Neonatal sepsis nursing: EOS vs. LOS, signs, NCLEX tips

Neonatal sepsis is a systemic bacterial, viral, or fungal infection occurring in the first 28 days of life. Its burden now falls mainly on preterm infants. In the NICHD Neonatal Research Network’s 2015–2017 cohort, 29% of preterm infants with early-onset sepsis died, while every term infant with early-onset sepsis survived; among VLBW infants with late-onset sepsis, mortality reaches 36% with gram-negative organisms. For nursing students, sepsis is one of the highest-yield neonatal topics on NCLEX-RN and a daily clinical reality in newborn nurseries and NICUs. Signs are subtle and non-specific; a low or unstable temperature is a classic red flag that is easy to blame on the environment; and the window between “looks slightly off” and hemodynamic collapse can be frighteningly narrow.

This reference covers the two major syndromes – early-onset sepsis (EOS) and late-onset sepsis (LOS) – along with their distinct pathogens and risk factors, the full clinical picture, the diagnostic workup including the Kaiser Permanente EOS Calculator, empiric antibiotic regimens, nursing priorities, CLABSI prevention, monitoring responsibilities, complications, and 10 high-yield NCLEX tips. Use alongside the neonatal nursing reference, neonatal resuscitation guide, and adult sepsis reference for contrast with the adult syndrome.

Quick reference: EOS vs LOS

Early-onset sepsis (EOS)

Early-onset sepsis occurs within the first 72 hours of life and is acquired through vertical transmission from the mother. The neonate aspirates or ingests infected amniotic fluid, vaginal secretions, or maternal blood during delivery. Once the organisms gain access – especially through the pulmonary epithelium or gut – the neonatal immune system, which is characterized by immature innate immunity, deficient opsonization, low complement levels, and a reduced neutrophil reserve, often cannot contain the infection before it becomes systemic.

Group B Streptococcus (GBS) is the leading cause of EOS in term infants in the United States. It accounted for about 43% of EOS cases in the 2006–2009 NICHD cohort (Stoll BJ et al., Pediatrics, 2011); in the 2015–2017 cohort, E. coli overtook it overall (37% vs 30%), although GBS still caused 52% of term-infant cases, and 53% of the GBS cases in that cohort were born to mothers whose antenatal GBS screen was negative (Stoll BJ et al., JAMA Pediatrics, 2020). Since intrapartum antibiotic prophylaxis (IAP) was introduced in the 1990s, CDC Active Bacterial Core surveillance has tracked GBS EOS falling from 1.7 per 1,000 live births in 1993 to 0.2 per 1,000 in 2023. IAP is considered adequate when penicillin, ampicillin, or cefazolin is administered at least 4 hours before delivery (AAP 2019).

Escherichia coli is the leading cause of EOS in preterm infants and VLBW neonates, responsible for about 29% of EOS cases in the 2006–2009 NICHD cohort and 37% in 2015–2017, when 52% of preterm EOS cases were E. coli. Unlike GBS, E. coli EOS rates have not declined with GBS prevention measures and rose in VLBW infants between the two cohorts (8.68 vs 5.07 per 1,000 live births). Ampicillin resistance is now the norm: only 22% of tested E. coli isolates in the 2015–2017 cohort were ampicillin-susceptible, and 8% were resistant to both ampicillin and gentamicin, which is why gentamicin carries the gram-negative coverage in the empiric regimen.

Listeria monocytogenes is a less common but clinically important pathogen – it is acquired from contaminated foods (unpasteurized cheeses, deli meats, raw sprouts) during pregnancy, crosses the placental barrier, and can cause severe early-onset disease including meningitis. It responds to ampicillin, which is why ampicillin remains in the EOS empiric regimen.

EOS risk factors

The Neonatal Early-Onset Sepsis Calculator (see Diagnostics section) synthesizes the most predictive maternal-obstetric risk factors:

• Prolonged rupture of membranes (≥18 hours) – loss of the amniotic fluid barrier and ascending microbial colonization
• Maternal GBS colonization – universal vaginal–rectal GBS culture at 36 0/7–37 6/7 weeks’ gestation. ACOG Committee Opinion 797 (2020) moved this window from the older 35–37 week recommendation and replaced the obstetric components of the CDC 2010 guideline; GBS prevention guidance is now issued by ACOG and AAP rather than CDC
• Intraamniotic infection (formerly clinical chorioamnionitis) – ACOG’s preferred term since Committee Opinion 712 (2017, reaffirmed 2025, with a July 2024 Clinical Practice Update) is intraamniotic infection, also described as “Triple I” (intrauterine inflammation or infection or both). ACOG makes the presumptive diagnosis when maternal temperature is ≥39.0°C, or 38.0–38.9°C plus at least one of: maternal leukocytosis, purulent cervical drainage, or fetal tachycardia. A temperature of 38.0–38.9°C with none of those findings is classed as isolated maternal fever, a separate category
• Prematurity – gestational age is the single strongest predictor of EOS (AAP 2018); in the NICHD 2015–2017 cohort, incidence was 1.08 per 1,000 live births overall and 18.47 per 1,000 at 22–28 weeks
• Inadequate or absent intrapartum antibiotic prophylaxis – GBS-positive mothers who did not receive adequate IAP before delivery
• Maternal intrapartum fever ≥38°C – independent of GBS status and antibiotic administration

Late-onset sepsis (LOS)

Late-onset sepsis begins at or after 72 hours of life and is predominantly nosocomial – acquired from the NICU environment, healthcare workers’ hands, and indwelling devices rather than the maternal birth canal. The NICHD Neonatal Research Network uses the 72-hour cutoff for VLBW infants (birthweight <1,500 g). The 7-day cutoff you may also see comes from GBS surveillance, where late-onset GBS disease means onset from 7 days to under 3 months of age. Preterm infants are especially exposed: about 40% of late-onset GBS cases occur in infants born at ≤34 6/7 weeks, and neither maternal IAP nor any newborn EOS practice prevents late-onset disease (AAP 2018).

Coagulase-negative Staphylococcus (CoNS) – primarily S. epidermidis – is the most common LOS pathogen in US NICU cohorts, accounting for 48% of culture-confirmed LOS episodes in VLBW infants, with gram-positive organisms overall causing 70% (Stoll BJ et al., Pediatrics, 2002). CoNS lives on skin and thrives in biofilm on intravascular catheters. Critically, CoNS bacteremia in a premature infant is clinically indistinguishable from bacteremia caused by more virulent organisms. In a symptomatic VLBW neonate, a CoNS-positive culture is treated as probable true infection until the clinical course and paired or repeat cultures show otherwise.

Staphylococcus aureus – including MRSA – causes a smaller proportion of LOS cases but is associated with higher morbidity, focal infection (osteomyelitis, endocarditis, pneumonia), and longer hospital stays. MRSA LOS requires vancomycin; MSSA responds to oxacillin or nafcillin.

Candida species – primarily C. albicans and C. parapsilosis – cause a smaller share of LOS than bacteria but are among the deadliest: in the NICHD VLBW cohort, 32% of infants with fungal LOS died (Stoll BJ et al., Pediatrics, 2002). Risk factors include extreme prematurity, prior broad-spectrum antibiotic exposure, TPN, central venous catheters, and endotracheal intubation (Downey LC et al., Early Human Development, 2010). Prophylactic fluconazole reduced Candida colonization and invasive disease in extremely-low-birthweight infants in a single-center randomized trial (Kaufman D et al., NEJM, 2001). A later multicenter randomized trial in infants under 750 g found that fluconazole reduced invasive candidiasis but did not significantly reduce the composite of death or invasive candidiasis (Benjamin DK Jr et al., JAMA, 2014), so prophylaxis is generally reserved for NICUs with a high baseline invasive candidiasis rate rather than used universally.

The central line-associated bloodstream infection (CLABSI) connection is direct: the primary driver of NICU LOS is the presence of a central venous catheter – umbilical venous catheter (UVC), percutaneously inserted central catheter (PICC), or surgically placed Broviac. CLABSI prevention bundles (hand hygiene, maximal sterile barrier, chlorhexidine skin antisepsis, optimal insertion site, daily line necessity review) are the most effective nursing-driven intervention for reducing LOS incidence.

Clinical signs and presentation

Neonatal sepsis signs are notoriously non-specific. The infant “just doesn’t look right” is a clinically valid nursing concern – and one of the most important things to communicate to the medical team. Early recognition depends on pattern recognition across multiple subtle signs.

Key signs by system

The single most important clinical message for nursing students: a neonate that was stable and feeding well who suddenly becomes hypothermic, lethargic, and feeding poorly has sepsis until proven otherwise. Waiting for a fever or an obvious source wastes the hours that matter most, so notify the provider and anticipate a sepsis workup.

Diagnostic workup

Complete blood count with differential

The CBC is part of almost every sepsis evaluation, but the AAP is blunt about its limits: EOS cannot be diagnosed with a CBC or CRP, and in two large multicenter studies of term and late-preterm infants, none of the CBC components performed well. Interpret results in context:

• White blood cell count – low counts are more concerning than high ones. Only extreme values carried meaningful likelihood ratios (WBC <5,000/µL, ANC <2,000/µL, or I:T >0.3 in one study; WBC <1,000/µL, ANC <100/µL, or I:T >0.5 in the other), and even those had very low sensitivity. A WBC above 20,000/µL was not associated with EOS (AAP 2018)
• Immature-to-total neutrophil ratio (I:T ratio) – calculated as bands + metamyelocytes + myelocytes divided by total neutrophils. Many unit protocols flag values above 0.2, but an elevated I:T should prompt reassessment of the infant and cannot diagnose sepsis by itself. Gestational age, sex, mode of delivery, maternal preeclampsia, and prolonged rupture of membranes all shift white cell values without infection (AAP 2018), and a normal value does not rule sepsis out
• Thrombocytopenia – platelet count <150,000/µL is the usual definition; severe thrombocytopenia (<50,000/µL) with prolonged PT/PTT suggests evolving DIC. Platelet counts did not predict EOS in the AAP-cited studies, so their main use is tracking complications
• Timing – a CBC drawn in the first hour after birth barely discriminates infected from uninfected infants; in a cohort of 67,623 term and late-preterm newborns, the area under the curve for WBC count rose from 0.52 at under 1 hour to 0.87 at 4 hours or later (Newman TB et al., Pediatrics, 2010). A single normal early CBC does not exclude sepsis

Blood cultures

Blood culture is the diagnostic gold standard. The AAP 2018 clinical reports call for at least 1 mL of blood; a second culture or bottle helps show whether a skin commensal such as CoNS is a true pathogen, which matters most in late-onset sepsis. Critical nursing responsibilities:

• Draw cultures before starting antibiotics – this is NCLEX-tested and is the standard of care, because antibiotic pre-treatment sharply reduces culture yield. The one exception runs the other way: if obtaining the culture would meaningfully delay antibiotics in a deteriorating infant, treat first. Antibiotics should not be held waiting on difficult access
• Use aseptic technique. The FDA relabeled chlorhexidine gluconate in 2012 from “do not use” in infants under 2 months to “use with care” in premature infants and infants under 2 months, and most US NICUs now use CHG for line-related antisepsis. Follow institutional policy on agent and concentration, and remove residual CHG after the procedure to limit skin irritation and absorption. Povidone-iodine is an alternative but carries a risk of transient hypothyroidism from iodine absorption in preterm infants with repeated exposure; 70% isopropyl alcohol is also used
• Minimum volume: pediatric blood culture bottles generally need at least 1 mL of blood for optimal recovery of organisms; modern systems reliably detect bacteremia of 1–10 colony-forming units per mL at that volume (AAP 2018), so an underfilled bottle undermines the test the whole workup depends on
• Two separate cultures let the team compare growth when a skin commensal such as CoNS appears, which helps separate true infection from contamination (AAP 2018)
• Once cultures are sterile at 36–48 hours of incubation, the AAP advises stopping empiric antibiotics unless there is clear evidence of a site-specific infection, so accurate culture timing documentation directly affects how long the infant stays on antibiotics

C-reactive protein (CRP) and procalcitonin

CRP lags behind the infection, so a single early CRP is often falsely reassuring. In a prospective study of suspected neonatal infection, the CRP drawn at the initial evaluation detected only 35% of proven early-onset sepsis, while CRP measured the next morning detected 79%; three serial values had a negative predictive value of 99.7% (Benitz WE et al., Pediatrics, 1998). Serial normal CRPs can therefore support stopping antibiotics when cultures are negative (Benitz WE, Clinics in Perinatology, 2010).

Procalcitonin (PCT) rises naturally over the first 24–36 hours after birth even in healthy newborns, and both CRP and PCT also rise with non-infectious stressors such as asphyxia and pneumothorax. The AAP’s position is that single values of either test are neither sensitive nor specific enough to guide EOS decisions; consistently normal values over the first 48 hours are associated with the absence of EOS, but serial abnormal values alone should not be used to continue antibiotics when cultures are negative (AAP 2018).

Lumbar puncture (LP)

LP for CSF analysis is indicated in any neonate with a positive blood culture (the AAP says it should be performed if not already done), clinical deterioration despite antibiotics, or in whom meningitis cannot be excluded. Meningitis complicates about 10% of early-onset and 31% of late-onset GBS disease (AAP 2019), and it does not always announce itself in the blood: in a cohort of 9,111 neonates ≥34 weeks who had an LP, 38% of those with culture-proven meningitis had a negative blood culture (Garges HP et al., Pediatrics, 2006).

CSF interpretation in neonates (normal ranges differ substantially from adults and older children):

Perform LP before starting antibiotics if the infant is clinically stable enough to tolerate the procedure – antibiotic pre-treatment reduces CSF culture yield. If the infant is too unstable (apnea, hemodynamic compromise), begin antibiotics immediately and perform LP when stabilized.

Neonatal early-onset sepsis calculator

The Kaiser Permanente Neonatal EOS Calculator (Escobar GJ et al., Pediatrics, 2014; available at neonatalsepsiscalculator.kaiserpermanente.org) applies to infants born at ≥34 weeks’ gestation and uses five maternal-obstetric variables to calculate an individual infant’s probability of EOS per 1,000 births:

1. Gestational age at delivery
2. Highest maternal antepartum temperature (°C or °F)
3. Duration of rupture of membranes (hours)
4. GBS status (positive, negative, unknown/not done)
5. Adequacy of intrapartum antibiotic prophylaxis

A common point of confusion for students: well-appearing, equivocal, and clinical illness are inputs the clinician enters. The calculator first produces a baseline risk from the maternal-obstetric variables, then asks the clinician to classify the infant’s examination during the first 12 hours into one of those three categories, and multiplies the baseline risk accordingly to produce a final risk estimate. The management recommendation follows from that final number: below roughly 1 per 1,000, routine vitals and no antibiotics; at or above roughly 1 per 1,000, blood culture and enhanced observation; at or above roughly 3 per 1,000, blood culture and empiric antibiotics. An infant classified as clinically ill receives empiric antibiotics regardless of the maternal risk estimate.

Clinicians also enter their local baseline EOS incidence, which sets the prior probability the maternal variables adjust. The calculator reduces unnecessary antibiotic exposure in well-appearing low-risk newborns – a significant advance over the older categorical risk-factor approach. The original model was derived from infants born in 1993–2007; because universal antepartum GBS screening and IAP guidance have changed since then, Kaiser re-estimated it on 412,595 infants born at ≥35 weeks in 2010–2020 (Kuzniewicz MW et al., Pediatrics, 2024). The updated model’s sensitivity was 0.80 versus 0.76 for the original (difference not statistically significant), with empiric antibiotics recommended for 3.7% versus 3.5% of infants, and the authors concluded both versions remain effective.

Nursing interventions and treatment

Empiric antibiotic regimens

Nursing priorities

Vascular access and specimen collection Establish IV access promptly. Blood cultures are drawn before any antibiotic dose. Work efficiently: for term infants and older children, the 2026 Surviving Sepsis Campaign children’s guidelines recommend antimicrobials ideally within 1 hour of recognition when septic shock is suspected, and within 3 hours for probable sepsis without shock after a time-limited evaluation. Document exact times for culture collection and first antibiotic administration.

Temperature regulation Neonates cannot thermoregulate independently. Place the infant in a servo-controlled incubator or radiant warmer set to maintain a neutral thermal environment. Monitor core temperature continuously; hypothermia perpetuates metabolic acidosis and worsens outcomes. Avoid overheating – hyperthermia in a septic neonate worsens cerebral injury and increases oxygen demand.

Cardiorespiratory monitoring Continuous cardiorespiratory monitoring (heart rate, respiratory rate, oxygen saturation by pulse oximetry). Be alert to apnea, bradycardia, and desaturation – in a septic neonate these signal clinical deterioration and warrant a sepsis-focused response even in an infant with a history of prematurity-related apnea. Have suction and resuscitation equipment immediately available. See the neonatal resuscitation reference for NRP algorithm review.

Glucose monitoring Sepsis drives both hypoglycemia (increased glucose consumption, poor feeding) and hyperglycemia (stress response, particularly in VLBW). Monitor glucose by point-of-care testing at the frequency and target range set by unit protocol, checking more often while the infant is unstable or not feeding. See neonatal hypoglycemia nursing reference for glucose management protocols.

Central line care (CLABSI prevention bundle) For infants with existing CVCs – UVC, PICC, or Broviac – the CLABSI prevention bundle is non-negotiable:

• Hand hygiene before every line access (single most important intervention)
• Maximal sterile barrier for line insertion (cap, mask, sterile gown and gloves, full drape)
• Chlorhexidine skin antisepsis at insertion, used “with care” in infants under 2 months per FDA labeling and institutional policy; wipe residual CHG from the skin afterward in premature infants
• Daily necessity assessment – does this infant still need the central line? Remove it as soon as clinically safe
• Scrub-the-hub: disinfect the hub, needleless connector, or injection port with friction before every access, for the contact time your unit’s bundle specifies
• Minimize line entries – bundle laboratory draws and medication administration

Antibiotic monitoring – gentamicin Gentamicin is nephrotoxic and ototoxic, and neonatal pharmacokinetics vary substantially by gestational age and postnatal age. Key nursing responsibilities:

• Draw the trough immediately before the second dose, and have the result available before the third dose (NICE NG195)
• Target trough: NICE adjusts the dosing interval to keep troughs below 2 mg/L (2 mcg/mL), and below 1 mg/L if the course runs longer than 3 doses; US units set their own targets, so follow the local protocol
• High trough → notify the provider, who will usually extend the interval; NICE advises against withholding a dose only because a trough result is delayed, unless there is evidence of impaired renal function (elevated serum urea or creatinine, or anuria)
• Trend serum creatinine and urine output, and report oliguria (<1 mL/kg/hour) promptly
• Cumulative gentamicin exposure → risk of sensorineural hearing loss; document and flag for audiology follow-up

Family-centered care Neonatal sepsis is terrifying for parents. Explain what sepsis is in plain language, what the workup involves, why antibiotics are started before results return, and what signs indicate improvement or deterioration. Encourage parental presence and skin-to-skin contact when medically stable – this supports thermoregulation, breastfeeding initiation, and attachment. Cluster care activities to minimize stimulation in critically ill neonates; excessive handling increases oxygen demand and metabolic stress.

Jaundice monitoring Sepsis can worsen jaundice through hemolysis, hepatic dysfunction, and direct bilirubin elevation. Monitor transcutaneous bilirubin or serum bilirubin per protocol; direct/conjugated hyperbilirubinemia in a septic neonate is a red flag for hepatic involvement. See neonatal jaundice nursing reference.

Complications and prognosis

Sepsis in neonates – particularly VLBW infants – carries a risk of serious complications that extend well beyond the acute infection:

Bacterial meningitis complicates about 10% of early-onset and 31% of late-onset GBS disease (AAP 2019). Clinical signs are often absent or nonspecific (no neck stiffness, often no fever). Survivors carry lasting harm: among 43 term and near-term survivors of GBS meningitis evaluated at a mean age of 6.8 years, 25% had mild-to-moderate impairment and 19% had severe impairment (Libster R et al., Pediatrics, 2012). This is why lumbar puncture is a standard part of the evaluation once a blood culture is positive.

Septic shock results from overwhelming infection with cardiovascular compromise – hypotension, poor perfusion, metabolic acidosis, organ dysfunction. For infants born at term, management follows the Surviving Sepsis Campaign children’s guidelines, updated in 2026 (Weiss SL et al., Pediatric Critical Care Medicine, 2026), which replaced the 2020 edition. Students should know the scope caveat: like the 2020 edition, the 2026 guidelines cover children born at 37 weeks’ gestation or later, so preterm sepsis management follows local NICU protocol.

Within that scope, the 2026 guidelines recommend measuring blood lactate at initial evaluation. Where intensive care is available, they suggest up to 40–60 mL/kg of bolus fluid in the first hour, given as 10–20 mL/kg boluses, and they favor balanced or buffered crystalloid over 0.9% saline. On vasoactive support, the 2020 edition had already moved away from the older teaching of dopamine as first-line, suggesting epinephrine or norepinephrine instead; the 2026 panel found insufficient evidence to prefer epinephrine over norepinephrine and now suggests starting vasoactive infusions through a peripheral vein rather than delaying for central access. Urgent source control (central line removal, drainage of a focal collection) sits alongside these.

Disseminated intravascular coagulation (DIC) – activation of the coagulation cascade by endotoxin and cytokines, resulting in consumption of clotting factors and platelets, paradoxical bleeding and thrombosis simultaneously. Monitor PT, PTT, fibrinogen, D-dimer, and platelet count. Fresh frozen plasma (FFP), cryoprecipitate, and platelet transfusions manage the coagulopathy while treating the underlying infection.

Necrotizing enterocolitis (NEC) – a devastating intestinal inflammatory condition disproportionately affecting VLBW preterm infants; sepsis is both a trigger and a complication of NEC. Signs include abdominal distension, bloody stools, bilious emesis, and absence of bowel sounds. Pneumatosis intestinalis (air in the bowel wall on abdominal X-ray) is the classic radiographic sign. See the NEC nursing reference for Bell staging and management.

Death – in the NICHD 2015–2017 cohort, 16% of all infants with early-onset sepsis died, all of them preterm (29% of preterm cases; median gestational age of those who died, 25.5 weeks). Among VLBW infants with late-onset sepsis, mortality was 18% overall, 36% with gram-negative organisms, and 32% with fungal infection. Survivors of severe neonatal sepsis have increased rates of neurodevelopmental impairment, chronic lung disease, and recurrent infection during infancy.

NCLEX tips

1. A falling temperature is a sepsis sign in a newborn. Neonates, especially preterm infants, may answer infection with temperature instability or hypothermia instead of a fever. A neonate who drops from 37°C to 35.8°C needs a sepsis assessment alongside any warming measures.

2. Blood cultures before antibiotics – always. Draw the blood culture (at least 1 mL; many units draw two) before administering the first antibiotic dose. This is NCLEX-tested repeatedly. Antibiotic pre-treatment significantly reduces culture yield.

3. Ampicillin + gentamicin is the EOS empiric standard. This combination, endorsed in the AAP’s 2018 early-onset sepsis clinical reports, covers GBS, E. coli, and Listeria – the three major EOS pathogens. Memorize it, and note that the AAP specifically discourages broader-spectrum empiric regimens, which drive resistance without improving outcomes.

4. GBS is the number one cause of EOS in term infants. Group B Streptococcus dominates EOS in term infants (52% of term cases in the NICHD 2015–2017 cohort), while E. coli leads in VLBW/preterm neonates.

5. No lab test diagnoses neonatal sepsis except a culture. An elevated I:T ratio (often flagged above 0.2), a low WBC, or a high CRP should raise concern, but the AAP states that EOS cannot be diagnosed with a CBC or CRP. Blood or CSF culture confirms it.

6. Lumbar puncture before antibiotics when the infant is stable. Antibiotic pre-treatment dramatically reduces CSF culture yield. If the infant tolerates the procedure, LP before the first dose. If unstable – treat first, LP when stabilized.

7. CoNS (coagulase-negative Staphylococcus) is the most common LOS pathogen in the NICU. S. epidermidis and other CoNS cause about half of NICU LOS episodes in VLBW infants, primarily through central line contamination.

8. Hand hygiene is the single most important CLABSI prevention intervention. Before every central line access, before and after patient care – consistent hand hygiene with soap and water or alcohol-based gel reduces nosocomial LOS more than any other single nursing action.

9. Gentamicin requires trough monitoring. Draw the trough immediately before the second dose. An elevated trough signals accumulation and nephrotoxicity risk, and usually means a longer dosing interval. Monitor urine output and creatinine throughout the course.

10. Bulging fontanelle and seizures are late signs of meningitis. By the time the fontanelle is bulging or the neonate is seizing, meningitis is advanced. The goal is LP-confirmed diagnosis and antibiotic initiation before these signs appear. A neonate with sepsis signs + altered tone + high-pitched cry should prompt LP consideration even before the fontanelle is bulging.

Related references

• Neonatal nursing reference – neonatal vital signs, NICU assessment, Ballard score, NEC staging, and NICU nursing priorities
• Necrotizing enterocolitis nursing – Bell staging, pneumatosis, feeding holds, and surgical indications
• Neonatal resuscitation nursing – NRP algorithm, APGAR scoring, PPV technique, chest compression protocol
• Neonatal hypoglycemia nursing – glucose screening protocols, at-risk groups, dextrose gel, IV dextrose management
• Neonatal jaundice nursing – TSB thresholds, phototherapy management, exchange transfusion criteria, breastfeeding jaundice
• Sepsis nursing reference (adult) – Sepsis-3 definitions, qSOFA, 1-hour SEP-1 bundle, vasopressor selection; compare with neonatal presentation
• Preterm labor nursing – prematurity as the strongest EOS risk factor; tocolysis, corticosteroids, GBS prophylaxis in the obstetric context

References

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