PERINATAL/NICU CONFERENCE Monthly Statistics Report November 2013 PERINATAL/NICU CONFERENCE Monthly Statistics Report November 2013 Maria Celeste B. Gomez, MD 3 rd Year Resident Pediatrics Giancarlo C. Santos, MD 3 rd Year Resident Obstetrics and Gynecology THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics TOTAL BIRTHS Births per Month, 4 th Quarter % 9% Total Births, November 2013 ACCORDING TO TYPE OF MOTHERSNUMBER Delivered from Normal Mothers 103 Delivered from High Risk Mothers 88 TOTAL BIRTHS 191 Total Births, November 2013 ACCORDING TO NUMBER OF FETUSNUMBER Singleton187 Multifetal (n = 2)2 TOTAL LIVE BIRTHS191 Total Births, November 2013 ACCORDING TO AGE OF GESTATIONNUMBER Term172 Preterm18 Postterm1 TOTAL LIVE BIRTHS191 Preterm Births as a Percentage of Live Births in the Philippines, 1994 to 2008 POGS CPG, november 2010 Preterm Births as a Percentage of Live Births in the United States, 1990 to Institute of Medicine. PRETERM BIRTH: CAUSES, CONSEQUENCES, AND PREVENTION Total Births, November 2013 ACCORDING TO PLACE OF PRENATAL CARENUMBER Registered189 Non-registered2 TOTAL LIVE BIRTHS191 Neonatal Morbidities, November 2013 NUMBER OF NEONATAL MORBIDITIES32 Incidence among total live births115 per 1000 LB Delivered from Normal Mothers12 Delivered from High Risk Mothers20 NEONATAL MORBIDITIES Top 5 Conditions Occurring Among High Risk Mothers, November 2013 Top 5 Maternal Conditions Associated with Neonatal Morbidities, November 2013 Prematurity = 6 LGA = 1 Prematurity = 6 LGA = 1 Top 5 Maternal Conditions Associated with Neonatal Morbidities, November 2013 Prematurity/Se psis = 4 LGA/Sepsis = 1 Prematurity/Se psis = 4 LGA/Sepsis = 1 Top 5 Maternal Conditions Associated with Neonatal Morbidities, November 2013 Prematurity = 4 RDS = 1 Prematurity = 4 RDS = 1 Top 5 Maternal Conditions Associated with Neonatal Morbidities, November 2013 Prematurity = 2 Top 5 Maternal Conditions Associated with Neonatal Morbidities, November 2013 Prematurity = 1 LGA = 1 Prematurity = 1 LGA = 1 CONGENITAL ANOMALIES Congenital Anomalies, November 2013 NUMBER OF NEONATES WITH CONGENITAL ANOMALIES 3 Incidence among total live births 15 per 1000 LB Delivered from normal mothers 1 Delivered from high risk mothers 2 Congenital Anomalies, November 2013 Coarctation of the Aorta + VSD1 Trisomy 211 Encephalocoele + Malposition of the Great Vessels 1 Congenital anomalies: November 2013 Antenatal detection and Neonatal outcome Congenital Anomalies NUltrasoundNeonatal outcome WHCCDone DetectedNot Detected Outside SurvivedDied Coarctation of the Aorta + VSD 1 Trisomy 21 1 Encephalocoele + Malposition of the Great Vessels 1 R. M. L. 33, G2P1 (1001), 38 6/7 Previous NSD CC: uterine contractions PNCU: 4mos AOG, unrecalled antibiotics Past Medical/Personal/Social/ Family History: U/R Stable Vital Signs IE: 4-5cm, 60%, -3, +B CTG: category 1 trace Intrapartum stay x 3hrs s/p NSD+MER(4) Female APGAR 9,9 3540g MT 39 AGA CASE 1: Coarctation of the Aorta + VSD 2 nd HOL Non-separation Good suck during latching Good cry and activity RUE: 73/39 LUE: 70/28 RLE: 76/31 LLE: 75/38 HR: 156 RR: 54 T:36.4 Noncyanotic Good air entry, regular cardiac rhythm Full pulses, CRT Term newborn female 17 th HOL Good suck during latching Good cry and activity With urine output and meconium passage HR: 145 RR: 52 T:36.6 Noncyanotic Good air entry Soft systolic murmur at left parasternal order Full pulses, CRT Term newborn female, probably in transitional circulation 40 th HOL Good suck during latching Good cry and activity With urine output and meconium passage HR: 140 RR: 40 T:37.3 Wt: 3425 grams (wt loss 115 grams, 3% BW) Noncyanotic Good air entry Grade 2/6 holosystolic murmur at left parasternal border A> Term newborn female, probably in transitional circulation rule out congenital heart disease 43 rd HOL 2D Echocardiography: 4mm ventricular septal defect 2-3mm patent ductus arteriosus with continuous flow Left sided aortic arch with a juxtaductal coarctation (2mm) Dilated main pulmonary artery, still R ventricle dominant heart PA pressure 60 mmHg CHD; VSD, Coarctation Small PDA RV and PA hypertension 48 th HOL Exclusively breastfed with good suck Good cry and activity Adequate urine output and meconium passage HR: RR: T:37.3 Noncyanotic Good air entry Grade 2-3/6 holosystolic murmur at left parasternal order Fair femoral pulses A> Term newborn female, CHD VSD, Coarctation NICU Referral Noncyanotic RUE: 88/34, 98% LUE: 91/34, 96% RLE: 67/47, 100% LLE: 63/38, 97% HR: 154 RR: 72 T:37.8 Noncyanotic Good air entry Grade 2-3/6 holosystolic murmur at left parasternal order Fair femoral pulses, left>right A> Term newborn female NICU Referral Feeding with expressed breastmilk continued IVF D10IMB at TFR 90ml/kg/day Diagnostics: CBCPC, Blood C&S, Chest XrayCBCPCBlood C&S Therapeutic: Ampicillin at mg/kg/day Gentamicin 3.95 mg/kg/dose Definitive management: Options: Open heart surgery: VSD and repair of coarctation Closed heart surgery: Coarctation repair OR coarctation repair + band Day 4 of life Underwent repair of coarctation and PA banding Procedure: Extended end-to-end anastomosis, PA banding Intraoperative findings: Short segment, preductal coarctation approximately 2 mm in diameter Hypoplastic aortic arch Postoperative Issues: Hypertension BP range: /46-69 mmHg Nitroglycerine started Assisted ventilation Commenced during operation Maintained and gradually weaned from mechanical ventilation Spontaneous respiratory capability was monitored via pulse oxymeter and blood gasesblood gases Extubated on day 1 post op Postoperative Issues: Increasing WBC Afebrile Chest xray showed presence of bilateral lung opacities Cefotaxime added to present antibiotics at 50 mg/kg/dose Final Diagnosis Live term baby girl delivered via NSD to a 33 years old G2P2 (2002) 38 6/7 wks AOG by LMP, MT 39 wks, AGA, AS 9,9 Congenital heart disease Coarctation of the aorta with large ventricular septal defect s/p coarctation of aorta repair (end to end anastomosis), pulmonary artery banding, thoracotomy CBC with platelet count HgbHctWBCBandNeuLymPlt 11/ STG 12/ STG 12/ Blood C&S: No growth after 7 days of incubation Electrolytes NaKiCaMgBUNCrea 11/ / / / Blood Gases pHpCO2HCO3pO2BEO2 Sat 11/ / / FiO2 40% PIP 16 PEEP 6 RR 45 IT / FiO2 21% PIP 14 PEEP 4 RR 20 IT 0.4 D. A. E. 45, G3P1 (1011), 38 6/7 PCS for Elderly Primi (43) and Fetal Macro (9.2lbs) CC: scheduled RCS PNCU and diagnostics (CAS): U/R Past Medical/Personal/Social History: U/R Family History: (+) DM Stable Vital Signs IE: cervix closed CTG: category 1 trace s/p Repeat CS Male APGAR 9,9 2860g MT 40 AGA CASE 2: Trisomy 21 Delivery Clear amniotic Fluid (+) Low set ears (-) Cleft lip/Cleft palate Good air entry Good cardiac tone, HR 150 Grossly male genitalia Extended scrotal skin over the penis Stay at the NICU Subjective 13th hour of life Given milk formula (Tolerates ml) Active (+) urine output (+) 2 meconium passage Objective T 36.7 C HR 120 bpm RR 50 cpm (+) Light jaundice to chest Low set ears Good air entry Good cardiac tone, no murmurs Soft abdomen Scrotal skin over penis Full pulses Assessment Term Baby Boy Plan For bilirubin levels Single phototherapy Referral to urologist Referral to geneticist Course in the NICU Subjective 27 th hour of life Tolerates milk formula ( ml every 2 hours) Active 6 urine output 4 meconium passages Objective T 36.8 C HR 145 bpm RR 45 cpm Weight 2656 g (+) jaundice to abdomen Low set ears Good air entry Good cardiac tone, no murmurs Soft abdomen Scrotal skin over penis Full pulses TB mg/ dl IB mg/ dl DB 0.69 mg/ dl Assessment Term baby boy Hyperbilirubinemia, unspecified Webbed penis Plan Continue single phototherapy For repeat bilirubin levels Continue observation Course in the NICU Subjective 3rd day of life (AM) Tolerates ml of milk feedings plus breastfeeding Active 7 urine output 5 meconium passages Objective Wt 2675 g T 36.9 C HR 138 bpm RR 34 cpm (+) light jaundice to upper chest Low set ears Good air entry Good cardiac tone, no murmurs Soft abdomen Scrotal skin over penis Full pulses TB 13.4 mg/ dl IB 2.82 mg/ dl DB 0.80 mg/ dl Assessment Term baby boy Hyperbilirubinemia, unspecified Webbed penis t/c Trisomy 21 Plan For 2D echo Continue observation Discontinue phototherapy Course in the NICU Subjective 4th day of life (AM) Tolerates ml of milk feedings plus breastfeeding Active 7 urine output 4 meconium passages Objective Wt 2695 g T 36.9 C HR 138 bpm RR 35 cpm (+) light jaundice to upper chest Good air entry Good cardiac tone, no murmurs Soft abdomen Full pulses Assessment Term baby boy Hyperbilirubinemia, unspecified Webbed penis t/c Trisomy 21 Plan Discontinue single phototherapy For chromosomal testing May go home Pertinent features Mild upslanting of palpebral fissure Median epicantic folds Dysplastic right helix Hypoplastic nipples Mid phalanx hypoplasia, 5 th digit with clinodactyly 2D Echo Normal echocardial structure Normal function Small PDA 1- 2 mm, continuous flow Transitional Circulation Trisomy 21/ Downs Syndrome Chromosomal condition associated with intellectual disability, a characteristic facial appearance, and hypotonia Each cell in the body has three copies of chromosome 21 instead of the usual two copies Epidemiology From January 1, 2009 to January 1, 2013: Features Decreased muscle tone at birth Excess skin at the nape of the neck Flattened nose Separated joints between the bones of the skull (sutures) Single crease in the palm of the hand Small ears Small mouth Upward slanting eyes Wide, short hands with short fingers Genetics: Trisomy 21 During reproduction and fertilization, the baby is a set of 46 chromosomes, 23 from the mother and 23 from the father (divided from the usual 46 chromosomes of each parent) An error occurs where the egg or sperm cell keeps both copies of the 21 chromosome hence the extra chromosome Complications Congenital heart defects Visual and hearing impairment (e.g. crossed- eyes, near- or far- sightedness or cataracts) Thyroid problems Leukemia Recurrent respiratory infection Intestinal problems Skeletal problems L. F. A. 35, G2P1 (1001), 39wks PCS for Failed Induction CC: scheduled RCS Regular PNCU 25wks: t/c encephalocoele Past Medical/Personal/Social History: U/R Family History: (+) DM Stable Vital Signs IE: cervix closed CTG: category 1 trace s/p Repeat CS + BTL Female APGAR 7,9 2560g MT 38 AGA CASE 3: Encephalocoele + Malposition of the Great Vessels Birth History Baby Girl Live, term Delivered via repeat Cesarean Section 36 y/o (G2P2) (2002) 39 1/7 weeks AOG MT: 38 weeks, AGA Anthropometrics BW 2560g BL 43 cm HC 32 cm CC 31 cm AC 28 cm Apgar Score 7,9 MT 38 AGA Upon delivery Weak cry, with good muscle tone Acrocyanosis Clear amniotic fluid No cord coil Heart rate: 90s APGAR SCORE SIGN012 Heart rateAbsentBelow 100Over 100 Respiratory effortAbsent Slow, irregular Good, crying Muscle toneLimpSome flexion of extremities Active motion Response to catheter in nostril (tested after oropharynx is clear) No responseGrimaceCough or sneeze ColorBlue, paleBody pink, extremities blue Completely pink Physical Examination General Survey weak cry and good activity Anthropometrics BW 2560g BL 43 cm HC 32 cm CC 31 cm AC 28 Apgar Score 7,9 MT 38 AGA HEENT Flat anterior fontanelle Sloped forehead Good elastic recoil, no ear tags Patent nares, no cleft lip, no cleft palate (+) occipital mass, soft (7cmx 7cm x 4cm) with intact skin Short neck Chest Symmetrical chest expansion Clear breath sounds Good air entry Cardiovascular Adynamic precordium, no murmurs Abdomen Globular abdomen, no masses palpated Umbilicus with 2 arteries, 1 vein Extremities Pulses full 2-3 syndactyly of both feeth Admitting Diagnosis Term baby girl Encephalocoele (occipital area) PLANS O2 support via nasal cannula at 1lpm Diagnostics: CBC Blood typing HGT Cranial MRI Chest and skull Xray Refer to Neurology, Neurosurgery & Geneticist Start IV antibiotics NPO Insert OGT 1 st hour of life With good cry No seizures With desaturations upto 88% Lateral positioning Thermoregulation Family conference CBC 11/25 Hgb160 Hct52 WBC10.8 Bands02 Neutrophils60 Lymphocytes30 Monocytes06 Eosinophils02 Platelet276 11/25 HGT65 mg/dL Blood typing O+ Hgt 65 mg/dL Chest and Cervical xray Skull xray Cranial mri Cranial Ultrasound 1 st -11 th hospital day With occasional desaturations No seizure, cyanosis With increased oral secretions With intermittent tachypnea IVF started O2 support Suctioning of secretions PO as needed Referral to Cardiology & Nephrology 2D Echo of the heart KUB ultrasound Family Conference Neural Tube Sequence, Encephaloco ele Pneumonia 2D Echocardiography of the Heart KUB Ultrasound Large VSD (8-9mm) Pulmonary artery overiding ventricular system Malposed great arteries Aorta arises from RV Small PFO vs ASD (4mm) Aortic arch predominantly at right parasternal area & right arching Small PDA Normal sized kidneys for age with intact morphology Partially filled urinary bladder with normal configuration Family conference Current situation discussed 1.Enlarging Encephalocoele 2.Congenital Heart disease (DORV, malposed great arteries) 3.No swallow reflex 4.Difficult airway Current & Possible actions discussed 1.Closure of encephalocoele 2.Pulmonary artery banding then complete repair later 3.Increase feeding until IVF could be discontinued Final Plan 1.Continue feeding per NGT 2.No procedure as of the moment 3.Send home FINAL DIAGNOSIS Encephalocoele Congenital Heart Disease,Taussig Bing Anomaly (Double outlet right ventricle, Malposition of great arteries, Ventricular septal defect, Atrial septal defect) Encephalocoele Neural tube defect Sac-like protrusions of the brain Due to failure of neural tube to close completely Occur in 1:5000 births worldwide Risk factors: Ethnicity Genetics Environmental factors Parental age Family history of spina bifida Treatment: Reparative Surgery during infancy Taussig Bing Anomaly Cyanotic congenital heart defect With both double outlet right ventricle and ventricular septal defect Both aorta and pulmonary artery are connected to right ventricle Only blood flow to the left ventricle is via VSD Occur in 1:10,000 live births Treatment: Palliative Pulmonary artery banding Systemic to pulmonary artery shunting Definitive Arterial switch operation Prognosis Pediatr Neurosurg. 2011;47(6): doi: / Epub 2012 Jul 7. Pediatr Neurosurg. Giant encephalocele: a study of 14 patients. Mahapatra AK. Mahapatra AK Source Department of Neurosurgery, AIIMS, New Delhi, India. Abstract BACKGROUND: Giant encephalocele is a rare condition and few published reports are available in the English literature. It is a challenge to neurosurgeons, even today. This series consists of 14 patients with giant encephaloceles treated at our institute. MATERIAL AND OBSERVATION: Over a period of 8 years, from 2002 to 2009, 110 patients with encephaloceles were managed at our institute. Amongst them, 14 were children with giant encephaloceles. All patients had CT/MRI or both prior to surgery, and all were operated upon. Four patients were neonates, under 1 month of age, and 9/14 patients (64%) were under 3 months. The youngest child was a newborn baby aged 2 days. Except for 1 with an anterior encephalocele, the rest were patients with occipital encephaloceles. A CT scan was performed on 5 and an MRI on 1 patient. Both CT and MRI scans were performed on the other 8 patients. MRI/CT showed hydrocephalus in 10/14 patients. Of these, 7 required ventriculoperitoneal (VP) shunt, and the remaining 3 with mild to moderate hydrocephalus did not. Of the 7 patients who underwent VP shunt, 5 had a shunt during the encephalocele repair and 2 had a postoperative shunt for increasing hydrocephalus. RESULTS: Other associated anomalies recorded were acquired Chiari malformation in 3 patients, secondary craniostenosis with microcephaly in 5, and syringomyelia in 1 patient. All the patients underwent repair of encephalocele and 4 had suturectomy of coronal suture for the secondary craniostenosis. There were 2 postoperative deaths due to hypothermia. Among the 12 surviving patients, 9 had a good outcome and 3 had poor mental development. The present study shows overall good outcomes in 9/14 (66%) patients. Copyright 2012 S. Karger AG, Basel. PMID: [PubMed - indexed for MEDLINE] Out of 14 patients who underwent repair of encephalocoele, 2 died of hypothermia post-opand 12 survived. Out of the 12, 9 (66%) had good outcomes Pediatr Cardiol Feb;33(2): doi: /s Epub 2011 Sep 30. Pediatr Cardiol. Short- and mid-term outcomes of total correction of Taussig-Bing anomaly. Al-Muhaya MA, Ismail SR, Abu-Sulaiman RM, Kabbani MS, Najm HK. Al-Muhaya MAIsmail SRAbu-Sulaiman RMKabbani MSNajm HK Source Department of Cardiac Sciences, National Guard Hospital Health Affairs, King Abdulaziz Medical City, Riyadh, Saudi Arabia. Abstract Double-outlet right ventricle (DORV)/Taussig-Bing (TB) anomaly is the second most common type of DORV. This study evaluates our experience and outcomes of total correction of DORV-TB anomaly at King Abdulaziz Cardiac Center. We conducted a retrospective study for all cases of TB anomaly repaired between June 2001 and April Patients were divided into two groups: Group A included patients repaired with arterial switch operation, and group (B) included patients repaired with Rastelli procedure. Thirteen patients with TB anomaly underwent total correction. There were 5 male (38%) and 8 female (62%) patients. Mean age and weight at surgery were 6.8 6 weeks and 3.6 0.7 kg, respectively. Of the 13 patients, 9 (69%) were in group A, and 4 (31%) were in group B. Aortic arch abnormalities were present in 9 patients (69%); abnormal coronary artery patterns were present in 7 patients (54%); side-by-side great arteries were present in 5 patients (38%); dextrotransposition of the great arteries was present in 7 patients (54%); and levo-malposition of the great arteries was present in 1 patient (8%). At postoperative follow-up, 4 patients (31%) had developed either left- or right-ventricular outflow tract (VOT) obstruction requiring surgical and/or catheter intervention. There was no early mortality, but there was 1 late mortality caused by left- ventricle dysfunction. DORV-TB is often associated with other congenital cardiac anomalies. In general, total repair is feasible in the majority of patients with satisfactory results and improved outcome. Residual lesion and development of VOT obstruction can occur, requiring close follow-up and intervention for residual lesion. PMID: [PubMed - indexed for MEDLINE] In general, total repair is feasible in the majority of patients with satisfactory results and improved outcome. Residual lesion and development of VOT obstruction can occur, requiring close follow-up and intervention for residual lesion. Am J Perinatol Aug;25(7): doi: /s Epub 2008 Aug 21. Am J Perinatol. Diagnosis and prognosis in double-outlet right ventricle. Gedikbasi A, Oztarhan K, Gul A, Sargin A, Ceylan Y. Gedikbasi AOztarhan KGul ASargin ACeylan Y Source Department of Obstetrics and Gynecology, Perinatology Unit, Istanbul Bakirkoy Maternity and Children Diseases HospitalIstanbul, Turkey. Abstract The aim of this study was to examine prenatal diagnosis of double-outlet right ventricle (DORV)- associated anomalies and prognosis of each case. Medical records were reviewed of fetuses with DORV who had fetal echocardiography at our institution from 2002 to Pre- and postnatal diagnosis and outcome were compared and evaluated. Twenty-one fetuses were diagnosed with DORV. The pregnancy was terminated in seven cases. Three cases had chromosomal abnormalities; three cases, hypoplastic left ventricle; and one case, encephalocele. Accurate prenatal diagnosis of the ventricular septal defect, outflow obstruction, and great artery relationship was achieved in 14 of 16 cases (87.5%). Only 2 of 13 live-born cases survived beyond 6 months. The overall prognosis for fetuses with DORV is poor. DORV is found in fetuses with a huge spectrum of associated cardiac and extracardiac anomalies. Careful assessment by fetal echocardiography can determine important anatomic details with adequate correctness for precise counseling. PMID: [PubMed - indexed for MEDLINE] In a study of 21 fetuses with DORV, 1 was associated with encephalocoele and only 2 lived beyond 6 months NEONATES WITH APGAR < 7 Neonates with APGAR < 7, November 2013 NUMBER OF NEONATES WITH APGAR < 7 1 Incidence among total live births 5 in 1000 LB Delivered from low risk mothers 0 Delivered from high risk mothers 1 M. N. M. 39, G2P1 (0101), 29 6/7 CC: uterine contractions no PNCU until 1 wk PTA; given steroids, tocolytics, antibiotics, bed rest G1: NSD: 2009: 32wks: 1.8kg: Pasig: Preec(?) Past Medical/Personal/Social History: U/R Family History: (+) HPN 176/80, HR 76, RR 17, 36.8C IE: fully dilated, bulging BOW, fetal parts not palpated s/p NSD Male APGAR 2,3,7,7,8 1180g MT 31 AGA CASE 4: APGAR 2,3,7,7,8 Preterm via normal spontaneous delivery 39 year old G2P2 (0202) 29 6/7 wks AOG, MT 32 AGA Apgar 2, 3, 7, 7, 8 B.M. BW 1180 g BL 43 cm HC 26 1/2 cm CC 23 cm AC 21 cm X XX X XX X 1 XX X 1 cord coil Flat fontanels No molding, caput No cleft lip or palate (-) alar flaring Intubated, Good air entry, subcostal retractions HR 150bpm, Good cardiac activity, Soft abdomen Grossly male genitalia with testes in the upper canal Full pulses Physical findings SUBJECTIVE Good cry (+) spontaneous inspiratory effort (-) cyanosis (-) seizure OBJECTIVE T C HR 130bpm BP RR 65 cpm O2 sats 93-96% (-) alar flaring Subcostal retractions Breath sounds louder on the right ASSESSMENT Preterm baby Respiratory distress syndrome vs neonatal pneumonia PLAN Neonatology consult Adjustment of ET tube mechanical ventilation UV cannulation D10 water 80ml/kg/day Ampicillin (100mkday) and Amikacin (18mkday) Surfactant therapy 15 th min OF LIFE pHPCO2PO2HCO3BEO2satImpression MV settings 11/23/ 13 10PM Metabolic Acidosis FiO2 80 PIP 16 PEEP 4 RR 50 NaHCO 3 2 meqs x 1 dose, NaHCO3 3 meq drip RR decreased to 40 FiO2 increased to 90, RR increased to 50 Chest Xray: Ground glass opacity at the Right lung field with air bronchogram Surfactant therapy (3.38mg/kg/dose) done pHPCO2 PO2 HCO3BEO2satImpression MV settings 11/23/ 13 9AM Compensate d Respiratory acidosis FiO2 80 PIP 16 PEEP 4 RR 40 CBCHgbHctWBCStNeuLymMonEosPC 11/ 15 th hour of life SUBJECTIVE No cyanosis No desaturation OBJECTIVE T C HR 145bpm RR 50 cpm O2 sats 100% Good air entry Shallow subcostal retractions Full pulses ASSESSMENT Preterm baby Respiratory distress syndrome s/p surfactant therapy PLAN IV fluids IV antibiotics RR decreased to 45, PIP decreased t0 15 Transferred to hospital of choice Awake, intubated RR 41-60cpm, good air entry, harsh breath sounds on PPV with subcostal retractions HR bpm BP 57/33mmHg, no murmur, full pulses Soft abdomen with UVC On Intravenous IV fluids and antibiotics 20 th hour of life Live preterm baby boy, delivered via normal spontaneous delivery at 29 6/7 weeks AOG, MT 32 weeks, AGA, AS 2,3,7,7,8 Respiratory Distress Syndrome S/p surfactant therapy Final diagnosis DISTRIBUTION OF BIRTHS November 2013 Distribution of Deliveries According to Birthweight Classification based on Best Score Wt (grams) < / > 42 Grand Total > Grand Total Relationship between AOG and Birth weight Relationship between Maturity Testing and Birthweight Wt (grams) < / > 42 Grand Total > Grand Total Small for Gestational Age Infants, November 2013 NUMBER OF SGA NEONATES 2 Incidence among total livebirths 10/1000 LB Delivered from normal mothers 2 Delivered from high risk mothers 0 A. Maternal factors0 B. Fetal Factors 0 C. Unknown factor 2 Large for Gestational Age Infants, November 2013 NUMBER OF LGA NEONATES 8 Incidence among total livebirths 41 /1000 LB Delivered from normal mothers 8 Delivered from high risk mothers 6 A. Maternal factors Gestational diabetes mellitus 0 B. Fetal Factors Fetal Macrosomia 6 DISTRIBUTION OF BIRTHS ACCORDING TO GESTATIONAL AGE ON DELIVERY Distribution of Births According to AOG on Delivery Livebirths = 191 Livebirths and Preterm Delivery, November 2013 NUMBER OF PRETERM NEONATES 18 Incidence among total livebirths 94 in 1000 LB Delivered from low risk mothers 12 Delivered from high risk mothers 6 ROOMING IN AND BREASTFEEDING RATES Rooming-In Total Eligible for Rooming In = 65/ 191(34%) MONTHNon Separation ( % MORTALITY CASES M. S. A. 40, G3P2 (2002), 31 5/7 PCS for Failed Induction CC: uterine contractions PNCU: regular (+) GDM, (+) CHPN Family History: (+) DM 161/93, HR 85, RR 18, 36.6C IE: 2, 60%, -3, +BOW IMU, Tocolysis, Steroids IE: 4, FE, -3, +BOW after 12h s/p RCS+BTL Male APGAR 9,9 1630g MT 33 AGA CASE 5: Mortality Case MSA Live, preterm, baby boy Delivered via stat cesarean section due to previous CS in labor 40 yo G3P3 ( ) LMP 31 5/7 weeks; MT 33weeks AGA APGAR score 9,9 BABY M 33 weeks Appropriate for gestational age Birthweight: 1630 g Birthlength: 41 cm Head Circ: 28cm Chest Circ: 25 cm Abd Circ: 21 cm Clear amniotic fluid HR 150s APGAR SCORE : 9,9 Upon delivery ASSESSMENT: Live preterm baby boy Delivered via stat CS for repeat CS in labor at 31 5/7 weeks AOG Apgar Score 9,9 ADMISSION Management Routine newborn care done Admitted to NICU Level 3 NPO O2 support via nasal canula IVF started Calcium gluconate started Septic workup: Blood CS: No growth in 72 hours Ampicillin, Amikacin started HgbHctWBCBandNeutLymMonPlt Course in the NICU 1 st Day of Life PROBLEMS Prematurity Probable sepsis Patient was placed in an isolette NPO IV fluid continued Hgt monitoring done Ampicillin, Amikacin continued 2 nd Day of Life PROBLEMS Jaundice Apnea O2 sat 86% HR 100 Nutritional buildup Phototherapy started Aminophylline started Continue O2 support until weaning Kept on NPO Aminosteril started 3 rd Day of Life PROBLEMS Vomiting of coffee ground material after feeding Kept on NPO Vitamin K given 4 th Day of Life PROBLEMS Nutritional buildup Feeding with expressed breast milk was started Intralipid was started 6 th Day of Life PROBLEMS Apnea Less than 10 seconds Improved by stimulation Cyanosis with hemodynamic compromise HR 9 iCa Seizure (t/c Intraventricular Hemorrhage) Phenobarbital 7 th Day of Life Desaturation despite bag tube ventilation Bradycardia (HR 40s), Hypotension (Undetectable) Resuscitation with chest compression and epinephrine After 45 minutes of resuscitation, patient was pronounced dead. Postmortem care done. FINAL DIAGNOSIS Prematurity Septic shock secondary to Acinetobacter baumannii Disseminated Intravascular Coagulation r/o Intraventricular Hemorrhage Neonatal Pneumonia Acute renal failure Acinetobacter baumannii The most resistant of the genospecies and has the greatest clinical importance Naturally inhabits water and soil Isolated from foods and arthropods In humans, can colonize: Skin, wounds Respiratory GI Can survive environmental dessication for weeks promotes transmission through fomite contamination in hospital RISK FACTORS AMONG NEONATES Low birth weight Total parenteral nutrition Central venous catheters Mittal N, Nair D, Gupta N, et al. Outbreak of Acinetobacter spp septicemia in a neonatal ICU. Southeast Asian J Trop Med Public Health 2003; 34:365. Huang YC, Su LH, Wu TL, et al. Outbreak of Acinetobacter baumannii bacteremia in a neonatal intensive care unit: clinical implications and genotyping analysis. Pediatr Infect Dis J 2002; 21:1105. Health Care Associated Infection Acinetobacter outbreaks have been traced to: 1.common-source contamination (particularly contaminated respiratory and ventilator equipment) 2.cross-infection by the hands of health care workers caring for colonized or infected patients Hartstein AI, Rashad AL, Liebler JM, et al. Multiple intensive care unit outbreak of Acinetobacter calcoaceticus subspecies anitratus respiratory infection and colonization associated with contaminated, reusable ventilator circuits and resuscitation bags. Am J Med 1988; 85:624. Maragakis LL, Cosgrove SE, Song X, et al. An outbreak of multidrug-resistant Acinetobacter baumannii associated with pulsatile lavage wound treatment. JAMA 2004; 292:3006. Bloodstream Infection Acinetobacter accounts for 1.5 to 2.4 percent of nosocomial bloodstream infections Most frequent source: vascular catheter, respiratory tract Less common: Wounds, urinary tract Septic shock develops in up to one-third of patients. Data regarding the prognosis of patients: limited Patients usually have longer ICU stay, higher rate of organ failure and higher mortality rates Risk factors for mortality: Imipinem resistence ICU stay Female gender Old age Pneumonia Diabetes Septic shock S. E. G. 37, G4P2 (1112), 30 1/7 CC: epigastric pain (+) CHPN+SIP admitted for BP given Nicardipine drip, steroids G1: PCS Preec: 2004: 32wks: 5.2lbs: Delgado Personal History: U/R Family History: (+) HPN,DM (200/120) 153/89, 104, 20, 37.0C IMU, Nicard drip, MgSO4, Steroids CTG: 140, min-mod var, no accelerations, (+) variable decels as low as 100bpm, no UC s/p RCS+BTL for NRFHRP MaleAPGAR 8,9 1020gMT 32 SGA Thinly Stained AF CASE 6: Mortality Case SEG Brief History Stat Primary CS due to Non-Reassuring Fetal Status of patient 37 yo G4P3 (1213) 30 weeks and 2/7 days AOG Maturity 32 weeks AGA Apgar 9,9 Wt 1020 g Physical Examination on Delivery HR= 150 RR= 54 T= 36.8 BP 58/35 O2 sat 99% at 02 hood at 2lpm pink soft flat and open anterior and posterior fontanelles eyes not fused patent nares no cleft lip and palate no clavicular fracture good air entry regular cardiac rhythm, soft abdomen umbilical cord 2 arteries, 1 vein grossly male genitalia, testes descending full and equal pulses Admitting Impression Live Term baby boy, delivered via Stat CS for Non Reassuring Fetal Status, at 30 2/7 weeks AOG, Maturity 32 weeks, AGA, Apgar 9,9 Sepsis, Unspecified Very Low Birth Weight, BW 1020g Timeline (Day 1-11) Birth Minimal O2 support Nepnatal Pneumonia Sepsis, Unspecified Hypocalcemia Ampicillin, Amikacin Day 2 Feeding started with EBM 1ml q3 Episodes of apnea Aminiphylline Day 6 NPO Shifted to Meropenem TPN with Lipids NEC Stage 1 Day 3-5 NPO Vomiting, Bilous drain from OGT TPN started Hyponatremia Septic Ileus Day 8-11 NPO Yellowish drain from OGT Decreased abdominal distention Active Timeline (Day 12-) Day Re-Feed EBM (+)residuals Metoclopromide given to improve gastric emptying Merop D7 Day Metabolic Acidosis Thrombocytopenia Hyponatremia Hypoglycemic episodes Add Fluconazole Metronidazole Day NPO Hypoalbuminemia Ascites BCS: Acinetobacter Baumanii d/c Merop Cefepime +Levofloxacin +Amikacin Day Re-Feed EBM Still Septic Hypoalbumnemia Anemia, Thrombocytopenia Repeat BCS: A. Baumanii Ceftazidime + Fluco +Metro d/c Amik PRBC, Platelet Concentrate Timeline (Day 29-30) Day 29 NPO Tachypneic, edematous Metabolic Acidosis Acute Renal Failure Furosemide Albumin Day 30 Episodes Desaturations, Bradycardia Septic Shock DIC EXPIRED Final Diagnosis Septic Shock with Severe Metabolic Acidosis 2 to Sepsis (Acinetobacter Baumanii) Necrotizing Enterocolitis Stage 1 Neonatal Pneumonia Acute Renal failure Prematurity Very Low Birth Weight (1020g) THANK YOU!!!