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Neonatal Jaundice Clinical Case

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• Clinical/Perinatal Neonatal Case Presentation
• Published: 23 December 1999

Clinical Perinatal/Neonatal Case Presentation

Collaborative Primary Care of the Prematurely Born Infant

• Susan Bakewell-Sachs PhD CPNP 1 , 2 &
• Trude Haecker MD 2  

Journal of Perinatology volume  19 ,  pages 603–607 ( 1999 ) Cite this article

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Family Nurse Practitioner Program (S. B.-S.), College of New Jersey School of Nursing, Ewing, NJ

Susan Bakewell-Sachs PhD CPNP

The Children’s Hospital of Philadelphia (S. B.-S., T. H.), Philadelphia, PA

Susan Bakewell-Sachs PhD CPNP & Trude Haecker MD

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Bakewell-Sachs, S., Haecker, T. Collaborative Primary Care of the Prematurely Born Infant. J Perinatol 19 , 603–607 (1999). https://doi.org/10.1038/sj.jp.7200278

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Published : 23 December 1999

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DOI : https://doi.org/10.1038/sj.jp.7200278

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Original Author(s): Dr Phil Jordan and Dr Umberto Piaggio Last updated: 16th February 2021 Revisions: 19

• 1 Introduction
• 2.1 Physiological jaundice
• 2.2 Pathological jaundice
• 3 Risk factors and history
• 4 Clinical Presentation
• 5.1 Bilirubin
• 5.2 Further investigations
• 5.3 As needed
• 6.1 Phototherapy
• 6.2 Fluid intake
• 6.3 Exchange Transfusion
• 6.4 IV Immunglobulin
• 7 Complications
• 8 Prognosis
• 9 References

Introduction

Jaundice is t he yellow colouring of skin and sclera caused by the accumulation of bilirubin in the skin and mucous membranes.

Neonatal jaundice  occurs in 60% of term infants and 80% of preterm infants [1] and is caused by hyperbilirubinaemia that is unconjugated (divided into physiological or pathological) or conjugated (always pathological).  High levels of unconjugated bilirubin have acute harmful effects as well as long term damage if left untreated, such as kernicterus .

10% of breast fed babies are jaundiced at 1 month.

Types of Jaundice

Physiological jaundice.

Jaundice in a healthy baby, born at term, is normal and may result from:

• Increased red blood cell breakdown: in utero the fetus has a high concentration of Hb (to maximise oxygen exchange and delivery to the fetus) that breaks down releasing bilirubin as high Hb is no longer needed
• Immature liver not able to process high bilirubin concentrations

Starts at day 2-3, peaks day 5 and usually resolved by day 10.   The baby remains well and does not require any intervention beyond routine neonatal care.

Physiological jaundice can progress to pathological jaundice if the baby is premature or there is increased red cell breakdown e.g. Extensive bruising or cephalohaematoma following instrumental delivery.

Pathological jaundice

Jaundice which requires treatment or further investigation.

• Onset less than 24 hours
• ?previous siblings treated for jaundice/family history/maternal rhesus status
• Maternal blood group (type O most likely to produce enough IgG antibodies to cause haemolysis)
• Requires investigation and treatment
• Onset after 24 hours
• likely dehydrated ?breast fed baby establishing feeding
• increased haemolysis due to bruising/cephalohaematoma
• Unwell neonate: jaundice as a sign of congenital or post-natal infection
• Metabolic: Hypothyroid/pituitarism, galactosaemia
• Breast milk jaundice: well baby, resolves between 1.5-4 months
• GI: biliary atresia, choledhocal cyst

Risk factors and history

Risk factors for pathological hyperbilirubinaemia: to be asked in history

• Prematurity, low birth weight, small for dates
• Previous sibling required phototherapy
• Exclusively breast fed
• Jaundice <24 hours
• Infant of diabetic mother

Clinical Presentation

• Colour: All babies should be checked for jaundice with the naked eye in bright, natural light (if possible). Examine the sclera, gums and blanche the skin. Do not rely on your visual inspection to estimate bilirubin levels, only to determine the presence or absence of jaundice.
• Drowsy: difficult to rouse, not waking for feeds, very short feeds
• Neurologically: altered muscle tone, seizures-needs immediate attention
• Other: signs of infection , poor urine output, abdominal mass/organomegaly, stool remains black/not changing colour

Investigations

• Transcutaneous bilirubinometer (TCB) can be used in >35/40 gestation and >24 hours old for first measurement. TCB can be used for all subsequent measurements, providing the level remains <250 µmol/L and the child has not required treatment
• Serum bilirubin to be measured if <35/40 gestation, <24 hours old or TCB >250 µmol/L
• Infants that are not jaundice to the naked eye do not need routine bilirubin checking.  
• Total and Conjugated Bilirubin is important if suspected; liver or biliary disorder, metabolic disorder, congenital infection or prolonged jaundice. Do not subtract conjugated from total to make management decisions for hyperbilirubinaemia.

Further investigations

• Serum bilirubin for all subsequent levels
• Blood group (Mother and Baby) and DCT
• FBC for haemoglobin and haematocrit
• U&Es if excessive weight loss/dehydrated
• Infection screen if unwell or <24 hours including Microbiological cultures if infection suspected: blood, urine, CSF. Consider TORCH screen.
• Glucose-6-phosphate dehydrogenase especially if Mediterranean or African origin
• LFTs if suspected hepatobiliary disorder

Phototherapy

Figure 1 – NICE treatment threshold graph [3]

• Above: If level is on or above the phototherapy line for their gestation and age (in days) phototherapy should be initiated and bilirubin monitored
• >50µmol/L below, clinically well with no risk factors for neonatal jaundice do not routinely repeat level
• <50µmol/L below, clinically well repeat level within 18 hours (risk factors present) to 24 hours (no risk factors present)
• Repeat bilirubin 4-6 hours post initiation to ensure not still rising, 6-12 hourly once level is stable or reducing.
• NB. Maximum skin coverage, eye protection for babies, breaks for breastfeeding/nappy changes/cuddles to be coordinated to maximise phototherapy
• Stop phototherapy once level >50µmol/L below treatment line on the threshold graphs
• Check for rebound of hyperbilirubinaemia 12-18 hours after stopping phototherapy

Fluid intake

Do not give additional fluids with phototherapy unless indicated and if possible expressed maternal milk is preferred. If phototherapy intensified or feeding poorly consider NGT feeding or IV fluids.

Give consideration to underlying cause i.e. infection, biliary obstruction

Exchange Transfusion

This is the simultaneous exchange of the baby’s blood (hyperbilirubinaemic) with donated blood or plasma (normal levels of bilirubin) to prevent further bilirubin increase and decrease circulating levels of bilirubin.

Performed via umbilical artery or vein and is indicated when there are clinical features and signs of acute bilirubin encephalopathy or the level/rate of rise (>8.5µmol/L/hour) of bilirubin indicates necessity based on threshold graphs. This will require admission to an intensive care bed.

IV Immunglobulin

IVIG can be used as adjunct to intensified phototherapy in rhesus haemolytic disease or ABO haemolytic disease.

Complications

Kernicterus , billirubin-induced brain dysfunction, can result from neonatal jaundice. Bilirubin is neurotoxic and at high levels can accumulate in the CNS gray matter causing irreversible neurological damage . Depending on level of exposure, effects can range from clinically undetectable damage to severe brain damage.

Depends on underlying cause but if correctly and promptly treated prognosis is excellent.

Always refer to local trust guidelines.

1st Author: Dr Phil Jordan

Senior Reviewer: Dr Umberto Piaggio

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A Case of a Full-Term Infant With Symptomatic Patent Ductus Arteriosus Successfully Closed With Indomethacin Treatment: Consideration of Mechanism for Ductus Arteriosus Closure

Junya tanabe.

a Postgraduate Clinical Training Center, Shimane University Faculty of Medicine, Shimane, Japan

Shigeki Nakajima

b Department of Pediatrics, Shimane University Faculty of Medicine, Shimane, Japan

Kenji Yasuda

Naoaki shibata, takeshi taketani, kazuaki tanabe.

c Division of Cardiology, Shimane University Faculty of Medicine, Shimane, Japan

Graphical abstract

• • Full-term infants have mature DA closure mechanisms.
• • Premature infants show delayed lung metabolism of prostaglandin.
• • IND may be a useful therapy for PDA.

Introduction

Patent ductus arteriosus (PDA) accounts for approximately 5% to 10% of all congenital heart diseases. Most cases of PDA are diagnosed and treated from infancy through childhood, but those clinically diagnosed in adulthood also are not rare. Basically, the presence of a heart murmur and symptomatic cases are considered to be indications for PDA treatment. If medical management does not lead to PDA closure, then indomethacin (IND) is administered intravenously, mainly in preterm infants. 1 , 2 However, the effectiveness of IND injection in full-term infants with PDA remains undetermined. We herein report our experience with a 12-day-old, full-term infant with symptomatic PDA successfully treated with IND therapy.

Case Presentation

A 12-day-old girl was referred to our hospital because of tachypnea and retractive breathing. The patient was born via elective cesarean section at 37 weeks and 0 days of gestation, weighing 2,955 g, with Apgar scores of 6/9. On day 6 after birth, a heart murmur was noted, and echocardiographic results led to the diagnosis of PDA. Tachypnea, retractive breathing, and tachycardia were observed, which were indicative of symptomatic PDA. Considering the potential need for surgical treatment, the patient was transferred to our hospital by neonatal transport on day 12 after birth. Her weight was 3,015 g, body temperature was 37.3°C, blood pressure was 87/43 mm Hg, heart rate was 155 beats/min and regular, respiratory rate was 67 breaths/min, and blood oxygen saturation (lower extremity) was 96% (room air). A continuous murmur was heard at the left upper sternal border. Respiratory sounds were clear, and tachycardia and retractive breathing were observed. Blood tests revealed no abnormalities. Chest radiography showed that the cardiothoracic ratio was 67%, indicating cardiomegaly, and lung permeability was reduced bilaterally ( Figure 1 ). Twelve-lead electrocardiography showed that the heart rate was 150 beats/min and regular, with right-axis deviation and left atrial overload with the downward deflection of the P wave in lead V 1 .

Chest radiography on admission demonstrates a cardiothoracic ratio (CTR) of was 67%, indicating cardiomegaly, and reduced lung permeability.

Initial echocardiography on admission demonstrated the presence of a large PDA measuring 6 mm on the aortic side and 5 mm on the pulmonary arterial side (Krichenko type A), and a left-to-right shunt of blood flow was shown by color Doppler ( Figure 2 ). A patent foramen ovale (PFO) was also present, with left-to-right shunt flow ( Figure 3 ). The right and left ventricles were almost the same size (left ventricular end-diastolic dimension 98% of normal predictive value; Figure 4 ), indicating the presence of volume overload in the left heart due to the PDA and in the right heart due to the PFO. The treatment strategy was to administer three doses of IND with a 12-hour interval between doses (first course, 0.2 mg/kg; second and third courses, 0.25 mg/kg); if no effects were obtained, we would perform surgery (PDA clipping). Thirty-six hours after first IND administration, no continuous murmur was heard with a stethoscope. Echocardiography revealed a reduction in PDA diameter to approximately 1 mm and rapid systolic left-to-right shunt flow ( Figure 5 ). Improvements were also noted in the heart rate (from 150–170 beats/min to 130 beats/min), as well as in the respiratory rate (from 70 to 40 breaths/min). Retractive breathing also showed resolution. No side effects were observed, such as decreased urine volume, hypoglycemia, or bleeding. The condition had improved at least to the point at which emergency surgery was not necessary. As the patient showed a favorable response to IND without side effects, the second course of IND therapy was initiated after a 1-day washout. Closure of the PDA was confirmed after the fourth dose of IND, and the treatment was therefore terminated. The fluid restriction was lifted, and the absence of PDA recanalization was confirmed. The patient remained in good systemic condition and was discharged from the hospital on day 20 after birth. Her 1-month checkup showed a substantial improvement in the cardiothoracic ratio (51%; Figure 6 ), and there were no signs of PDA recanalization ( Figure 7 ).

Echocardiography on admission demonstrates the presence of a large PDA measuring 6 mm on the aortic side and 5 mm on the pulmonary arterial side, and a left-to-right shunt of blood flow is shown by color Doppler. AAo , Ascending aorta; DAo , descending aorta; MPA , main pulmonary artery; RPA , right pulmonary artery.

A PFO was also present, with left-to-right shunt flow. LA , Left atrium; RA , right atrium.

Apical four-chamber view shows that the right ventricle (RV) and left ventricle (LV) are almost the same size, indicating the presence of volume overload.

After IND treatment, echocardiography reveals a reduction in PDA diameter to approximately 1 mm. AAo , Ascending aorta; MPA , main pulmonary artery.

Chest radiography at 1-month checkup shows a substantial improvement in the cardiothoracic ratio (CTR).

Echocardiography at 1-month checkup shows no signs of PDA recanalization. AAo , Ascending aorta; LPA , left pulmonary artery; MPA , main pulmonary artery; RPA , right pulmonary artery.

Mechanisms for ductus arteriosus (DA) closure are roughly classified into two types. One is the constriction of the DA itself following the start of pulmonary respiration at birth, induced by oxygen stimulation resulting from increased partial pressure of oxygen in blood and the disappearance of vasodilators due to decreased production of prostaglandin E 2 (PGE 2 ) and reduced PGE 2 receptor (EP4). 3 , 4 The other is attributable to the histologic structure of the DA. During the fetal period, PGE 2 is produced mainly in the placenta and DA; PGE 2 stimulation increases the production of hyaluronic acid, which induces the migration of DA smooth muscle cells, causing intimal thickening of the DA.Additionally, one of the characteristics of the histologic structure of the DA is poor formation of elastic fibers. Unlike the great arteries, a vessel without elastic fibers is unlikely to be restored to its original size after intense vasoconstriction. 5 , 6 , 7 There is also a relatively old report suggesting that elastic fibers were abnormally distributed in the vascular wall of the DA (particularly elastic fibers under endothelial cells) in infants ≥4 months of age. 8 Therefore, it is reasonable that persistently PDA until adulthood may have a different histologic structure.

Because a full-term infant has a mature DA closure mechanism and is highly reactive to oxygen, functional closure of the DA generally occurs within a few days after birth. Following vascular remodeling, the anatomic closure of the DA is completed in several days to a few months. In a premature infant, however, the DA is poorly responsive to oxygen, and premature infants with compromised or immature respiratory function show a delay in lung metabolism of prostaglandin, resulting in delayed or failed closure of the PDA. 9

Symptomatic premature infants with PDA are managed through fluid restriction, correction of anemia, use of diuretics, and other appropriate interventions. If the DA remains patent, the prostaglandin synthesis inhibitor IND is injected intravenously. IND can affect the smooth muscle tone of the DA and promote ductal constriction. The PDA closure rate in premature infants on IND is said to be 70% to 90%. 10 In a study that examined IND therapy for PDA in full-term infants, the response rate was 61%. 11 There was no significant difference between responders and nonresponders of IND in gestational age, body weight, Apgar score at 1 min, minimum diameter of the DA before treatment, age at the initiation of treatment, or DA flow pattern. If full-term infants have unstable perinatal conditions such as hypoxia or acidosis, it may lead to delayed DA closure and subsequent heart failure. Delayed ductal closure often perpetuates hypoxia in infants and vice versa. Apgar scores can provide essential information on the perinatal condition, which plays an important role in the development of PDA. 12 The present patient was a full-term infant with a mature DA closure mechanism. However, her Apgar scores at 1 min were low (6/9), indicating that she had some form of pulmonary prematurity. Lung metabolism of PGE 2 was thereby delayed, resulting in persistent and symptomatic PDA. This patient had a PFO, and left-to-right shunt flow was observed on day 12 after birth, but the possibility of right-to-left shunt of PFO leading to systemic hypoxemia at birth cannot be denied. However, the patient had a good response to IND therapy. Still, as shown by the present case, there is a possibility that IND may be a useful therapy for PDA without side effects and that it would, therefore, be worthwhile to consider the use of IND therapy before performing surgery.

We experienced a full-term infant with symptomatic PDA successfully treated with IND administration. Even in full-term infants, unstable perinatal conditions such as hypoxia or acidosis may lead to delayed prostaglandin metabolism and DA closure. Thus, IND administration might be a useful medical treatment option before considering surgery for PDA in full-term infants.

Conflicts of interest: The authors reported no actual or potential conflicts of interest relative to this document.

Management of Neonatal Sepsis

Nov 17, 2014

540 likes | 1.18k Views

Management of Neonatal Sepsis. Niki Kosmetatos, MD Anthony Piazza, MD Ira Adams-Chapman, MD J. Devn Cornish, MD Emory University Department of Pediatrics. Note: Dr. Cornish does not have any financial relationships to disclose nor will he discuss any non-approved drug or device uses.

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• fetal tachycardia
• maternal temp 38
• maternal intrapartum fever 38

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Management of Neonatal Sepsis Niki Kosmetatos, MD Anthony Piazza, MD Ira Adams-Chapman, MD J. Devn Cornish, MD Emory University Department of Pediatrics Note: Dr. Cornish does not have any financial relationships to disclose nor will he discuss any non-approved drug or device uses.

Babies and Bacteria… Gram positive bacteria (anthrax) Gram negative bacteria (pseudomonas)

…Don’t mix!

Incidence • Mortality • 13-69% world wide • 13-15% of all neonatal deaths (US) (8th cause) • Meningitis • 0.4-2.8/1000 live births (US 0.2-0.4/1000) • Mortality 13-59%; US 4% of all neonatal deaths • Sepsis • 1-21/1000 world wide; US,1-2/1000 live births • Culture proven 2/1000 (3-8% of infants evaluated for sepsis); 10-20/1000 VLBW • Prematures <1000 g 26/1000 1000 - 2000 g 8-9/1000

Predisposing Factors General Host Factors Prematurity (OR 25 if < 1,000 gms) Race – GBS sepsis blacks>whites (x4) Sex – sepsis & meningitis more common in males, esp. gram negative infections Birth asphyxia, meconium staining, stress Breaks in skin & mucous membrane integrity (e.g. omphalocoele, meningomyelocoele) Environmental exposure Procedures (e.g. lines, ET-tubes)

Predisposing Factors • Maternal/Obstetrical Factors • General– socioeconomic status, poor prenatal care, vaginal flora, maternal substance abuse, known exposures, prematurity, twins • Maternal infections –chorioamnionitis (1-10% of pregnancies), fever (>38° C/100.4° F), sustained fetal tachycardia, venereal diseases, UTI/bacteriuria, foul smelling lochia, GBS+ (OR 204), other infections • Obstetrical manipulation – amniocentesis, amnioinfusion, prolonged labor, fetal monitoring, digital exams, previa/abruption? • Premature & Prolonged ROM, preterm labor

Predisposing Factors Overall sepsis rate 2/1000 Maternal Fever 4/1000 PROM 10-13/1000 Fever & PROM 87/1000

Preterm Labor/PROM • Prematurity (~10%) 15-25% due to maternal infection • >18-24h term; >12-18h preterm • Bacterial infection •  synthesis of PG • Macrophage TNF/IL stimulate PG synthesis, cytokine release** • Release of collagenase & elastase ROM • + Amniotic fluid cultures 15% (with intact membranes)

SEPSIS ORGANISMS (all babies) • Group B strep (most common G+) 41% • Other strep 23% • Coliforms(E. coli most common G-) 17% • Staph aureus 4% • Listeria2% • Nosocomial infections • Candida • Note: 73% G+ and 27% G-

SEPSIS ORGANISMS (VLBW) • Group B strep (most common G+) 12% • Other strep 9% • Coliforms(E. coli most common G-) 41% • CONS 15% • Listeria2% • Nosocomial infections • Candida 2% • Note: 45% G+ and 53% G- Source: Stoll et al PedInfDis 2005, 24:635

Routes of Infection • Transplacental/Hematogenous • Ascending/Birth Canal • Aspiration • Device Associated Infection • Nosocomial • Epidemic

Transplacental/Hematogenous • Organisms (Not just “TORCHS”) Toxoplasmosis Parvovirus Rubella Gonorrhea Cytomegalovirus Mumps Herpes* TB Syphilis Varicella Acute Viruses HIV Coxsackie Polio Adenovirus GBS Echo Malaria Enterovirus Lyme

Ascending/Birth Canal • Organisms - GI/GU flora, Cervical/Blood E. Coli Herpes GBS Candida Chlamydia HIV UreaplasmaMycoplasma Listeria Hepatitis Enterococcus Anaerobes Gonorrhea Syphilis HPV

Nosocomial • Organisms – Skin Flora, Equipment/Environment Staphylococcus – Coagulaseneg & pos MRSA Klebsiella Pseudomonas Proteus Enterobacter Serratia Rotavirus Clostridium – C dificile Fungi

Infection Timing • Onset • Early Onset 1st 24 hrs 85 % 24-48 hrs 5% • Late Onset 7-90 days

Symptoms • Non-specific/Common • Respiratory distress (90%) - RR, apnea (55%), hypoxia/vent need (36%), flaring/grunting • Temperature instability, feeding problems • Lethargy-irritability (23%) • Gastrointestinal – poor feeding, vomiting, abdominal distention, ileus, diarrhea • Color—Jaundice, pallor, mottling • Hypo- or hyperglycemia • Cardiovascular – Hypotension(5%), hypoperfusion, tachycardia • Metabolic acidosis NICHD data

Symptoms • Less common • Seizures • DIC • Petechiae • Hepatosplenomegaly • Sclerema • Meningitis symptoms • Irritability, lethargy, poorly responsive • Changes in muscle tone, etc.

Evaluation • Non-specific • CBC/diff, platelets – ANC, I/T ratio • Radiographs • CRP • Fluid analysis – LP, U/A • Glucose, lytes, gases • Specific – Cultures, stains • Other – immunoassays, PCR, DNA microarray

Results “Trigger Points” • CBC • WBC <5.0, abs neutro <1,750, bands >2.0 • I/T ratio > 0.2* • Platelets < 100,000 • CRP > 1.0 mg/dl • CSF > 20 WBC’s with few or no RBC’s • Radiographs: infiltrates on CXR, ileus on KUB, periosteal elevation, etc.

Treatment • Prevention – vaccines, GBS prophylaxis, HAND-WASHING • Supportive – respiratory, metabolic, thermal, nutrition, monitoring drug levels/toxicity • Specific – antimicrobials, immune globulins • Non-specific – IVIG, NO inhibitors & inflammatory mediators

Neonatal Sepsis:the special case ofGroup B Strep Sepsis

Mother to Infant Transmission GBS colonized mother (20-30% in US) 50% 50% Non-colonized newborn Colonized newborn 98% 2% Early-onset sepsis, pneumonia, meningitis Asymptomatic

GBS SEPSIS RISK FACTORS • Previous GBS-infected baby • Gestational age <37 wks • Maternal disease (esp. GBS UTI) • Ruptured membranes > 18 hours • Location of delivery (e.g., home) • Infant/Fetal symptommatology • Clinical suspicion Note: incidence has fallen 80% since CDC prevention guidelines were published in 1996

Mothers in labor or with ROM should be treated if: • Chorioamnionitis • History of previous GBS+ baby • Mother GBS+ or GBS-UTI this preg. • Mother’s GBS status unknown and: • < 37 wks gestation • ROM ≥ 18 hrs • Maternal temp ≥ 38o (100.4oF)

Group B Strep Association formed 1st ACOG & AAP statements CDC draft guidelines published Rate of Early- and Late-onset GBS Disease in the 1990s, U.S. Consensus guidelines Schrag, New Engl J Med 2000 342: 15-20

GBS SEPSIS INFANTS TO BE SCREENED • Maternal “chorioamnionitis” • Maternal illness (i.e. UTI, pneumonia) • Maternal peripartum fever > 38o(100.4oF) • Prolonged ROM ≥ 18 hrs (≥ 12 hrs preterm) • Mother GBS+ with inadequate treatment (< 4 hrs) • No screening necessary if C-section delivery with intact membranes

GBS SEPSIS INFANTS TO BE SCREENED • Prolonged labor (> 20 hrs) • Home or contaminated delivery • “Chocolate-colored”/foul smelling amniotic fluid • Persistent fetal tachycardia • SYMPTOMATIC INFANT • treat immediately (in DR if possible)

GBS SEPSIS SEPSIS SCREEN • CBC with differential • Platelet count • Blood culture x 1-2 (ideally 1 ml) • Chest X-ray &/or LP if symptommatic • Close observation and frequent clinical evaluation • Role of CRP

Algorithm for Neonate whose MotherReceivedIntrapartum Antibiotics Maternal Rx for GBS? Maternal antibiotics for suspected chorioamnionitis? Signs of neonatal sepsis? Full diagnostic evaluation * Empiric therapy++ Gestational age <35 weeks? Limited evaluation$ & Observe ≥ 48 hours If sepsis is suspected, full diagnostic evaluation and empiric therapy ++ Duration of IAP before delivery < 4 hours # No evaluation No therapy Observe ≥ 48 hours** YES YES YES NO NO * CBC, blood cx, & CXR if resp sx. If ill consider LP. ++ Duration of therapy may be 48 hrs if no sx. $ CBC with differential and blood culture # Applies only to penicillin, Ampicillin, or cefazolin. ** If healthy & ≥ 38 wks & mother got ≥ 4 hours IAP, may D/C at 24 hrs. NO

Careful Observation & Immediate Antibiotics Careful Observation pending review of screen • Symptomatic INFANT • Maternal intrapartum fever > 38.6o • “Chocolate” or foul smelling fluid • Ill mother • Fetal tachycardia • Home delivery • Maternal fever < 38.6o • PROM • Mat GBS with < 2 dose abx (-) Screen(+) Screen(-) Screen(+) Screen Cont abx until bld cx neg for 48o if asympt. Use clini-cal judgement for cessation of abx if pt is/was sympt d/c abx; careful obs and monit bld cx until d/c Careful obs and monit bld cx until d/c Initiate abx & cont until bl cx (-) for 48o. Clinical judgement for cessation of abx if pt sympt Blood Culture Positive Initiate, resume or continue abx therapy and treat for 7-10 days for gram pos organism or longer if gram neg organism cultured. LP may be performed at the discretion of attending, especially in seriously symptomatic pt

SEPSIS SIGNS and SYMPTOMS • temp instability • lethargy • poor feeding/residuals • resp distress • glucose instability • poor perfusion • hypotension • bloody stools • abdominal distention • bilious emesis • apnea • tachycardia • skin/joint findings

SEPSIS LABORATORY EVALUATION • Provide added value when results are normal • high negative predictive value • low positive predictive value • abnl results could be due to other reasons and not infection • IT < 0.3, ANC > 1,500 (normal) do not start abx, or d/c abx if started, if pt remains clinically stable • IT > 0.3, ANC < 1,500 consider initiation of abx pending bldcx in “at-risk” pt who was not already begun on antibiotics for other factors

SEPSIS LABORATORY EVALUATION • Positive screen • total WBC < 5,000 – I/T > 0.3 • ANC < 1,500 – platelets < 100,000 • Additional work-up • CXR, urine cx, and LP as clinically indicated • CRP • no added value for diagnosis of early onset sepsis • best for negativepredicativevalue or when used serially • not to be used to decide about rx, duration of rx or need for LP • positive results for a single value obtained at 24 hrs ranges > 4.0 - 10.0 mg/dL

SEPSIS TREATMENT • Review protocol • Antibiotics • Ampicillin 100 mg/kg/dose IV q 12 hours • Gentamicin 4 mg/kg/dose IV q 24 hours • IM route may be used in asymptomatic pt on whom abx are initiated for maternal risk factors or to avoid delays when there is difficulty obtaining IV • For meningitis: Ampicillin 200-300 mg/kg/d • Symptomatic management • respiratory, cardiovascular, fluid support

Prognosis • Fatality rate 2-4 times higher in LBW than in term neonates • Overall mortality rate 15-40% • Survival less likely if also granulocytopenic (I:T > 0.80 correlates with death and may justify granulocyte transfusion).

Infection and Outcome • Leviton, et al, Ped Res 1999 • 1078 infants <1500 grams and/or <32 wks • Infants with IUI were more likely to have PVL • Chorioamnionitis was associated with a 4-fold increased risk of CP (17% vs. 3%) • Nelson, et al reported increased cytokine response in population based study of term but not preterm infants

Infection and ND Outcome • IUI and postnatal infection both appear to increase the risk for adverse ND outcome • Role of inflammatory mediators/SIRS in brain injury in the preterm infant • Pressure passive CNS circulation • Direct cytotoxicity to the developing brain • Inherent vulnerability of the oligodendrocyte precursor

Postnatal Infection and ND Outcome: PDI < 70 Infection Groups Compared to Uninfected by Logistic Regression Clinical Infection (N=1415) Sepsis Alone (N=1740) Sepsis+NEC (N=252) Sepsis+Meningitis (N=152) 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 Adjusted Odds Ratios and 95% CIs Stoll, JAMA 2004

Postnatal Infection and ND Outcome: Cerebral Palsy Infection Groups Compared to Uninfected by Logistic Regression Clinical Infection (N=1415) Sepsis Alone (N=1740) Sepsis+NEC (N=252) Sepsis+Meningitis (N=152) 0.0 1.5 2.5 3.0 3.5 0.5 1.0 2.0 Adjusted Odds Ratios and 95% CIs Stoll, JAMA 2004

Late Onset Infection • Majority of ELBW infants will develop late onset sepsis • Significant associated morbidity and mortality • CONS still the most common pathogen • Gram-negative pathogens increasing in prevelance and are associated with higher mortality rate

Neonatal Infection and Outcome • Increased risk of adverse ND outcome in ELBW infants with LOS • Increased risk of poor growth at 18 months AA in ELBW with LOS • Poor outcome associated with NEC • ?Role of cytokines and inflammatory mediators in CNS

Prevention of Nosocomial Infections • HANDWASHING • HANDWASHING • Universal precautions • Limit use devices and catheters • Minimize catheter manipulation • Nursery design • Meticulous skin care • Education

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