THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics PERINATAL/NICU CONFERENCE Monthly Statistics.

THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics PERINATAL/NICU CONFERENCE Monthly Statistics Report January Marco Manzano and Clarissa Pangilinan, MD 3rd Year Resident – Pediatrics Maria Edwardina G. De Leon, MD 3rd Year Resident – Obstetrics and Gynecology Perinat Report Mortality Anna Aspiras Morbidity Ma. Joycelyn Panganiban (poor APGAR) Jolet Ayaso (poor APGAR) Catherine Banes (skipped beats) Congenital Anomalies Paderanga, Michaela (Cleft palate) Rivera, Maria Christina (Imperforate anus)

TOTAL BIRTHS Number (%) Total Births 200 Live births 200 (100.0%)
Stillbirths 0 (0.0%) Delivered from normal mothers (%) 117 (58.5 %) Delivered from high risk mothers (%) 83 (41.5 %) 2 sets of twins both from high risk moms

Total Births, January 2014 ACCORDING TO TYPE OF MOTHERS NUMBER
Delivered from Normal Mothers 117 Delivered from High Risk Mothers 83 TOTAL BIRTHS 200

Total Births, January 2014 ACCORDING TO NUMBER OF FETUS NUMBER
Singleton 196 Multifetal (n = 2) 4 TOTAL LIVE BIRTHS 200 There were 2 cases of twin deliveries: Hung & Mabazza

Total Births, January 2014 ACCORDING TO AGE OF GESTATION NUMBER Term
181 Preterm 18 Postterm 1 TOTAL LIVE BIRTHS 200

Total Births, January 2014 ACCORDING TO PLACE OF PRENATAL CARE NUMBER
Registered 198 Non-registered TOTAL LIVE BIRTHS 200

NURSERY ADMISSIONS

December vs January

January 2013 vs January 2014

Deliveries By Levels

NICU Referral (n=9) Inborn Transfer = 8 Inborn Readmission = 1

Isolation (n=8) Inborn Transfer = 2 Inborn Readmission = 2
Outborn Admission = 4

NEONATAL MORBIDITIES

Neonatal Morbidities, January 2014
NUMBER OF NEONATAL MORBIDITIES 36 Incidence among total live births 115 per 1000 LB Delivered from Normal Mothers 19 Delivered from High Risk Mothers 17 47.2% normal mothers 52.8% high risk mothers 14 14

Top 5 Conditions Occurring Among High Risk Mothers, January 2014
Dm = 28 = 14.14% = 4 preterm Anemia = 27 = 13.64% = 3 preterm, 1 SGA, 1 low birth weight, 2 LGA Hpn = 23 = 11.62% = 4 preterm, 1 LGA, 1 low birth weight Uti = 21 = 10.61% = 1 preterm, 3 LGA Baniae = 8 = 4.04% = 1 poor Apgar, 1 LGA URTI = 7 = 3.54% = 0 Thyroid = 1 = 0.51% = 15

Top 5 Maternal Conditions Associated with Neonatal Morbidities, January 2014
Prematurity = 4 Dm = 28 = 14.14% = 4 preterm Anemia = 27 = 13.64% = 3 preterm, 1 SGA, 1 low birth weight, 2 LGA Hpn = 23 = 11.62% = 4 preterm, 1 LGA, 1 low birth weight Uti = 21 = 10.61% = 1 preterm, 3 LGA Baniae = 8 = 4.04% = 1 poor Apgar, 1 LGA URTI = 7 = 3.54% = 0 16

Prematurity = 3 LGA = 2 SGA = 1 Low birth weight = 1 Dm = 28 = 14.14% = 4 preterm Anemia = 27 = 13.64% = 3 preterm, 1 SGA, 1 low birth weight, 2 LGA Hpn = 23 = 11.62% = 4 preterm, 1 LGA, 1 low birth weight Uti = 21 = 10.61% = 1 preterm, 3 LGA Baniae = 8 = 4.04% = 1 poor Apgar, 1 LGA URTI = 7 = 3.54% = 0 17

Prematurity = 4 LGA = 1 Low birth weight = 1 Dm = 28 = 14.14% = 4 preterm Anemia = 27 = 13.64% = 3 preterm, 1 SGA, 1 low birth weight, 2 LGA Hpn = 23 = 11.62% = 4 preterm, 1 LGA, 1 low birth weight Uti = 21 = 10.61% = 1 preterm, 3 LGA Baniae = 8 = 4.04% = 1 poor Apgar, 1 LGA URTI = 7 = 3.54% = 0 18

Dm = 28 = 14.14% = 4 preterm Anemia = 27 = 13.64% = 3 preterm, 1 SGA, 1 low birth weight, 2 LGA Hpn = 23 = 11.62% = 4 preterm, 1 LGA, 1 low birth weight Uti = 21 = 10.61% = 1 preterm, 3 LGA Baniae = 8 = 4.04% = 1 poor Apgar, 1 LGA URTI = 7 = 3.54% = 0 Prematurity = 1 LGA = 3 19

Dm = 28 = 14.14% = 4 preterm Anemia = 27 = 13.64% = 3 preterm, 1 SGA, 1 low birth weight, 2 LGA Hpn = 23 = 11.62% = 4 preterm, 1 LGA, 1 low birth weight Uti = 21 = 10.61% = 1 preterm, 3 LGA Baniae = 8 = 4.04% = 1 poor Apgar, 1 LGA URTI = 7 = 3.54% = 0 LGA = 1 Poor APGAR = 1 20

CONGENITAL ANOMALIES

Congenital Anomalies, January 2014
NUMBER OF NEONATES WITH CONGENITAL ANOMALIES 2 Incidence among total live births 15 per 1000 LB Delivered from normal mothers 1 Delivered from high risk mothers c/o Pedia 22 22

Congenital Anomalies, January 2014
Cleft Palate 1 Imperforate Anus c/o Pedia

Congenital anomalies: January 2013 Antenatal detection and Neonatal outcome
N Ultrasound Neonatal outcome WHCC Done Detected Not Detected Outside Survived Died Cleft Palate 1 R Imperforate Anus Cleft palate- Imperforate anus- Encephalocoele – cas done at whcc Trisomy 21 – cas and 2d echo done at whcc Coa – none done 24

CASE 1: Cleft Palate Stable Vital Signs IE: 3cm, 50%, -3, (-)BOW
CTG: Category 1 trace Intrapartum stay x 10hrs s/p PCS Female APGAR 9,9 3140 g MT 38 AGA M. M. P. 28, G1P0, 39 CC: vaginal bleeding PNCU: regular, unremarkbale Past Medical/Personal/Social/Family History: U/R Michaela Anicia Mejia Paderanga January 30, 2013 Under Dr.Vicencio HPI: vaginal bleeding with associated moderate uterine contractions Married, nurse, denies smoking, occasional alcoholic beverage drinker CAS 27 weeks AOG CS for nonreassuring fetal heart rate pattern(persistent variable decelerations with late component as low as 80bpm)

CASE: Cleft Palate S.M.P. BW 3140 g
Full term via stat cesarean section due to NRFHRP 28 year old G1P1 (0101) 39 1/7 weeks AOG, MT 38 AGA Apgar 9, 9 BW 3140 g BL 51 cm HC 34 cm CC 34 cm AC 30 cm Aileen Elbo Dailo November 19, 2013 Under Dra. M. Saludares Normal CAS (August 28, 2013) and 2d echo Homemaker, college graduate, no vices HPI: asymptomatic

Personal/Social History OB History: Feeding history
Maternal History: UTI- 1st trimester, treated with cefuroxime Past Medical History: (+) asymptomatic MVP Family History: Diabetes, Hypertension, Heart disease, Stroke Personal/Social History Unremarkable OB History: G1 – present pregnancy Feeding history Mixed feeding, expressed breastmilk+milk formula

Physical Findings Thinly meconium-stained amniotic fluid
Flat fontanels No molding Cleft palate (-) alar flaring Good air entry, no retractions HR 150bpm, Good cardiac activity, Soft abdomen Grossly female genitalia Full pulses

Diagnosis Live Term Baby Girl Cleft palate

PLAN NPO ENT Referral Therapeutics:
Obturator fitting c/o pedia dentist OGT feedings Feeding plate Breast feed as tolerated Strict aspiration precautions

Course in the NICU Subjective Day 1 of life
Tolerates milk formula (10-15 ml every 2 hours) Active No vomiting or regurgitation 5 urine output 3 meconium passages Objective T – 36.8 C HR 146 bpm RR 49 cpm Weight 3020 g (+) cleft palate OGT at level 17 Good air entry Good cardiac tone, no murmurs Soft abdomen Full pulses Assessment Term baby girl Cleft Palate, Incomplete Plan Continue feedings Referral to pedia dentist

Course in the NICU Subjective Day 2 of life Tolerates milk formula (15-20 ml every 2 hours) Active No vomiting or regurgitation 5 urine output 6 meconium passages Objective T – 36.9 C HR 145 bpm RR 49 cpm (+) cleft palate Good air entry Good cardiac tone, no murmurs Soft abdomen Full pulses Assessment Term baby girl Cleft Palate, Incomplete Plan Pedia dentist: No need for obturator plate at this time Referral to maxillofacial surgeon For obturator fitting as outpatient pending surgical intervention Adivsed proper feeding position with dropper or soft baby bottle with nipple. BF is encouraged FF-up as soon as 1st tooth erupts

Cleft Palate Failure of the palatal shelves to fuse
Cleft palate: 1 in 2500 (Caucasians) Cleft lip+/- cleft palate: 1 in 750 Cleft palate: Females > Males Cleft lip: Males > Females Syndromes associated w/ Cleft Lip +/- cleft palate : >200 Ethnic factors (Cleft lip +/- cleft palate) Native Americans (1 in 230 to 1,000) Asians (1 in 400 to 850) African Americans (1 in 1,300 to 5,000) Incidence of associated congenital malformations and of impairment in development is increased: Cleft palate alone > cleft lip Most common in Native Americans (1 in 230 to 1,000) and Asians (1 in 400 to 850) least common in African Americans (1 in 1,300 to 5,000) Samanich, J. Cleft Palate . Pediatrics in Review 2009;30;230

Clefting Defects between the 6th and 9th weeks AOG
primary palate begins to form at about 35 days complete lip development by the 6th week palatal fusion follows Cleft lip: interruption or hypoplasia of the mesenchymal layer  failure of fusion of the medial nasal process, maxillary process, and lateral nasal process (unilateral or bilateral) Cleft palate: palatal shelves fail to fuse Multifactorial traits: Genetic: mutations in single genes (TBX22, IRF6, MSX1); Part of chromosomal aneuploidy or deletion syndromes (trisomy 13, velocardiofacial syndrome) environmental factors: teratogens (anticonvulsants) Most common in Native Americans (1 in 230 to 1,000) and Asians (1 in 400 to 850) least common in African Americans (1 in 1,300 to 5,000) Samanich, J. Cleft Palate . Pediatrics in Review 2009;30;230

Cleft Palate Occurs in the midline and might involve only the uvula or can extend into or through the soft and hard palates to the incisive foramen When associated with cleft lip: involve midline of the soft palate and extend into the hard palate on one or both sides, exposing one or both of the nasal cavities as a unilateral or bilateral cleft palate Can also have a submucosal cleft indicated by a bifid uvula, partial separation of muscle with intact mucosa, or palpable notch at the posterior of the palate Kliegman et al Nelson’s Textbook of Pediatrics. 19th Edition

Pierre Robin sequence (PRS)
micrognathia (small mandible) retropositioned tongue U-shaped cleft palate failure of the mandible to grow properly  positioning of the tongue in the back of the pharynx  blocks the ability of the palatal shelves to fuse properly severe respiratory distress: mortality rate as high as 30% careful monitoring: first 1 to 4 weeks over time, the lower jaw generally “catches up” in growth vs. surgical intervention (jaw expansion) isolated birth defect, but may be part of syndromes such as trisomy 18 or Stickler syndrome An important type of clefting defect to recognize in the neonatal period is Pierre Robin sequence (PRS), which includes micrognathia (small mandible), a retropositioned tongue, and a U-shaped cleft palate. The initial embryologic event is believed to be failure of the mandible to grow properly, leading to positioning of the tongue in the back of the pharynx, which blocks the ability of the palatal shelves to fuse properly. Affected children often experience severe respiratory distress, leading to a mortality rate as high as 30% and requiring interventions ranging from prone positioning to allow the tongue to fall forward out of the airway to intubation and tracheostomy. Children who have PRS require careful monitoring, particularly in the first 1 to 4 weeks after birth. Over time, the lower jaw generally “catches up” in growth, but sometimes surgical intervention is required for jaw expansion. PRS generally occurs as an isolated birth defect, but may be part of syndromes such as trisomy 18 or Stickler syndrome. Samanich, J. Cleft Palate . Pediatrics in Review 2009;30;230

Trisomy 18 Edward’s Syndrome
second most common autosomal trisomy after trisomy 21 severe psychomotor and growth retardation, microcephaly, microphthalmia, malformed ears, micrognathia or retrognathia, microstomia, distinctively clenched fingers, and other congenital malformations

Stickler Syndrome distinctive facial appearance, eye abnormalities, hearing loss, and joint problems somewhat flattened facial appearance underdeveloped bones in the middle of the face, including the cheekbones and the bridge of the nose High myopia, glaucoma, cataracts, retinal detachment Hearing loss Loose or hypermobile joints, arthritis, scoliosis, khyphosis, platyspondyly

Velocardiofacial Syndrome
structural or functional palatal abnormalities, cardiac defects, unique facial characteristics, hypernasal speech, hypotonia, and defective thymic development DiGeorge Syndrome (10%) at least 2 of the following features: Conotruncal cardiac anomaly Hypoparathyroidism, hypocalcemia Thymic aplasia, immune deficiency Velo: cleft palate Cardio: interrupted aortic arch type B (50%),truncus arteriosus (34.5%) and tetralogy of Fallot (16%). Other cardiac defects include pulmonary atresia with ventricular septal defect Facial:

Pediatrics in Review 1988;9;331 Lorraine Suslak and Franklin Desposito
Infants with Cleft Lip/Cleft Palate

Cleft Palate: Treatment
Immediate problem: Feeding Difficulty creating sufficient suction in the mouth to complete a feeding without tiring Soft artificial (cross-cut) nipples with large openings, a squeezable bottle Plastic obturator Small, frequent feedings, not longer than 30mins Burped 2-3x during a feeding: bottle positioned as upright as possible to avoid air in the nipple, or fed with an angled bottle Timing of surgical correction is individualized Width of the cleft Adequacy of the existing palatal segment Morphology of the surrounding areas Neuromuscular function of the soft palate and pharyngeal walls Complete rehabilitation can require years of special tx by a team consisting of a pedia, plastic surgeon, ent, oral and maxillofacial surgeon, pedia dentist, prosthodontist, orthodontist, speech therapist, geneticist, medical social worker, psychologist, and public health nurse Parents have the added concern that the baby must gain weight before the cleft can be repaired Infants who have a CP have a connection between the mouth and the nose and, therefore, have difficulty creating sufficient suction in the mouth to complete a feeding without tiring. Often they are unable to obtain enough nutrition by breastfeeding alone. Mothers should be encouraged to try breastfeeding, but if weight gain is poor,supplementation with a bottle, ideally using pumped human milk, will be needed. SWALLOW MORE AIR: should be burped two to three times during a feeding, with the bottle positioned as upright as possible to avoid air in the nipple, or fed with an angled bottle. be cautioned not to stop for too long in the middle of the feeding to burp the baby or the infant may lose interest in completing the feeding squeezable bottles, which allow them to provide the force for giving a mouthful of milk to the baby, rather than having the baby suck to provide the force 3 months of age when the infant has shown satisfactory weight gain and is free of any oral, respiratory, or systemic infection. Modified Millard rotation-advancement technique: a staggerred suture line minimizws notching of the lip and retraction of scar tissue

Cleft lip: “rule of 10s”– 10lbs, 10 weeks old, and hgb of 10.0 g/dL Goals of surgery: Union of the cleft segments Intelligible and pleasant speech Reduction of nasal regurgitation Avoidance of injury to the growing maxilla Cleft palate: Usually by 1 year of age (speech development) Furlow double-opposing Z-plasty (most common) may need revisions as they grow older When delayed beyond 3rd year: a contoured speech bulb can be attached to the posterior of the maxillary denture Cleft palate: usually crosses the alveolar ridge and interferes with teeth formation in the anterior maxillary region May be displaced, malformed, or missing (replaced by prosthetics) When delayed beyond 3rd year: a contoured speech bulb can be attached to the posterior of the maxillary denture So that contraction of the pharyngeal and velopharyngeal muscles can bring tissues into contact with the bulb to accomplish occlusion of the nasopharynx and help the child develop intelligible speech. Kliegman et al Nelson’s Textbook of Pediatrics. 19th Edition Samanich, J. Cleft Palate . Pediatrics in Review 2009;30;230

Postoperative management: gentle aspiration of nasopharynx (minimizes atelectasis or pneumothorax which are common complications) Maintenance of clean suture line and avoidance of tension on the sutures Bottle-fed with arms restrained and with elbow cuffs Fluid or semi-fluid diet for 3 wks Hands, toys, and other foreign bodies are kept away from the surgical site Kliegman et al Nelson’s Textbook of Pediatrics. 19th Edition

Cleft Palate: Sequelae
Recurrent otitis media and subsequent hearing loss Displacement of maxillary arches and teeth malposition Misarticulations and velopharyngeal dysfunction (10-20% after repair) Emission of air from the nose Hypernasal quality Compensatory misarticulations (glottal stops) Middle ear infection: anomalies of the insertion of the tensor and levator veli palatini muscles into the eustachian tube, affected children are unable to open and ventilate the middle ear adequately Speech defect: inadequacy of palatal and pharyngeal muscles After CP repair, about 10% to 20% of patients experience velopharyngeal insufficiency, a phenomenon in which the soft palate cannot form a tight closure with the pharynx, causing air to escape through the nose rather than being directed through the mouth during speech. This effect manifests as audible nasal air escape and as hypernasal resonance during speech, particularly when making the s, z, sh, f, p, and b sounds. Affected children may develop maladaptive compensatory articulation errors for these sounds, making their speech more difficult to understand. Children who have CP also may have speech problems caused by dental malocclusion from the cleft or from fistula formation after surgery. Fistulas can develop between the oral and nasal cavities, leading to air escape during speech and to regurgitation of food or liquids through the nose. Surgical correction of velopharyngeal insufficiency, fistula, or other structural anomalies generally is necessary before speech therapy, an integral part of treatment for the child who has CP, can be successful. Kliegman et al Nelson’s Textbook of Pediatrics. 19th Edition Samanich, J. Cleft Palate . Pediatrics in Review 2009;30;230

CASE 2: Imperforate Anus
M. B. R. 33, G2P1 (1001), 38 s/p PCS for arrest of descent CC: irregular uterine contractions PNCU: U/R Past Medical: s/p Harrington rod insertion Personal/Social History: U/R Family History: (+) DM, Hypertension Stable Vital Signs IE: 1cm, 50% CTG: category 1 trace s/p Repeat CS Male APGAR 9, 9 3350 g MT 38 AGA Maria Christina Felicidad Bautista Rivera January 17, 2013 Under Dr. Rivera HPI: irregular uterine contractions without bloody or watery vaginal discharge, good fetal movements Married, executive, no vices

Pertinent Data: Imperforate Anus
PBR Delivered via Scheduled Repeat Cesarean Section 33 year old G2P2 (2002) AOG: 38 1/7 weeks MT: 38 AGA Apgar Score: 9,9 Anthropometrics: BW= 3350 grams BL= 52 cm HC= 34 1/2 cm CC= 34 cm AC= 29 cm

Pertinent History: Imperforate Anus
Maternal History: 3rd Trimester, Cough and Colds, no medications given Past Medical History: Scoliosis s/p Spine surgery (1993) Family History: Diabetes, Hypertension OB History: G PCS for Arrest of descent- LFT- Male- TMC- No FMC G2: Present Pregnancy Personal Social: Post-graduate, Works as a market researcher, no vices

Physical Examination: Imperforate Anus
Had good cry and activity Clear amniotic fluid Flat and open fontanelles Good air entry, no retractions Regular cardiac rhythm, HR at 150 bpm Soft Abdomen Grossly male genitalia Imperforate Anus Full pulses

Diagnosis: Imperforate Anus
Term Baby Boy t/c Imperforate Anus

PLANS: Transfer to Level III care Maintain on NPO Referral to Surgery

Course in the NICU: Imperforate Anus
Subjective Objective Assessment Plan 5th HOL On NPO No vomiting Active T: 36.7, HR 143, RR: 44 Good air entry, no retractions Good cardiac tone Soft abdomen (+) Imperforate anus Term Baby Boy t/c Imperforate Anus Insert OGT For Babygram Observe for any fecalith material with UO IVF HGT monitoring

Subjective Objective Assessment Plan 7th HOL On NPO No vomiting Active (+) UO: no Fecalith matter noted T: 36.9, HR 147, RR: 42 Good air entry, no retractions Good cardiac tone Soft abdomen (+) Imperforate anus Babygram: Normal Term Baby Boy t/c Imperforate Anus IVF

Subjective Objective Assessment Plan 20th HOL On NPO No vomiting Active (+) UO T: 36.7, HR 151, RR: 43 Good air entry, no retractions Good cardiac tone Soft abdomen, slightly dilated (+) Imperforate anus Term Baby Boy t/c Imperforate Anus For cross table lateral abdominal X-ray in prone position For anoplastly Start Ampicillin and Gentamycin

Subjective Objective Assessment Plan 26th HOL No vomiting (+) UO Evacuation of meconium intra-op Stable vital signs Good air entry, no retractions Good cardiac tone Soft abdomen (+) Anal pack Term Baby Boy Imperforate Anus s/p Anoplasty Feedings resumed

Subjective Objective Assessment Plan 3rd DOL Tolerates 20 ml every 2 hours with breastfeeding No vomiting (+) UO (+) meconium Good air entry, no retractions Good cardiac tone Soft abdomen Full pulses Term Baby Boy Imperforate Anus s/p Anoplasty For rooming in (Discharged at the 5th DOL)

Imperforate Anus Absence of an anal opening Occurs in 1 in 5000 births
- May have other associated problems: VACTERL

VACTERL/VATER association is typically defined by the presence of at least three of the following congenital malformations: vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula, renal anomalies, and limb abnormalities. In addition to these core component features, patients may also have other congenital anomalies. Although diagnostic criteria vary, the incidence is estimated at approximately 1 in 10,000 to 1 in 40,000 live-born infants Orphanet J Rare Dis. 2011; 6: 56. Published online 2011 August 16. doi: /

Cross table lateral prone Xray
If the air column is more than 1 cm from the perineum, a colostomy is indicated. 1.58 cm for our patient. Cross table lateral prone Xray

The presence of meconium at the perineum, a bucket-handle malformation (ie, a prominent skin tag located at the anal dimple, below which an instrument can be passed), and an anal membrane (through which meconium is visible). A flat bottom or flat perineum, as evidenced by the lack of a midline gluteal fold and the absence of an anal dimple, indicates that the patient has poor muscles in the perineum. Newborn boys Anoplasty - Rectoperineal fistula Colostomy - Rectobulbar urethral fistula, rectoprostatic urethral fistula, rectobladderneck fistula, imperforate anus without fistula, rectal atresia Anoplasty Colostomy

NEONATES WITH APGAR < 7

Neonates with APGAR < 7, January 2014
NUMBER OF NEONATES WITH APGAR < 7 2 Incidence among total live births 5 in 1000 LB Delivered from low risk mothers Delivered from high risk mothers 63 63

CASE 3: APGAR 5, 4 J. C. A. 148/92, HR 66, RR 18, 36C 32, G1P0, 40
CC: watery vaginal discharge Past Medical: GDM – 9 wks AOG, on Insulin 26u BID; Asthma – Symbicort inhaler PRN; Thyroid disease Personal/Social History: U/R Family History: (+) DM 148/92, HR 66, RR 18, 36C SE: moderate pooling of greenish amniotic fluid IE: 4cm, 70%, -3, (-) BO W s/p STAT PCS Male APGAR 5, 4, 4 4210 g MT 39 LGA Jolet Cristobal Ayaso PRELR: 6:00am, BABY OUT: 6:50AM January 8, 2014 Under Dr. Cotas-Cruz HPI: watery vaginal discharge an hour PTC with moderate uterine contractions every 15 minutes and minimal vaginal bleeding, good fetal movements LMP: April 8, EDD: Jan. 8, 2014 GDM at 9 weeks AOG, 75g OGTT 1 level elevated, referred to Endo, on Insulin ; BANIAE since CH last attack Dec 2013 on Symbicort inhaler PRN; Thyroid disease since 2007, s/p thyroidectomy, LTFT: June 2013 with normal results Married, homemaker, denies smoking, occasional alcoholic beverage drinker

Jolet Cristobal Ayaso PRELR: 6:00am, BABY OUT: 6:50AM
January 8, 2014 Under Dr. Cotas-Cruz HPI: watery vaginal discharge an hour PTC with moderate uterine contractions every 15 minutes and minimal vaginal bleeding, good fetal movements LMP: April 8, EDD: Jan. 8, 2014 GDM at 9 weeks AOG, 75g OGTT 1 level elevated, referred to Endo, on Insulin ; BANIAE since CH last attack Dec 2013 on Symbicort inhaler PRN; Thyroid disease since 2007, s/p thyroidectomy, LTFT: June 2013 with normal results Married, homemaker, denies smoking, occasional alcoholic beverage drinker

Identifying Data Live, term, baby boy delivered via STAT caesarian section for nonreassuring fetal heart rate pattern to a 33 year old G1P1 (1001) at 40 weeks age of gestation BW= 4210g BL= 452 cm HC= 35 ½ cm CC= 37 cm AC= 32 cm MT 39 weeks LGA AS 5, 4, 4

Maternal History 1st trimester 2nd trimester
Started prenatal check-up (13x for the whole pregnancy) Ultrasound 5x = normal Threatened abortion given Isoxilan and bed rest for 2 months 2nd trimester Gestational Diabetes = FBS = 250, referred to endocrinologist  started on insulin 12 ‘u’ BID FBS repeat after a month = 180, insulin increased to 14 ‘u’ BID until 26 ‘u’ 2x/day (+) UTI (pus cells = 50-60) treated with Cefalexin for 7 days, repeat urinalysis = normal Upon admission, noted to have variable decelerations with latest at 70 bpm 3x, with thickly stained amniotic fluid

Past Medical History Bronchial asthma since childhood on Symbicort 350mcg 1 puff PRN Thyroid nodule 2007 s/p total thyroidectomy, no maintenance medications, last thyroid function test  June 2013 (normal results)

Family History Maternal grandparents : diabetes
Maternal grandfather: hypertension Maternal grandmother: thyroid disease

Personal Social History
College undergraduate Entrepreneur No vices

Upon delivery Had thickly stained amniotic fluid, with weak cry, heart rate of 150s, cyanotic, with some flexion and grimace Suctioning and stimulation done At 5 minutes: still cyanotic, no cry but with spontaneous respiration, heart rate of 80s  positive pressure ventilation done  heart rate now 120s, with acrocyanosis, no cry

intubated with ET size of 3.5 level 12
At 6 minutes, heart rate became 70  positive pressure ventilation done  heart rate of 110, still with no cry, and acrocyanosis  intubated with ET size of 3.5 level 12 Pink, with some flexion, heart rate 160, Good air entry, rales on both lung fields, good cardiac tone, soft abdomen, 2 umbilical arteries and 1 vein, stained cord, full pulses

Transferred to Level 3 Hooked to a mechanical ventilation support Placed on NPO Work-up: CBCPC, Blood Culture and Sensitivity, CRP Chest Xray obtained VBG done Antibiotics and Dobutamine drip started at 5mcg/kg/min IV fluids started BP and O2 saturations obtained

Complete Blood Count CRP: 0.49 mg/dl Hgb Hct WBC N L M E band Plt 160
23.7 29 63 06 02 172 CRP: 0.49 mg/dl

Chest Xray Impression: Meconium Aspiration Pneumonia with superimposed pulmonary edema

10th Hour of Life Noted to have desaturations to 70’s, with alar flaring and subcostal retractions Dopamine started for heart support however held due to tachycardia Surfactant 4ml/kg given Referred to Cardiology for evaluation and management 2D Echo done

2D Echo Situs Solitus AV & VA concordance Normal venous connections
Patent foramen ovale 6mm Intact IV septum Moderate TR Mildly dilated RA & RV Patent ductus areteriosus 3-4mm Conclusion: Consistent with Persistent Pulmonary Hypertension

16th hour of life O2 saturations at 83-88% Minimal urine output
Milrinone started at 0.5mcg/kg/min for pulmonary vasodilation Dobutamine increased to 10/mcg/kg/min

Day 1-2 of life S O A P Intubated
With spontaneous respirations, occasional desaturations, no cyanosis With episodes of agitation Adequate urine output 1.7cc/kg/hr BP 67/25 CR 154 RR 68 Pre O2sats 94% Post O2 sats 92% Flat fontanelles Light jaundice to abdomen +subcostal retractions, good air entry, rales on both lung fields Regular cardiac rhythm, no murmur Soft abdomen Full pulse Persitent Pulmonary Hypertension Meconium Aspiration Syndrome Mech.Vent.Settings adjusted Phototherapy started IVF adjusted Dobutamine, Milrinone Drip continued Morphine Drip Started Antibiotic continued Fentanyl given as relaxant as needed VBG obtained

Day 3 of Life S O A P (+) Fever Intubated
With spontaneous respirations With ocassional desaturations, no cyanosis BP 68/27 CR 154 RR 72 O2sats 98% T37.8 Flat fontanelles Light jaundice to abdomen +subcostal retractions, good air entry, harsh breath sounds Regular cardiac rhythm, no murmur Soft abdomen Full pulse Persitent Pulmonary Hypertension Meconium Aspiration Syndrome Feeding with EBM started Mech.Vent.Settings adjusted Phototherapy continued IVF adjusted Dobutamine, Milrinone, Morphine Drip continued Antibiotic shifted to Ceftazidime and Oxacillin CBC, CRP, BCS repeated Electrolytes, Bilirubin levels obtained Repeat Chest Xray done

Complete Blood Count Hgb Hct WBC N L M E band Plt 142 43 8.5 63 28 04
01 148 CRP Mg Na K 0.49 2.51 142 4.2 Total Bilirubin Direct Bilirubin Indirect Bilirubin 14.85 2.12 12.95 High Risk Zone

Chest Xray Impression: Interval regression of bilateral infiltrates/edema

Day 4 of Life S O A P No recurrence of Fever Intubated
With spontaneous respirations With ocassional desaturations, no cyanosis BP 74/39 CR 165 RR 61 O2sats 98% Flat fontanelles Very Light jaundice to face +shallow subcostal retractions, good air entry, harsh breath sounds Regular cardiac rhythm, no murmur Soft abdomen Full pulse Persitent Pulmonary Hypertension Meconium Aspiration Syndrome Midazolam Drip started at 0.5mcg/kg/min BCS (Staph. Haemolyticus) Transferred to isolation

Day 5 of life S O A P Intubated With spontaneous respirations
No desaturations, no cyanosis BP 68/31 CR 167 RR 50 O2sats 94% Flat fontanels Very Light jaundice to face +subcostal retractions, good air entry, harsh breath sounds Regular cardiac rhythm, no murmur Soft abdomen Full pulse Persitent Pulmonary Hypertension Meconium Aspiration Syndrome Mech.Vent.Settings adjusted Phototherapy discontinued Feeding increased and IVF adjusted Dobutamine drip discontinued Milrinone and Morphine drip decreased Midazolam Drip continued Lumbar puncture done

Day 6 of life Day 7 of life Blood CS: Staph. Haemolyticus Sensitive to Vancomycin, resistant to Ceftazidime Antibiotic shifted to Vancomycin Milrinone drip discontinued Mech.Vent. adjusted + coughing episodes Midazolam drip discontinued Given Ipratropium Bromide + Salbutamol nebulization for cough

Day 8 of life Extubation done
no desaturation, tachypnea, not in distress Hooked to CPAP then discontinued Nebulization with Salbutamol for 24hrs Repeat cbc, crp, blood cs done

Complete Blood Count CRP: 1.4 mg/dl Hgb Hct WBC N L M E band Plt 176
54 17.2 69 20 08 03 114 CRP: 1.4 mg/dl

Day 9 – Day 14 of life Good cry and activity
No cyanosis, tachypnea, sign of respiratory distress Feeding increased then fed as tolerated Vancomycin completed for 10days Referred to Pediatric Ophtalmologist for Retina screening and Development Pedia for evaluation Discharged

Final Diagnosis Live Term Baby Meconium Aspiration Syndrome
Persistent Pulmonary Hypertension Sepsis (Staphylococcus Haemolyticus) Hyperbilirubinemia Unspecified

Meconium Aspiration Syndrome and Persistent Pulmonary Hypertension

Meconium passage in utero  gasping by the fetus or newly born infant can cause aspiration of meconium-contaminated amniotic fluid  can obstruct airways, interfere with gas exchange, and cause severe respiratory distress Meconium-stained amniotic fluid: 10-15% births; term and post term Meconium aspiration syndrome: 5%, 30% require mechanical ventilation, 3-5% usually die May be depressed and require resuscitation at birth At increased risk of PPHN

Aspirated meconium  vasospasm, hypertrophy of the pulmonary arterial musculature, and pulmonary hypertension that lead to extrapulmonary right-to-left shunting through the ductus arteriosus or the foramen ovale results in worsened ventilation-perfusion mismatch, leading to severe arterial hypoxemia  persistent pulmonary hypertension of the newborn (PPHN) Aspirated meconium also inhibits surfactant function.

Diagnosis PPHN should be suspected in all term infants who have cyanosis with or without fetal distress, IUGR, moconium stained amniotic fluid, hypoglycemia, and others. A PaO2 gradient between a preductal (right radial artery) and a postductal (umbilical artery) site of blood sampling >20mmHg sugests right-to-left shnting throughthe ductus arteriosus 94

Diagnosis Real-time 2D echo combined with doppler flow studies
-demonstrates right to left shunting across a patent foramen ovale and a ductus arteriosus. Tricuspid or Mitral insufficiency Holosystolic murmur Can be visualized in the 2D echo with poor contractility when PPHN is associated with myocardial ischemia Tricuspid or Mitral insufficiency may be noted on ausculatation 95

Treatment Directed correctingany predisposingdisease
Hypoglycemia, polycythemia To improve poor tissue oxygenation Response unpredictable, transient, and complicated by the adverse effects of drugs or mechanical ventilation 96

Treatment Initial management Oxygen
Correction of acidosis, hypotension, and hypercapnia Intubation and mechanical ventilation - hyperventilation is used to reduce pulmonary vasoconstriction by lowering pCO2 (~25mmHg) and increase the pH ( ) 97

Treatment Inhaled NO Potent and selective pulmonary vasodilator
Initial dose 1-20ppm Improves oxygenation Reduces the need for ECMO Initial improvement but not sustained, ECMO is required If there’s sustained improvement, usually weaned by the 5th day of therapy. 98

Treatment Extracorporeal Membrane Oxygenation (ECMO)
When response to 100% oxygen, mechanical ventilation, and drugs is poor A form of cardiopulmonary bypass that augments systemic perfusion and provides gas exchange 99

Venous bypass: Blood is initially pumped through the ECMO circuit at arate ~80% of the estimated cardiac output of ml/kg/min Venous return passes through a membrane oxygenator, warmed, and returns to the aortic arch. 100

This requires complete heparinization to prevent clotting in the circuit, patients at high risk for IVH are not candidates Complications: thromboembolism, bleeding, stroke, air embolization, others 101

Prognosis Survival varies
Long term outcome for patients is reated to the associated HIE and the ability to reduce pulmonary vascualr resistance Long term prognosis who survive after treatment with hyperventilation is comparable to that infants who have underlying illnesses of equivalent severity Birth asphyxia Hypoglycemia ECMO: favorable, 85-90% survive, 60-75% of survivors appear normal at yrs of age 102

CASE 4: APGAR 7, 5 M. I. P. 34, G2P0 (0010), 29 CC: vaginal bleeding G weeks AOG, spontaneous abortion Past Medical/Personal/Social History/Family History: U/R 103/72, HR 98, RR 19, 36.5C SE: minimal pooling of blood with some clots IE: 1cm, <50%, -3,(+)BOW CTG: Category I trace s/p NSD Male APGAR 7, 5 1510 g MT 31 AGA Ma. Joycelyn Idio Panganiban IMU: 1am, BABY OUT: 1:15AM January 24, 2014 Under Dr. Rivera HPI: vaginal bleeding IMU-for tocolysis with Isoxuprine drip, Dexamethasone 6mg IM was given for 1 dose, Utrogestan 200mg Q6 PO However, contractions were not controlled and on physical exam patient was fully dilated, station +1  delivery Married, accountant, no vices

Ma. Joycelyn Idio Panganiban IMU: 1am, BABY OUT: 1:15AM
January 24, 2014 Under Dr. Rivera HPI: vaginal bleeding IMU-for tocolysis with Isoxuprine drip, Dexamethasone 6mg IM was given for 1 dose, Utrogestan 200mg Q6 PO However, contractions were not controlled and on physical exam patient was fully dilated, station +1  delivery Married, accountant, no vices

Baby I.P. Live, Baby Boy NSD 34 year old, G2P1 (0111)
Preterm at 29 weeks AOG by LMP 31 weeks, AGA by Maturity Testing APGAR Score: 7 and 5

Anthropometrics: Birth weight: 1510 grams Birth lenght: 41 cm
Head Circumference: 29 cm Chest Circumference: 25 cm Abdominal Circumference: 23 cm Appropriate for Gestational Age

Maternal History: Day of admission  vaginal spotting, preterm labor  admitted at IMU for tocolysis

Personal/Social History:
Past Medical History: unremarkable Family History: Diabetes mellitus Personal/Social History: Non smoker, Non alcoholic drinker

OB History: G1 – 2012: spontaneous abortion at 8 weeks AOG , D&C done
G2-2014: Present Pregnancy

UPON DELIVERY: Clear amniotic fluid One loose cord coil

At the Delivery Room 1st min 2nd min 3rd- 5th min 6th min Grimace
Some flexion HR HR decreased HR= HR improved Spont. Respirationthen Acrocyanosis Color improved 1st min nd min rd- 5th min 6th min Drying, wrapping Stimulation PPV initiated Chest compression ET pulled out Suctioning secretions Intubation PPV continued Free flow O Epinephrine given thenreintubation done

Upon Transfer to NICU ET tube in place Equal breath sounds
Patient had pink color HR Better activity Good respirations

Admitting Diagnosis: Live, Baby Boy
Preterm at 29 weeks AOG by LMP, 31 weeks by Maturity testing Appropriate for Gestational Age Respiratory Distress Syndrome Sepsis Unspecified

PROBLEMS: Respiratory Distress Syndrome Intubation  CPAP
Surfactant therapy VBGs Chest Xray

Chest Xray Compensated Respiratory Acidosis
Surfactant deficiency disease considered, Neonatal pneumonia less likely 1/24 pH pCO2 pO2 HCO3 O2Sat BE 7.391 50.7 26.9 30.7 49.4 5.4 Compensated Respiratory Acidosis 1/25 pH pCO2 pO2 HCO3 O2Sat BE 7.382 47.2 40.2 28 73.5 2.7 Compensated Respiratory Acidosis 1/26 pH pCO2 pO2 HCO3 O2Sat BE 7.293 52.7 35.9 25.4 60.4 -1.7 Respiratory Acidosis

Sepsis unspecified Antibiotics (Ampicillin, Amikacin) CBC Blood CS CRP

Blood CS: No growth for 7 days HGT: 63 – 89 - 112
Hgb Hct WBC Neu Lym Mon Eos Plt 1/24 152 46 10.9 52 40 06 02 263 Hgb Hct WBC Neu Lym Mon Eos Plt 1/26 133 40 8.8 36 55 05 04 208 CRP: 0.01 Blood CS: No growth for 7 days HGT: 63 –

Hyperbilirubinemia unspecified
Phototherapy

The End

CASE 5: Skipped beats C. G. B. 103/72, HR 98, RR 19, 36.5C
25, G1P0, 38 5/7 CC: uterine contractions Past Medical/Personal/Social History: U/R Family History: Hypertension 103/72, HR 98, RR 19, 36.5C SE: minimal pooling of blood with some clots IE: 1cm, <50%, -3,(+)BOW CTG: Category 1 trace s/p PCS Female APGAR 9, 9 2890 g MT 39 AGA Catherine Gerona Banes January 21, 2014 Under Dr. AJavier HPI: uterine contractions with associated vaginal spotting and good fetal movements, no watery vaginal discharge Married, homemaker, college graduate, no vices CS for arrest of cervical dilatation

Catherine Gerona Banes
January 21, 2014 Under Dr. AJavier HPI: uterine contractions with associated vaginal spotting and good fetal movements, no watery vaginal discharge Married, homemaker, college graduate, no vices CS for arrest of cervical dilatation

Birth History ARB Delivered via STAT Primary Cesarean Section for arrest in cervical dilatation 25 year old G1P1 (1001) AOG: 38 5/7 weeks MT: 39 AGA Apgar Score: 9,9 Anthropometrics: BW= 2890 grams BL= 47 cm HC= 35 cm CC= 32 cm AC= 27 cm

Maternal History: 1st Trimester, Cough and Colds, no medications given
Past Medical History: Breast cyst, Left, s/p Excision(2012) Family History: Hypertension OB History: present pregnancy Personal Social: College graduate, housewife, no vices

Upon Delivery Good cry and activity, no cyanosis Clear amniotic fluid
Flat and open fontanelles Good air entry, no retractions Irregular cardiac rhythm, HR 140 bpm, no murmur (skipped beats, x per minute) Soft Abdomen Grossly normal female genitalia Full pulses

Initial Impression Term Baby Girl r/o Cardiac Pathology

Transfer to Level 3 of care hook to cardiac monitor
PLAN: Transfer to Level 3 of care hook to cardiac monitor Refer to a pediatric cardiologist Hook to cardiac monitor BP and oxygen saturations on all extremities

Course in the NICU Subjective Objective Assessment Plan 3rd HOL
Good suck, cry, and activity Able to latch T: 36.8, HR 146, RR: 44 No cyanosis, no alar flaring Good air entry, no retractions Irregular cardiac rhythm, with 1-2 skipped beats/minute Full pulses Live term baby girl r/o cardiac pathology Monitor vital signs every hour Hook to cardiac monitor BP and O2 sats on all extremities Watch out for skipped beats/minute

Oxygen saturations on all extremities: 100%
Stable vital signs BP on all extremities: Oxygen saturations on all extremities: 100% 61/31 63/38 65/30 61/35

Course in the NICU Subjective Objective Assessment Plan 10th HOL
Good suck, cry, and activity Tolerates 10-15ml of milk feedings T: 37, HR 122, RR: 44 No cyanosis, no alar flaring Good air entry, no retractions Irregular cardiac rhythm, with 2-5 skipped beats/minute Full pulses Live term baby girl r/o cardiac patholog Bed side 2D-echo EG-7

2D echo Cardiology remarks: PFO 4.2mm Left to right shunt
Trivial mitral regurgitation PDA 1.8 continuous blow Normal transitional circulation; no arrhythmia Cardiology remarks: Common incidental finding in newborns Structural abnormality ruled out No signs of heart failure noted Refer for >5 skipped beats per minute

EG7 results: Na: 138 mmo/L K: 4.3 mmo/L iCal: 1.21 mmo/L Hct: 47%
pH: 7.37 pCO2: 47 mmHg pO2: 38mmHg (80-105) HCO3: 27 mmo/L TCO2: 28 mM Beecf: 2 mM sO2: 69% (95-98) tHB: 16 g/dL

Course in the NICU Subjective Objective Assessment Plan 24th HOL
Good suck, cry, and activity Tolerates 10-15ml of milk feedings every 2 hours T: 36,5, HR 148, RR: 56 No cyanosis, no alar flaring Good air entry, no retractions Regular cardiac rhythm, no skipped beats Full pulses Live term baby girl Rooming in

Course in the NICU Subjective Objective Assessment Plan Day 2 of life
Good suck, cry, and activity Breastfeeding T: 36,5, HR 148, RR: 56 No cyanosis, no alar flaring Good air entry, no retractions Regular cardiac rhythm, no skipped beats Full pulses Live term baby girl May go home For ECG - Normal

Neonatal Arrhythmias Arrhythmias in fetuses and newborns are relatively common -- up to 90% of newborns and 1% to 3% of pregnancies Life-threatening arrhythmias are uncommon

Almost all arrhythmias fall into one of three categories
irregular tachycardic bradycardic

Arrhythmias are found in 1–5% of newborns during the first 10 days of life
Most are premature supraventricular beats that will disappear during the first month of life The development of symptoms depends on the rate and duration of the arrhythmia tachyarrhythmia - 240–300bpm Bradyarrhythmia - <100bpm

Normal Newborn ECG

Sinus Pause

Sinus Arrhythmia

Sinus pauses from 800 to 1,000 msec may occur in healthy newborns
Such pauses usually are followed by escape beats from the atria or the atrioventricular (AV) junction Pauses of more than 2 seconds are considered abnormal

Possible causes: oversedation, (drugs passed through the placenta)
hypothermia central nervous system abnormalities increased intracranial pressure increased vagal tone obstructive jaundice hypothyroidism

DISTRIBUTION OF BIRTHS January 2014

Distribution of Deliveries According to Birthweight
87% of infants were appropriate for age. 11% were large for gestational age. 2% were SGA

Classification Based on Best Score
SGA AGA LGA TOTAL Preterm 2 16 18 Term 1 157 23 181 Post Term 3 174 200 This table shows the birth weight and AOG on delivery. Majority of our babies were born term, and most were AGA.

Small for Gestational Age Infants, January 2014
NUMBER OF SGA NEONATES 3 Incidence among total live births 10/1000 LB Delivered from normal mothers 1 Delivered from high risk mothers 2 A. Maternal factors 2 B. Fetal Factors C. Unknown factor 1 Duque, Maridel 31 G2P1 (0100), 1290g, 35 SGA, CHPN+SIP Jimenez, Karen Grace 32 G2P1 (1001), 2025g, 38 SGA, no comorbids Duterte, Cherry Anne 30 G1P0, 2140g, 37 SGA, GDM 146 146

Large for Gestational Age Infants, January 2014
NUMBER OF LGA NEONATES 23 Incidence among total livebirths 41 /1000 LB Delivered from normal mothers 15 Delivered from high risk mothers 8 A. Maternal factors Gestational diabetes mellitus 5 B. Fetal Factors Fetal Macrosomia 3 CHECK BMI’s Laus, Clarisse 24 G2P1 (1001), BMI , 4145g, 42 LGA, no comorbids Amor, Karina 32 G4P2 (2012), BMI , 3860g, 38 LGA, no comorbids Franquia, J 27 G1P0, BMI , 3625g, 38 LGA, no comorbids Modaressi Mohavedi, Fatemeh 22 G1P0, BMI , 3770g, 39 LGA, no comorbids Dizon, Imelda 32 G3P1 (1011), BMI , 3710g, 39 LGA, GDM Rabago, Nina 31 G1P0, BMI , 3765g, 39 LGA, no comorbids(anemia) Blake, Margarita 36 G5P3 (3013), BMI , 3560g, 38 LGA, no comorbids Gopez, Rochelle 31 G2P1 (1001), BMI , 3855g, 39 LGA, no comorbids Cruz, Consuela 31 G1P0, BMI , 3270g, 39 LGA, no comorbids Rebanal, Maica 26 G1P0, BMI , 3750g, 39 LGA, no comorbids Aldeon, Veronica 32 G1P0, BMI , 3975g, 40 LGA, no comorbids (UTI) Kisteria, Liza 35 G1P0, BMI , 3800g, 39 LGA, no comorbids Bacala, Gladys, 27 G1P0, BMI , 4020g, 40 LGA, no comorbids Ngo, Vinalyn 36 G2P1 (1001), BMI , 3505g, 37 LGA, GDM Bragais, Sarah 29 G1P0, BMI , 3120g, 37 LGA, GDM Dee, Lilet, 35 G3P2 (2001), BMI , 3705g, 40 LGA, no comorbids Nepomuceno, Rosalie 32 G1P0, BMI , 3705g, 38 LGA, GDM Chua, Melanie 30 G1P0, BMI , 3650g, 38 LGA, GDM Periquet, Alexis 30 G1P0, BMI , 3810g, 39 LGA, no comorbids Gesmundo, Charmaine 37 G2P1 (1001), BMI , 3595g, 38 LGA, no comorbids Estrella, Jeany Rose 26 G1P0, BMI , 3665g, 37 LGA, no comorbids Carbonell, Rosario 26 G1P0, BMI , 3515g, 38 LGA, no comorbids (BANIAE) Lontok, Shearon 37 G2P1 (1001), BMI , 3530g, 37 LGA, no comorbids 147 147

DISTRIBUTION OF BIRTHS ACCORDING TO GESTATIONAL AGE ON DELIVERY

Distribution of Births According to AOG on Delivery
Livebirths = 200 Last month, 90% of the total births were delivered term while 9% were delivered preterm based on AOG. 1% were post term delivery.

Weight vs MT 9 169 19 200 Wt (grams) <28 28-29 30-31 32-33 34-35
/7 37-39 40-42 > 42 Grand Total 1 2 5 3 10 13 67 73 56 7 63 29 6 35 >3800 9 169 19 200 This table shows the relationship between AOG and birthweight . Majority of our babies were born term, and within the birthweights of grams.

Weight vs LMP 13 146 31 200 Wt (grams) <28 28-29 30-31 32-33 34-35
/7 37-39 40-42 > 42 Grand Total 2 1 5 3 4 12 8 56 7 72 60 11 71 22 30 >3800 13 146 31 200 This table shows the relationship between AOG and birthweight . Majority of our babies were born term, and within the birthweights of grams.

Weight vs Best Score 150 32 200 Wt (grams) <28 28-29 30-31 32-33
34-35 /7 37-39 40-42 > 42 Grand Total 1 2 5 4 6 12 57 9 72 61 10 71 22 8 30 >3800 150 32 200 This table shows the relationship between AOG and birthweight . Majority of our babies were born term, and within the birthweights of grams.

Livebirths and Preterm Delivery, January 2014
NUMBER OF PRETERM NEONATES 18 Incidence among total livebirths 94 in 1000 LB Delivered from low risk mothers 6 Delivered from high risk mothers 12 Among the preterm neonates, 12 were delivered from high risk mothers. Duque-CHPN+SIP, 35 Bilan-Preec, GDM, 36 late preterm Tiangco-33, no comorbids Sumpaico-GDM, anemia, 37 SGA Ocampo-GHPN, 36 late preterm Mayo-36, late preterm, no comorbids Mabazza twins-BANIAE, 37 late preterm??? Aspiras-CHPN, GDM, 32, mortality Geroy-37, no comorbids ??? Pesigan-32, no comorbids, in PTL Pasco-36, late preterm, no comorbids(anemia) Fababaer-36, late preterm, previous history of preterm delivery Panganiban-31, no comorbids (anemia) Hung-twinB, 36, late preterm Duterte-GDM, 37 ??? Sumulong-37, no comorbids??? Verdeflor-36, late preterm, no comorbids 153 153

ROOMING IN AND BREASTFEEDING RATES
C/O PEDIA

Rooming-In Rate Total No. of Babies Eligible for Rooming In = 182/ 200 (91%) Rooming-In Rate = 180/182 (98.9%)

Breastfeeding Rates

JCI: 92.80% (exclusively BF/Term NB -exclusions)
BREASTFEEDING RATE N (Total deliveries) = 200 JCI: 92.80% (exclusively BF/Term NB -exclusions) BFHI: 92.86% (exclusively BF + w/medical indications of not BF/total no of live births) Level Pure Mixed Formula Only None Donor Total Level I (n=58) Roomed in (n=57) 50 8 1 58 Level II (n=134) 79 52 3 134 Level III (n=7) 7 Isolation (n = 1) 4 Grand Total 130 64 6 200

GENERAL INDICES OF PERINATAL DEATH

Neonatal Mortality, January 2014
NUMBER OF MORTALITIES 1 Incidence among total live births 5 per 1000 LB PERINATAL MORTALITY RATE Crude Perinatal Mortality Rate 1 mortality / 200 total births 5 per 1000 TB Corrected Perinatal Mortality Rate 0 non-lethal mortalities+0 stillbirth /200 total births 159

MORTALITY CASE

CASE 6: Mortality Case AAA
137/93, HR 108, RR 17, 36.8C IE: soft, closed, uneffaced CTG: Category 2 trace s/p STAT PCS Female APGAR 5, 4 1420g MT 32 AGA A. A. A. 27, G1P0, 33 2/7 CC: minimal variability on CTG (+) GDM, (+) GHPN s/p repair of cleft lip Family History: (+) DM Anna Arcenas Aspiras WITH PERINAT REFERRAL; PRELR: 9:30AM, BABY OUT: 10:49PM January , 2014 Under Dr. Campana/Cango-Castor HPI: on regular PNCU, patient had DV (normal results) and NST with minimal variability, OB wise asymptomatic, advised admission for close monitoring GDM = 2nd trimester – 1 level at 75g ogtt, diet & cbg; GHPN-3rd trimester, 140/90 on MD 250 TID, s/p repair of cleft lip, unrecalled Married, employee IMU –Dexamethasone 12mg/im q12h x 1 dose only, aldo 250TID500 TID, referred to perinat and neonat, CTG: 120bpm, minimal variability, no A, spontaneous decelerations as low as 90 bpm with gradual recovery, no UC  STAT CS

Anna Arcenas Aspiras WITH PERINAT REFERRAL; PRELR: 9:30AM, BABY OUT: 10:49PM
January , 2014 Under Dr. Campana/Cango-Castor HPI: on regular PNCU, patient had DV (normal results) and NST with minimal variability, OB wise asymptomatic, advised admission for close monitoring GDM = 2nd trimester – 1 level at 75g ogtt, diet & cbg; GHPN-3rd trimester, 140/90 on MD 250 TID, s/p repair of cleft lip, unrecalled Married, employee IMU –Dexamethasone 12mg/im q12h x 1 dose only, aldo 250TID500 TID, referred to perinat and neonat, CTG: 120bpm, minimal variability, no A, spontaneous decelerations as low as 90 bpm with gradual recovery, no UC  STAT CS

G. A. Live Preterm Baby Girl
Stat Cesarean Section for Non-reassuring Fetal Status 27 y/o G1P1 (0101) 33 2/7 weeks AOG Anthropometrics: BW: 1420 gms; BL 41 cm; HC 28 cm; CC 24 cm; AC 23 cm Maturity Test: 32 weeks AGA

APGAR SCORE 1 2 5 4 6 7 1st minute 3rd minute 5th minute 10th minute
Appearance 1 2 Pulse Grimace Activity Respiration TOTAL 5 4 6 7

Problems Prematurity Respiratory and Cardiac Metabolic
Persistent Desaturations despite mechanical ventilation Metabolic Persistent Acidosis despite correction

2D Echocardiography Bilobed Liver Dilated hepatic veins
Aorta anterior and left to the spine IVC to the right of the spine, same level as aorta Heart is mesocardiac in position pointing to the left Poor RV function Severe Tricuspid Regurgitation

Mild Mitral Regurgitation
Mild Aortic Insufficiency Multichamber enlargement Dilated coronary arteries Ejection fraction 61%

Final Diagnosis Intractable Metabolic Acidosis
Heart Failure secondary to Neonatal Myocarditis Respiratory Distress Syndrome s/p Surfactant Therapy Poor APGAR Prematurity

THANK YOU!!!

THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics PERINATAL/NICU CONFERENCE Monthly Statistics.

Similar presentations

Presentation on theme: "THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics PERINATAL/NICU CONFERENCE Monthly Statistics."— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics PERINATAL/NICU CONFERENCE Monthly Statistics.

Similar presentations

Presentation on theme: "THE MEDICAL CITY Department of Obstetrics and Gynecology: Section of Perinatology and the Department of Pediatrics PERINATAL/NICU CONFERENCE Monthly Statistics."— Presentation transcript:

Similar presentations

About project

Feedback