PERINATAL/NICU CONFERENCE Monthly Statistics Report January 2014 PERINATAL/NICU CONFERENCE Monthly...

PERINATAL/NICU PERINATAL/NICU CONFERENCECONFERENCE

Monthly Statistics Report Monthly Statistics Report January 2014 January 2014

Marco Manzano and Clarissa Pangilinan, MD3rd Year Resident – Pediatrics

Maria Edwardina G. De Leon, MD3rd Year Resident – Obstetrics and Gynecology

THE MEDICAL CITYDepartment of Obstetrics and Gynecology: Section of Perinatology

and theDepartment of Pediatrics

TOTAL BIRTHS

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

Total Births, January 2014ACCORDING TO NUMBER OF FETUS NUMBER

Singleton 196Multifetal (n = 2) 4TOTAL LIVE BIRTHS 200

Total Births, January 2014ACCORDING TO AGE OF GESTATION NUMBER

Term 181 Preterm 18 Postterm 1TOTAL LIVE BIRTHS 200

Total Births, January 2014ACCORDING TO PLACE OF PRENATAL CARE NUMBERRegistered 198Non-registered 0TOTAL 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

NEONATALMORBIDITIES

Neonatal Morbidities, January 2014NUMBER OF NEONATAL MORBIDITIES 36Incidence among total live births 115 per 1000 LBDelivered from Normal Mothers 19Delivered from High Risk Mothers 17

Top 5 Conditions Occurring Among High Risk Mothers, January 2014

Top 5 Maternal Conditions Associated with Neonatal Morbidities, January 2014

Prematurity = 4Prematurity = 4

Prematurity = 3LGA = 2SGA = 1

Low birth weight = 1

Prematurity = 3LGA = 2SGA = 1

Prematurity = 4LGA = 1

LGA = 1Poor APGAR = 1

CONGENITALANOMALIES

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 1

Congenital Anomalies, January 2014

Cleft Palate 1

Imperforate Anus 1

Congenital anomalies: January 2013Antenatal detection and Neonatal outcome

CongenitalAnomalies

N Ultrasound Neonatal outcomeWHCC Done

Detected

Not Detecte

Outside Survive

Cleft Palate 1

Imperforate Anus1

• M. M. P.• 28, G1P0, 39• CC: vaginal bleeding• PNCU: regular,

unremarkbale• Past

Medical/Personal/Social/Family History: U/R

• Stable Vital Signs• IE: 3cm, 50%, -3, (-)BOW• CTG: Category 1 trace• Intrapartum stay x 10hrs

• s/p PCS• Female

APGAR 9,93140 gMT 38 AGA

CASE 1: Cleft Palate

• S.M.P.• 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

CASE: Cleft Palate

• 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

• NPO• ENT Referral• Therapeutics:

– Obturator fitting c/o pedia dentist– OGT feedings– Feeding plate– Breast feed as tolerated

Course in the NICU

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

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)

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. 2011. 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

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

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

Cleft Palate: Treatment• 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)

Kliegman et al. 2011. Nelson’s Textbook of Pediatrics. 19th EditionSamanich, J. Cleft Palate . Pediatrics in Review 2009;30;230

Cleft Palate: Treatment

• 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

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)

• 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, 93350 gMT 38 AGA

CASE 2: Imperforate Anus

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: • G1- 2009- 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

- 7th HOL- On NPO- No vomiting- Active- (+) UO: no

Fecalith matter noted

- T: 36.9, HR 147, RR: 42

- Good cardiac tone

- Soft abdomen

- Babygram: Normal

- Term Baby Boy

- 20th HOL- On NPO- No vomiting- Active- (+) UO

- T: 36.7, HR 151, RR: 43

- Good cardiac tone

- Soft abdomen, slightly dilated

- Term Baby Boy

- For cross table lateral abdominal X-ray in prone position

- For anoplastly

- Start Ampicillin and Gentamycin

- 26th HOL- No vomiting- (+) UO- Evacuation

of meconium intra-op

- Stable vital signs

- Good cardiac tone

- Soft abdomen

- (+) Anal pack

- Term Baby Boy

- Imperforate Anus

- s/p Anoplasty

- Feedings resumed

- 3rd DOL- Tolerates 20

ml every 2 hours with breastfeeding

- No vomiting- (+) UO- (+)

meconium

- 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

Orphanet J Rare Dis. 2011; 6: 56.Published online 2011 August 16. doi: 10.1186/1750-1172-6-56

Cross table lateral prone Xray

If the air column is more than 1 cm from the perineum, a colostomy is indicated.

Anoplasty Colostomy

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.

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).

NEONATES WITHAPGAR < 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 mothers0

• J. C. A.• 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, 44210 gMT 39 LGA

CASE 3: APGAR 5, 4

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

– 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

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 Hgb Hct WBC N L M E band Plt

160 49 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 fontanellesLight jaundice to abdomen+subcostal retractions, good air entry, rales on both lung fieldsRegular cardiac rhythm, no murmurSoft abdomenFull 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 LifeS O A P

• (+) Fever• Intubated• With

spontaneous respirations

• With ocassional desaturations, no cyanosis

BP 68/27 CR 154 RR 72 O2sats 98% T37.8Flat fontanellesLight jaundice to abdomen+subcostal retractions, good air entry, harsh breath soundsRegular cardiac rhythm, no murmurSoft abdomenFull pulse

• Feeding with EBM started

• 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

142 43 8.5 63 28 04 01 04 148

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 LifeS O A P

• No recurrence of Fever

• With ocassional desaturations, no cyanosis

BP 74/39 CR 165 RR 61 O2sats 98% Flat fontanellesVery Light jaundice to face+shallow subcostal retractions, good air entry, harsh breath soundsRegular cardiac rhythm, no murmurSoft abdomenFull pulse

• Midazolam Drip started at 0.5mcg/kg/min

• BCS (Staph. Haemolyticus)

• Transferred to isolation

Day 5 of lifeS O A P

• No desaturations, no cyanosis

BP 68/31 CR 167 RR 50 O2sats 94% Flat fontanelsVery Light jaundice to face+subcostal retractions, good air entry, harsh breath soundsRegular cardiac rhythm, no murmurSoft abdomenFull pulse

• 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

176 54 17.2 69 20 08 0 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

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 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

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 (7.5-7.55)

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.

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

Treatment

Venous bypass: Blood is initially pumped through the ECMO circuit at arate ~80% of the estimated cardiac output of 150-200ml/kg/min

Venous return passes through a membrane oxygenator, warmed, and returns to the aortic arch.

Treatment

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

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 1-3.5 yrs of age 102

• M. I. P.• 34, G2P0 (0010), 29• CC: vaginal bleeding• G1-2012-8 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

CASE 4: APGAR 7, 5

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

• 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 Drying, wrapping Stimulation PPV initiated Chest compression ET pulled

out Suctioning secretions Intubation PPV

continued Free flow O2 Epinephrine given

thenreintubation done

Grimace Some flexion HR 160 HR decreased HR= 60 HR improvedSpont. RespirationthenAcrocyanosis Color improved

Upon Transfer to NICU

• ET tube in place• Equal breath sounds• Patient had pink color• HR 120-130• 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:

1. Respiratory Distress Syndrome

• Intubation CPAP• Surfactant therapy• VBGs• Chest Xray

1/24 pH pCO2 pO2 HCO3 O2Sat BE

7.391 50.7 26.9 30.7 49.4 5.4

• Chest Xray

• Surfactant deficiency disease considered, Neonatal pneumonia less likely

Compensated Respiratory Acidosis

7.382 47.2 40.2 28 73.5 2.7

Compensated Respiratory Acidosis

7.293 52.7 35.9 25.4 60.4 -1.7

Respiratory Acidosis

2. Sepsis unspecified

• Antibiotics (Ampicillin, Amikacin)• CBC• Blood CS• CRP

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 – 89 - 112

3. Hyperbilirubinemia unspecified

• Phototherapy

The End

• C. G. B.• 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

CASE 5: Skipped beats

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, 10 -13x per minute)• Soft Abdomen• Grossly normal female genitalia• Full pulses

Initial Impression

• Term Baby Girl• r/o Cardiac Pathology

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 NICUSubjective 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

- Irregular cardiac rhythm, with 1-2 skipped beats/minute

- Full pulses

Live term baby girlr/o cardiac pathology

- Monitor vital signs every hour

- Hook to cardiac monitor

- BP and O2 sats on all extremities

- Watch out for 25-30 skipped beats/minute

• Stable vital signs• BP on all extremities:

• Oxygen saturations on all extremities: 100%

Course in the NICUSubjective Objective Assessment Plan- 10th HOL- Good suck, cry,

and activity- Tolerates 10-

15ml of milk feedings

- T: 37, HR 122, RR: 44

- Irregular cardiac rhythm, with 2-5 skipped beats/minute

- Full pulses

Live term baby girlr/o cardiac patholog

- Bed side 2D-echo

- EG-7

• 2D echo– 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 NICUSubjective 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

- Regular cardiac rhythm, no skipped beats

- Full pulses

Live term baby girl - Rooming in

Course in the NICUSubjective Objective Assessment Plan- Day 2 of life- Good suck, cry,

and activity- Breastfeeding

- T: 36,5, HR 148, RR: 56

- 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

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 0

C. Unknown factor 1

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 5B. Fetal Factors Fetal Macrosomia 3

DISTRIBUTION OFBIRTHS ACCORDING

TO GESTATIONALAGE ON DELIVERY

Distribution of Births According to AOG on Delivery

Livebirths = 200Livebirths = 200

Wt (grams)

<28 28-29 30-31 32-33 34-3536-36 6/7

37-39 40-42 > 42Grand Total

600-999

1000-1499

1500-1999

1 2 1 1 5

2000-2499

3 10 13

2500-2999

3 67 3 73

3000-3499

56 7 63

3500-3800

29 6 35

>3800 6 3 9Grand Total

2 2 1 7 169 19 0 200

Weight vs MT

Wt (grams)

<28 28-29 30-31 32-33 34-3536-36 6/7

37-39 40-42 > 42Grand Total

600-999

1000-1499

1500-1999

1 2 1 1 5

2000-2499

3 4 4 1 12

2500-2999

1 8 56 7 72

3000-3499

60 11 71

3500-3800

22 8 30

1 2 2 5 13 146 31 200

Weight vs LMP

Wt (grams)

<28 28-29 30-31 32-33 34-3536-36 6/7

37-39 40-42 > 42Grand Total

600-999

1000-1499

1500-1999

2 1 2 5

2000-2499

1 4 6 1 12

2500-2999

57 9 72

3000-3499

61 10 71

3500-3800

22 8 30

2 2 4 10 150 32 0 200

Weight vs Best Score

Livebirths and Preterm Delivery, January 2014

NUMBER OF PRETERM NEONATES 18

Incidence among total livebirths 94 in 1000 LB

Delivered from low risk mothers6

ROOMING IN ANDBREASTFEEDING

Rooming-In Rate

• Total No. of Babies Eligible for Rooming In = 182/ 200 (91%)

• Rooming-In Rate = 180/182 (98.9%)

Breastfeeding Rates

Level Pure MixedFormula Only

None Donor Total

Level I (n=58)Roomed in (n=57)

50 8 0 0 1 58

Level II (n=134) 79 52 0 0 3 134

Level III (n=7) 1 3 0 0 3 7

Isolation (n = 1) 0 1 4 0 0 1

Grand Total 130 64 4 0 6 200

BREASTFEEDING RATEN (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)

GENERAL INDICESOF PERINATAL DEATH

Neonatal Mortality, January 2014

NUMBER OF MORTALITIES 1Incidence 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

5 per 1000 TB

MORTALITY CASE

• A. A. A.• 27, G1P0, 33 2/7• CC: minimal variability on

CTG• (+) GDM, (+) GHPN• s/p repair of cleft lip• Family History: (+) DM

• 137/93, HR 108, RR 17, 36.8C

• IE: soft, closed, uneffaced• CTG: Category 2 trace

• s/p STAT PCS• Female

APGAR 5, 41420gMT 32 AGA

CASE 6: Mortality Case AAA

• 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 SCORE1st minute 3rd minute 5th minute 10th minute 15th minute

Appearance

1 1 1 1 2

Pulse 2 2 1 2 2

Grimace 1 1 1 1 1

Activity 0 0 0 1 1

Respiration 1 1 1 1 1

TOTAL 5 5 4 6 7

Problems

• Prematurity• Respiratory and Cardiac

– 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!!!

PERINATAL/NICU CONFERENCE Monthly Statistics Report January 2014 PERINATAL/NICU CONFERENCE Monthly...

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