic polymers of catheters.

• Proteins on the organism enhance attachment to the surface.

• This creates a capsule between the microbe and the catheter preventing C3 deposition and phagocytosis.

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• Pneumonia is the most common invasive bacterial infection in the newborn.

• PMNs are vital in elimination of bacteria but they are deficient in chemotaxis and killing in neonates because of ↓ adherence to endothelial lining reduced ability to marginate and leave intravascular space.

• Deficient humoral deficiency due to ↓IgG.• Infant T cells do not proliferate as fast as adult T cells.

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• Hypovolemia from intravascular fluid losses occurs through capillary leak.

• Cardiogenic shock results from the myocardial-depressant effects of sepsis.

• Distributive shock is the result of decreased systemic vascular resistance.

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• Age < 60/90days• One or more of:

– Change in level of activity– Bulging fontanelle– History of convulsions– Feeding difficulty– Temp ≥37˚C or <35.5˚C– Fast breathing? Resp rate ≥60bpm– Severe chest wall indrawing– Grunting– Cyanosis/ Pulse oximetry

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• Also check– Jaundice– Capillary refill– Severe pallor– PROM > 18hrs if aged <7days– Localized severe infection – joints, abdominal distension– Weight loss

• If no sign of serious illness check for:– Pus from eye, ear, umbilicus and redness of abdominal

skin– Few large, pus-filled blisters/ septic spots

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• Characterise symptoms ruling out differentials• Risk factors• Interventions• Complications

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PHYSICAL EXAMInitially nonspecificGeneral exam: sick looking, resp. distress, AVPU <A, LBW, Hyper/hypothermia(temp instability), pallor, mottled skin, skin rash, petechiae, jaundice• RS-tachypnea >60, grunting, LCWI, Intercostal recession,

head nodding, Low SpO2• CNS-Lethargy, excessive crying, bulging fontanelle,

irritability, convulsions, neck stiffness, sunset eyes, • GIT- feed intolerance, abd distension,

hepatosplenomegaly• CVS- Cap refill delayed, tachycardia or bradycardia,• Septic spots• Omphalitis- umbilical flare, oozing pus

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Predicting severe illness in young infants (2)

Symptom / Sign WHO Kenya

Reduced Feeding Ability Reduced / Abnormal Movements Breathing difficulty History of convulsions a

Temperature > 38.00C Respiratory rate > 60bpm Severe lower chest wall indrawing Cyanosis Prolonged capillary refill b

Bulging fontanelle







a – very uncommon, b – not assessed

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Lab:Blood culture, Complete blood count(I/T ratio), Lumbar Puncture(microscopy, culture, biochem, sensitivity), Swab of infected cord or skin lesion, Random Blood sugar (hypo/hyperglycemia), Coagulation studies(DIC), CRP, PITC, HSV PCR

Supportive Ix such as UECs, LFTs as requiredImaging:Chest xray, Cranial Ultrasound

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SUPPORTIVE• Ensure hydration/electrolyte balance.• Thermal-neutral environment.• Ensure nutrition (parenteral if indicated). Weigh daily• Isolate/barrier nursing especially if MRSA.• Remove all indwelling catheters.• Vit K 1ml PO and TEO if not given.

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Things to take into account:• Organisms• Antibiotic sensitivity• Is there meningitis?

Treatment could be supportive or definitive with close monitoring of.

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• Check for hypoglycaemia, treat if unable to measure glucose. 2mls/kg of D10

• Give Oxygen if cyanosed or resp rate >60bpm• Phenobarbital for seizures. IM LD 20mg/kg, MD 5mg/kgIV ABXGentamicin 3mg/kg or 5mg/kg (if >2kg)OD and xpen 50,000IU/kg BD. Xpen can be substituted with 3rd gen cephalosporin eg ceftriaxone 50mg/kg OD or cloxacillin if Staph. suspected. Vancomycin for MRSA.ORAL ABXAmoxycillin/ampicillin/flucloxacillin 50mg/kg BD• Acyclovir for HSV

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Duration of treatment for neonatal sepsisSigns of neonatal Infection in a baby breast feeding well.IV/IM Abx could be stopped after 48 hours if all the signs of possible sepsis have resolved and the child is feeding well and LP , if done, is normal.Give oral treatment to complete 5 days in total. Advise the mother to return with the child if problems recur.Skin infection with signs of generalised illness such as poor feeding IV/ IM Abx could be stopped after 72 hours if the child is feeding well without fever and has no other problem and LP , if done, is normal.Oral Abx should be continued for a further 5 days.Clinical or radiological pneumonia. IV/ IM Abx should be continued for a minimum of 5 days or until completely well for 24 hrs.Severe Neonatal Sepsis The child should have had an LP . I V/ I M Abx should be continued for a minimum of 7 days or until completely well if the LP is clearNeonatal meningitis or severe sepsis and no LP performed I V/ I M Abx should be continued for a minimum of 14 days.If Gram negative meningitis is suspected treatment should be iv for 3 weeks.

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Antibiotic prophylaxisXpen + Gentamicin given as soon as possible after birth to all newborns (term and preterms) with any one of the following risk factors:

PROM>18 hours mother with fever (T > 38⁰ C)Suspected or Confirmed chorioamnionitis Mother Rx for sepsis at any time during labour or in the last 24 hours before and after birth.

Given for 48-72 hours (at least 4 doses of Penicillin + 2 doses of gentamicin) and may be stopped if the baby has remained entirely well during this period. If there are no risk factors then DO NOT initiate Abx treatment. A well baby born preterm < 37 wks or Low birth weight with low risk factors does not require antibiotic treatment.

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• Good antenatal care.• Good delivery suite practices e.g aggressively

treat chorio-amnionitis with rapid delivery of the infant.

• Prevent nosocomial infections by observing infection control strategies such as hand washing between infants, reduce over crowding,good umbilical stump care.

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• Shock,circulatory collapse, DIC, severe jaundice, NEC.

• Long term…..due to meningitis/ mental retardation and other neurological disorders.

……due to NEC / short bowel syndrome following resection of non-viable gut.