Presentation is loading. Please wait.

Presentation is loading. Please wait.

Case Discussion 2016/12/06 R2郭舒涵.

Similar presentations


Presentation on theme: "Case Discussion 2016/12/06 R2郭舒涵."— Presentation transcript:

1 Case Discussion 2016/12/06 R2郭舒涵

2 Patient profile Name:謝O帆之女 Chart number: 1793xxxx Age: 0 d/o
Gender: female Admission date: 2016/11/26 Chief complaint: Nasal flaring and grunting after birth

3 Present illness 0-day-old girl infant
Born to a 33 year-old mother, G1P1, GA 39+6 weeks Prenatal care at 陳澤彥OBS, and was uneventful Mother had no GDM, gestational hypertension/preeclampsia except seizure history since childhood with lamotrigine use during pregnancy fever with APN and treated with antibiotics for 2 weeks at gestational age about 5 to 6 months, no more fever after that GBS(-) at GA 37 weeks not received amniocentesis Level II sonography : no obvious fetal anomaly

4 Present illness-2 Due to labor pain, she was admitted to delivery room at 11/25 night No PROM, no maternal fever This baby was born at 2016/11/26 00:41 via NSD, Apgar score:89 Nasal flaring and grunting around 2016/11/26 05:30 (5 hours old) SpO2: 85% O2 5-6L/min SpO2 >95% Transfer to our NICU

5 Physical examination T/P/R: 36.7/171/90 BP: 61/43(49) O2: Room air
SpO2:95% BL: 51cm(50-75%) BW: 3040gm(25-50%) AC: 33cm HC: 33cm Tachypnea, grunting Suprasternal/subcostal retraction(+) Breath sound: bilateral crackles, no wheezing, no stridor Regular heart beats, no specific heart murmur Abdomen: soft and distended, normoactive bowel sounds

6 11/26 I/T ratio: 0.28 >0.2 A reduced pH level raises concern about poor cardiac output and pending shock, which can be seen in cases of severe hypoxemia and/or heart failure. metabolic acidosis with respiratory compensation

7 11/26 diffuse peri-hilar interstitial infiltration with minor fissure (+) and blunt cost-phrenic angle no cardiomegaly enlarged liver(+)

8 Impression and plan Respiratory distress, favor pneumonitis
Polycythemia Plan: Septic workup Empirical antibiotics with ampicillin and gentamycin Bubble CPAP support, FiO2 21% Adequate hydration

9 BP drop to 53/32 mmHg, MAP 36-39 mmHg, HR: 150bpm
CRP: 75.7 mg/L Lumbar puncture Room air 7:30 Hold dopamine GPC BP drop to 53/32 mmHg, MAP mmHg, HR: 150bpm dopamine 4mcg/kg/min UOP: 2-3 cc/kg/hr BP:67-78/32-50 mmHg 08:35 NBP drop to 48/26(33) mmHg ABP 45/34(38) mmHg dopamine 5.5mcg/kg/min 810 Off dopamine

10 Culture CSF culture: No aerobic bacteria isolated
Brain echo: Normal, no ventriculitis Repeat Blood culture: no growth  Ampicillin for 10 days

11 檢驗名稱(單位) 11-29 11-27 11-26 CRP(mg/L) 38.3 75.7 <7.0

12 11/28

13 Final diagnosis Septic shock with GBS bacteremia Polycythemia

14 Group B streptococcus disease
Discussion Group B streptococcus disease

15 EPIDEMIOLOGY Major cause of neonatal bacterial sepsis in the United States in the late 1960s Incidence: /1,000 liveborn infants in the United States early-onset disease (<7 days of age): 1.7->0.25 / 1,000, decreasing late-onset disease ( ≥7– 90 days of age): / 1,000, remained stable Vaginal or rectal colonization occurs in up to approximately 30% of pregnant women and is the usual source for GBS transmission to newborn infants 7 days of age Avery's Neonatology

16

17 Risk factors For early-onset disease : For late-onset disease :
Maternal GBS colonization Prolonged rupture of membranes Chorioamnionitis Intrapartum fever Prematurity Maternal bacteriuria during pregnancy Previous delivery of an infant who developed GBS disease Infected route: Via ascending infection or during passage through the birth canal For late-onset disease : less-well defined May follow vertical transmission, or acquired later from maternal or nonmaternal sources Pneumothorax in respiratory distress syndrome (RDS) has been associated with increased risk of intraventricular hemorrhage

18 (CAM, PROM, preterm labor)
type III strains are implicated in most cases of late-onset neonatal GBS disease and meningitis. Type III strains are taken up by brain endothelial cells more efficiently in vitro than are strains of other serotypes, Ten GBS capsular types have been identified: types Ia, Ib, II, III, IV, V, VI, VII, VIII, and IX

19 CLINICAL MANIFESTATIONS-1
Early-onset disease: appear ill at the time of delivery, and most infants become ill within the 1st 24 hr of birth In utero infection may result in septic abortion >80% of early-onset GBS disease presents as sepsis without a focus of infection Pneumonia (10%) and meningitis (7%) are other common manifestations Nonspecific signs such as hypothermia or fever, irritability, lethargy, apnea, and bradycardia may be present Respiratory signs are prominent include cyanosis, apnea, tachypnea, grunting, flaring, and retractions Fulminant course with hemodynamic abnormalities, including tachycardia, acidosis, and shock

20 CLINICAL MANIFESTATIONS-2
Late-onset disease: most commonly manifests as bacteremia without a focus (45- 65%) but more frequently develop meningitis (25-35%) than EOS Focal infections involving bone and joints, skin and soft tissue, the urinary tract, or lungs may also be seen Maternal obstetric complications are not risk factors for the development of late- onset GBS disease Often less-severely ill on presentation than infants with early-onset disease, and the disease is often less fulminant

21 Management Empirical therapy Definitive therapy In cases of meningitis
ampicillin + aminoglycoside Definitive therapy Penicillin G In cases of meningitis high doses of penicillin(450, ,000 units/kg/day) or ampicillin (300 mg/kg/day) suggest repeat lumbar puncture at 24 to 48 hours of therapy to document sterilization of CSF before changing antimicrobial therapy

22 PROGNOSIS 1970s-1980s : up to 30% of infants surviving GBS meningitis had major long-term neurologic sequelae developmental delay, spastic quadriplegia, microcephaly, seizure disorder, cortical blindness, or deafness Periventricular leukomalacia and severe developmental delay may result from GBS disease and accompanying shock in premature infants, even in the absence of meningitis. Focal GBS infections outside of the central nervous system, such as bone or soft- tissue infections, is generally favorable Mortality is higher in premature infants GA <33 wk : fatality rate of 30% GA ≥37 wk : 2%

23 PREVENTION-1 Universal prenatal culture-based screening for vaginal and rectal GBS colonization of all pregnant women at weeks' gestation, except for those with GBS bacteriuria during the current pregnancy or a previous infant with invasive GBS disease. Indications of intrapartum antibiotics (IAP) Any woman with a positive prenatal screening culture GBS bacteriuria during pregnancy Previous infant with invasive GBS disease Culture status is unknown and deliver prematurely (<37 wk gestation), Prolonged rupture of membranes (≥18 hr) or Intrapartum fever (≥38°C)  significant reduction in the incidence rates of EOD Intrapartum fever (≥38°C

24 PREVENTION-2 Penicillin remains the preferred agent for maternal chemoprophylaxis Ampicillin is an acceptable alternative Recent reports indicating frequent resistance of GBS to clindamycin (up to 20%) Cefazolin should be used in most cases of intrapartum chemoprophylaxis for penicillin-intolerant women Unfortunately, antenatal screening and IAP have not changed the incidence of LOD and no specific strategies are at present With wider implementation of maternal chemoprophylaxis, an increasing percentage of early-onset neonatal disease has been in patients born to women with negative cultures false-negative screens rate 4-8%

25 Algorithm for secondary prevention of EOD among newborns from CDC guideline
CDC MMWR Recomm Rep 59[RR-10]:22, 2010 Algorithm for secondary prevention of early-onset group B streptococcal disease among newborns.

26 The Changing Face of Early-onset Neonatal Sepsis After the Implementation of a Maternal Group B Streptococcus Screening and Intrapartum Prophylaxis Policy The GBS screening rate increased from 10.11% in 2004 to 65% in 2008 and the IAP rate increased from 40% in 2004 to 90% in 2008. The most common EOS pathogen in Period 1 was GBS (45.4%), which decreased to 20% in Period 2 (p=0.081; trend p=0.009 The percentage of EOS because of Escherichia coli in Period 1 was 40.9% but increased to 70% in Period 2 (p=.059). E coli EOS increased in extremely low birth weight premature babies weighing g from Period 1 to Period 2 (p=0.031 The incidence of ampicillin-resistant E coli EOS was relatively high, but no significant change (88.9% vs. 92.9%) after implementation of GBS screening and IAP was noted. Pediatrics and Neonatology (2011) 52, 78-84

27

28

29 Neurological Complications after Neonatal Bacteremia: The Clinical Characteristics, Risk Factors, and Outcomes


Download ppt "Case Discussion 2016/12/06 R2郭舒涵."

Similar presentations


Ads by Google