CASE DISCUSSION

Legaspi, LuisOntok, Abdul-AzizPayumo, Edelissa

Pelayo, May AngelaRodriguez, MelissaSamson, Edgardo

HISTORY

• Baby Boy J.C.

• Full Term, 37 weeks by P.A.

• 2600 g, appropriate for G.A.

• Cephalic presentation

• Repeat low-segment C.S.

• 23 year old, G2P2

Identifying Data

• OB Index: G2P2 (2002)• Previous Pregnancy:

Date: 2007

Sex: Male

BW: 2.7 kg

Place: Perpetual Help Hospital

Delivery Type: 1o Low-segment C.S.

AOG: Full Term

Complications: Cephalopelvic Disroportion

Maternal Obstetrical History

• LMP: September 04, 2008

• Prenatal Checkups: 2 at PGH

• Medications Taken: None

• Illnesses/Infection: None

• Alcohol/Tobacco Use: None

Antenatal History

• Onset of Uterine Activity:

Spontaneous

• Intensity of Contractions:

Moderate

• Membrane Status: Intact

• Analgesia: None

Labor

• Mode: Abdominal

• Amniotic Fluid: Slightly

Meconium Stained

• Analgesia: Subarachnoid

Block

Delivery

History of Present Illness

Limp, HR 60’s, acrocyanotic, with no

response

•Thermoregulation•Suctioning•Tactile stimulation

(+) grimace, HR 50’s, acrocyanotic, some

flexion

•Weaned off from O2

(+) grunting, (+) retractions

• APGAR Score: 5, 9

• Resuscitation: Supplementary O2 10 LPM via hood

Positive Pressure-Ventilation

Immediate Neonatal Period

• (-) Hypertension

• (-) Diabetes Mellitus

• (-) Bronchial Asthma

• (-) Blood Dyscrasias

Family History

PHYSICAL EXAMINATION

PHYSICAL EXAM

• GENERAL APPEARANCE:limp, in respiratory distress

• VITAL SIGNS: T: 36.6oC HR: 130 bpm RR: 50 cpmWt: 2600 g Lt: 49 cm HC: 32.5 cmCC: 31 cm AC: 28 cm

PHYSICAL EXAM

• SKIN: acrocyanotic, (-) lesions, (+) cracking, rare veins

• HEAD:(-) molding, (-) cephalhematoma, both fontanels flat and soft, (-) overlapping sutures, BT: 8cm, BP: 9cm, SOB: 9cm, OF: 10.5cm, OM: 11.5cm

• EYES:(-) discharges, anicteric sclerae, both pupils equally reactive to light

PHYSICAL EXAM

• EARS: (-) low-set ears, formed, firm with instant recoil

• MOUTH:(-) circumoral cyanosis, (-) cleft lip, formed tongue, (-) cleft palate

• CHEST/LUNGS:barrel-shaped, (+) subcostal & intercostal retractions, raised areola with 3-4 mm bud, (+) grunting, (-) tachypnea

PHYSICAL EXAM

• HEART:adynamic precordium, (-) thrills, normal rate, regular rhythm, (-) murmur

• ABDOMEN:globular but not distended, nonpalpable liver

• UMBILICUS:translucent, (-) meconium stained, 2 arteries & 1 vein

• BACK:lanugo with bald areas, (-) dimpling, straight spine

PHYSICAL EXAM

• GENITALIA:both testes descended, scrotum with good rugae

• ANUS:patent, (+) passage of meconium

• EXTREMITIES:(-) polydactyly, (-) hip dislocation, plantar crease over anterior 2/3, equally strong & palpable pulses

• NEUROLOGIC EXAM:(+) moro reflex, (+) sucking reflex, (+) grasping reflex

PRIMARY IMPRESSION

• Meconium Pneumonitis

• Full term 37 weeks by PA 2600 grams AGA cephalic presentation delivered by repeat LSCS, AS 5,9

Primary Working Impression

(+) history of meconium staining

baby received non-vigorous, HR 60s, poor muscle tone, with no response

(+) tachypnea (+) grunting (+) retractions

MECONIUM PNEUMONITIS

DIFFERENTIAL DIAGNOSIS

DIFFERENTIALSDifferential Rule-in Rule-out

Hyaline Membrane Disease

(+)tachypnea(+) grunting(+)retractions

-rare in term neonates-mother not GDM-worsens / peaks at 48-36 hours

Transient Tachypnea of the Newborn

-usually follows uneventful normal FT SVD or cesarean section

-Early onset tachypnea with or without retractions

(+) expiratory grunting

-cyanosis relieved by minimal 02-with rapid recovery in 3 days-PE: lungs clear w/o rales or rhonchi-benign, self-limited course

Neonatal Pneumonia (+)tachypnea(+) grunting(+)retractions(+) cyanosis

Pre-natal history suggests infection-usually predisposed by pre-mature labor, PROM, increased IE-CBC usually: neutropenia, leukocytosis-cannot be fully ruled-out

Meconium Aspiration Syndrome

(+) history of meconium staining-baby received non-vigorous, HR 60s, poor muscle tone, with no response(+)tachypnea(+) grunting(+)retractions

-cannot be fully ruled-out

Neonatal Sepsis Respiratory distress(+)tachypnea(+) grunting(+)retractions

Cannot be fully ruled out

COURSE IN THE WARD

• Born at PGH Nursery on May 7, 2009 with APGAR score 5, 9

• Started on Piperacillin-Tazobactam (75mkd) 195 mg IV q12

• Started on Amikacin (15mkd) 40 mg IV OD

Catcher’s Area

Catcher’s AreaPiptazo Combination antibiotic

containing the extended-spectrum penicillin and the B-lactamase inhibitor tazobactam

Amik An aminoglycoside With synergistic effect with B-lactams

• Labs:• CBC with PC Na, K, Cl, Ca,

• Blood typing CXR APL

• ABG Blood C/S

• Venoclysis started with D10W (80) @

9cc/hr• NPO, Hgt q8• O2 support at 10 lpm/hood

Catcher’s Area

NICU

• Admitted at NICU 3 on May 7, 2009

• Received with fair pulses BP 30-40/20’s

• Given total of 50 cc/kg PNSS IV bolus, BP improved to 40-50/30’s but still with fair pulses

• Started on Dopamine @ 10mcg/kg/min to run for 1cc/hour

(Dopamine 0.9cc + D5W 23.1cc)

• UVC inserted

On Admission

On Admission

50 cc/kg PNSS IV bolus

To increase BP

Dopamine @ 10mcg/kg/min to run for 1cc/hour (Dopamine 0.9cc + D5W 23.1cc)

Maintenance bp

• Due to persistent desaturation (O2 sats 80’s), patient intubated with MV settings 100%, 18/3, RR 60 LT 0.4

• O2 sats improved to 98-100%• ABGs ordered• D10W increased to run for 10

cc/hour• STAT NaHCO3 5 meqs given

On Admission

On Admission

NaHCO3 5 meqs To counteract metabolic acidosis

MV settings 100%, 18/3, RR 60 LT 0.4

?

ABG

pH 7.189

pCO2 51.20

pO2 76.00

HCO3 19.80

BEb -8.2

O2sat 91.40%

05/07/09 23:10 100% O2 hood

Respiratory AcidosisDecrease VentilationHypoxemia

ABG

pH 7.252

pCO2 39.70 N

pO2 188.00

HCO3 17.70

BEb -8.5

O2sat 99.50%

05/08/09 00:18 S/P INTUBATION 100% 18/3 60 0.4

Metabolic AcidosisNaHCO3 5 meqs

ABG

ABG

pH 7.407 N

pCO2 28.00

pO2 146.00

HCO3 17.80

BEb -5

O2sat 99.30%

05/08/09 06:51 AFTER CORRECTION 100% 18/3 60 0.4

ABG

Component 05/07/09 Reference Range

Unit

WBC 5.56 5.0 – 30.0 X109/L

RBC 3.74 4.0 – 6.0 X1012/L

HGB 129 120-180 g/L

HCT 0.386 0.370 – 0.540

MCV 103.2 80.0 – 100.0 Fl

MCH 34.5 27.0 – 31.0 Pg

MCHC 334 320 – 360 g/L

RDW 17.2 11.0 – 16.0 %

Platelet 227 150 – 450 X109/L

NRBC 2/100

Complete Blood Count

Component 05/07/09 Reference Range

Unit

Neutrophil 0.697 0.500 – 0.700 %

Lymphocyte 0.182 0.200 – 0.500 %

Monocyte 0.101 0.020 – 0.090 %

Eosinophil 0.016 0.000 – 0.060 %

Basophils 0.004 0.000 – 0.020 %

Stab %

Metamyelocyte

Myelocyte

Promyelocyte

Blast

Atypical Lymphocyte

Complete Blood CountComplete Blood Count

Electrolytes

Test 05/09/09 05/12/09 Units Normal Values

Calcium 1.60 1.92 mmol/L 2.12 – 2.52

Sodium 143 140 mmol/L 136.00 – 145.00

Potassium

3.9 4.3 mmol/L 3.50 – 5.10

Chloride 108 106 mmol/L 98.00 – 107.00

• PWI: FT 37 weeks PA, 2600g, AGA, ceph, repeat LSCS, LBB, AS 5,9; Neonatal Pneumonia vs MAS; PPHN precaution r/o sepsis

• MV settings maintained

• IVF shifted to D10IMB Ca 300 @ 10cc/hr

1st HD, 1st DOL

1st HD, 1st DOL

D10IMB Ca 300 @ 10cc/hr

To correct hypocalcemia

• Decrease RR to 50 then decrease by 2 q2 until 30

• Decrease FiO2 by 5 q2 until 60%

1st HD, 1st DOL

ABG

pH 7.468

pCO2 14.40

pO2 191.00

HCO3 10.50

BEb -9.8

O2sat 99.80%

05/08/09 17:00 100% 18/3 60 0.4

Dec. RR to 50 then dec by 2 O2 til 30Dec.. FiO2 by 5 O2 til 60%

ABG

Babygram 5/08/09 (1st hospital day)

Pneumonia, both inner lung zones

• MV setting at 80%, 18/3, 44, 0.4

• ABGs ordered

• Once FiO2 60%, may start feeding with 5cc EBM q3/OGT with SAP

2nd HD, 2nd DOL

• Start feeding 5cc EBM as ordered, if tolerated 3x, start increments: increase 5cc every feeding until 30cc

• MV setting: 60% 18/5 26 0.4• Wean FiO2 by 5 q2 til 21%• Wean RR by 2 q2 til 10• Extract ABGs at RR=10

2nd HD, 2nd DOL

ABG

pH 7.360

pCO2 32.70

pO2 149.00

HCO3 18.40

BEb -5.1

O2sat 99.20%

05/09/09 09:32 WEANING 80% 18/3 44 0.4

ABG

• Prepare for extubation

• Prepare O2 hood FiO2 30%

• MV settings at 21%, 18/3, 14, 0.4

• Revise inotropes: Dopamine 0.5cc + D5W 23.5 cc to run at 1cc/hour then consume then discontinue

3rd HD, 3rd DOL

• S/P Extubation

• Placed on O2 hood FiO2 30%

• Racemic epinephrine nebulization started to continue 2 more doses 15 minutes apart

3rd HD, 3rd DOL

• Patient noted to be jaundiced up to thighs

• For TB DB IB

• Increase feeding to 35cc q3/OGT

3rd HD, 3rd DOL

• For CPT with proper shields• Dopamine discontinued• NCPAP 30% PEEP 5• ABGs• Noted vomiting with feeding; abdomen soft but distended

• Feeding decreased to 30cc

3rd HD, 3rd DOL

ABG

pH 7.324 N

pCO2 38.60 N

pO2 84.00

HCO3 20.30 N

BEb -4.7

O2sat 95.60%

05/11/09 04:13 S/P EXTUBATION 30%

Maintain now

ABG

• Increased feeding to 35cc• TB DB IB noted• Maintained on phototherapy• PWI: FT 37 wks by PA, 2600 g, AGA, cephalic, delivered via primary LSCS, LBG, AS 5,9; Neonatal pneumonia; Hyperbilirubinemia no set-up

4th HD, 4th DOL

Bilirubin

Test 05/11/09

05/12/09

Units Normal Values

TB 16.1 14.6 umol/L 17.00 – 180.00

DB 0 0.0 umol/L 0.00 – 10.00

IB 16.1 14.6 umol/L 10.00 – 180.00

• 13cc of feeding residual noted; no abdominal distention

• Feeding deferred

• Wean FiO2 by 5 q2 until 21%

• Coffee-ground noted

4th HD, 4th DOL

• NPO

• Start Famotidine 1mg IV q12

• Give Vit K 2mg slow IV push

• ABGs ordered at 25% PEEP 5

4th HD, 4th DOL

ABG

pH 7.329

pCO2 40.80

pO2 68

HCO3 21.80

BEb -3.5

O2sat 92.40

05/11/09 17:00 25% 18/3 60 0.4

ABG

Babygram 05/11/09 (4th hospital day) S/P Extubation

Atelectasis, Right Upper LobeAtelectasis/Consolidation, Medial Segment of R Lower Lobe

• PWI: FT, 37 wks by PA, 2600g, AGA, cephalic, rpt LSCS, LBG, AS 5,9; neonatal pneumonia; hyperbilirubinemia with no set-up; rule out nosocomial sepsis

• Still with jaundice and coffee ground material

5th HD, 5th DOL

• For repeat CBC with PC, blood CS, eletrolytes

• To start Ceftazidime (50mkd) 130mg IV q12h

• NPO• IVF revised to: D10IMB Ca 400 @

13cc/hr• Please put patient on right side

up

5th HD, 5th DOL

Component

05/07/09 05/12/09 Reference Range

Unit

WBC 5.56 24.42 5.0 – 30.0 X109/L

RBC 3.74 3.66 4.0 – 6.0 X1012/L

HGB 129 122 120-180 g/L

HCT 0.386 0.358 0.370 – 0.540

MCV 103.2 97.8 80.0 – 100.0 Fl

MCH 34.5 33.3 27.0 – 31.0 Pg

MCHC 334 341 320 – 360 g/L

RDW 17.2 17.3 11.0 – 16.0 %

Platelet 227 142 150 – 450 X109/L

NRBC 2/100 1

Complete Blood CountComplete Blood Count

Component

05/07/09 05/12/09 Reference Range

Unit

Neutrophil 0.697 0.77 0.500 – 0.700 %

Lymphocyte

0.182 .07 0.200 – 0.500 %

Monocyte 0.101 0.10 0.020 – 0.090 %

Eosinophil 0.016 0.006 0.000 – 0.060 %

Basophils 0.004 0.000 – 0.020 %

Stab %

Metamyelocyte

Myelocyte

Promyelocyte

Blast

Atypical Lymphocyte

Complete Blood CountComplete Blood Count

MECONIUM ASPIRATION SYNDROME

Meconium-stained amniotic fluid may be aspirated during labor and delivery, causing neonatal respiratory distress.

Because meconium is rarely found in the amniotic fluid prior to 34 weeks' gestation, meconium aspiration chiefly affects infants at term and postterm.

3 major constituents of meconium:1. Intestinal secretions2. mucosal cells3. solid elements of swallowed

amniotic fluid are the 3 major solid constituents of meconium.

Water - major liquid constituent, (85-95%)

Meconium Aspiration Syndrome

Factors that promote meconium passage in utero include: • placental insufficiency, • maternal hypertension, • preeclampsia, • oligohydramnios, and • maternal drug abuse, especially

of tobacco and cocaine.

PathophysiologyIn utero meconium passage results from neural stimulation of a mature GI tract and usually results from fetal hypoxic stress. As the fetus approaches term, the GI tract matures, and vagal stimulation from head or cord compression may cause peristalsis and relaxation of the rectal sphincter leading to meconium passage.

Pathophysiology

Meconium directly alters the amniotic fluid, reducing antibacterial activity and subsequently increasing the risk of perinatal bacterial infection. Meconium is irritating to fetal skin, thus increasing the incidence of erythema toxicum.

Pathophysiology

However, the most severe complication of meconium passage in utero is aspiration of stained amniotic fluid before, during, and after birth.

Pathophysiology

Aspiration induces hypoxia via 4 major pulmonary effects:  1. airway obstruction 2. surfactant dysfunction 3. chemical pneumonitis

Pathophysiology

1. Airway obstructionComplete obstruction - atelectasis. Partial obstruction - ball-valve effect.

Hyperdistention of the alveoli occurs from airway expansion during inhalation and airway collapse around inspissated meconium in the airway, causing increased resistance during exhalation.

Pathophysiology

2. Surfactant dysfunction

free fatty acids of the meconium (eg, palmitic, stearic, oleic), have a higher minimal surface tension than surfactant

Meconium strip it from the alveolar surface, resulting in diffuse atelectasis.

Pathophysiology3. Chemical pneumonitis

Enzymes, bile salts, and fats in meconium irritate the airways and parenchyma, causing a release of cytokines

results in a diffuse pneumonia that may begin within a few hours of aspiration.

HistoryPresence of meconium in amniotic fluid is required to cause meconium aspiration syndrome (MAS), but not all neonates with meconium-stained fluid develop meconium aspiration syndrome. The presence of thick particulate meconium in the amnionic fluid increases the likelihood of prenatal aspiration.

Green urine may be observed in newborns with meconium aspiration syndrome less than 24 hours after birth. Meconium pigments can be absorbed by the lung and can be excreted in urine.

Clinical Manifestations•Cyanosis •End-expiratory grunting •Alar flaring •Intercostal retractions •Tachypnea •Barrel chest in the presence of air trapping •Auscultated rales and rhonchi (in some cases)•Yellow-green staining of fingernails, umbilical cord, and skin may be observed.

– Placental insufficiency – Maternal hypertension – Preeclampsia – Oligohydramnios – Maternal drug abuse, especially of tobacco and

cocaine – Maternal infection/chorioamnionitis – Fetal gasping secondary to hypoxia – Inadequate removal of meconium from the airway

prior to the first breath – Use of positive pressure ventilation (PPV) prior to

clearing the airway of meconium

Factors that promote the passage of meconium in utero :

Laboratory Studies

Acid-base status • Metabolic acidosis from perinatal stress is

complicated by respiratory acidosis from parenchymal disease and persistent pulmonary hypertension of the newborn (PPHN).

• ABG measurement of pH, partial pressure of carbon dioxide (pCO2), partial pressure of oxygen (pO2), and continuous measurement of oxygenation by pulse oximetry are necessary for appropriate management.

Laboratory Studies

Serum electrolytes: Obtain sodium, potassium, and calcium concentrations when the infant with MAS aged 24 hours because the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and acute renal failure are frequent complications of perinatal stress.

Laboratory Studies

CBC count • In utero or perinatal blood loss, as well as infection, contributes to postnatal stress.

• Hemoglobin and hematocrit levels must be sufficient to ensure adequate oxygen-carrying capacity.

• Neutropenia or neutrophilia with left shift of the differential may indicate perinatal bacterial infection.

Chest Findings gross overaeration of the lungs and

bilateral nodular infiltrates The nodular infiltrates represent

areas of patchy or focal alveolar atelectasis and the overaerated spaces in between, compensatroy, focal alveolar overdistension

ManagementWhen aspiration occurs, intubation and

immediate suctioning (tracheal suctioning) of the airway can remove much of the aspirated meconium

No clinical trials justify suctioning based on the consistency of meconium. Do not perform the following harmful techniques in an attempt to prevent aspiration of meconium-stained amniotic fluid:

• Squeezing the chest of the baby • Inserting a finger into the mouth of the baby

guidelines for management of the baby exposed to meconium

The American Academy of Pediatrics Neonatal Resuscitation Program Steering Committee

If the baby is not vigorous (defined as minimal or absent respiratory effort, poor muscle tone, or heart rate <100 beats/min): Use direct laryngoscopy, intubate, and suction the trachea

immediately after delivery. Suction for no longer than 5 seconds. If no meconium is retrieved, do not repeat intubation and suction. If meconium is retrieved and no bradycardia is present,

reintubate and suction. If the heart rate is low, administer positive pressure ventilation

and consider suctioning again later.

Medical Care If the baby is vigorous (defined as good respiratory effort, crying, good muscle tone, and heart rate >100 beats/min): Do not electively intubate. Clear secretions and meconium from the mouth and nose with a bulb syringe or a large-bore suction catheter.

In either case: The remainder of the initial resuscitation steps should ensue and include drying, stimulating, repositioning, and administering oxygen as necessary.

Continued care in the NICU• Maintain an optimal thermal environment

• Minimal handling

• Sedation - to decrease agitation

• Continue respiratory care. Oxygen therapy via hood or positive pressure is crucial in maintaining adequate arterial oxygenation. If mechanical ventilation is required, make concerted efforts to minimize the mean airway pressure and to use as short an inspiratory time as possible. Oxygen saturations should be maintained at 90-95%.

Continued care in the NICU• Surfactant therapy

• For treatment of persistent pulmonary hypertension of the newborn (PPHN), inhaled nitric oxide is the pulmonary vasodilator of choice

• Pay careful attention to systemic blood volume and blood pressure. Volume expansion, transfusion therapy, and systemic vasopressors are critical in maintaining systemic blood pressure greater than pulmonary blood pressure, thereby decreasing the right-to-left shunt through the patent ductus arteriosus.

Complications

1. chronic lung disease2. infections

PrognosisMost with complete recovery of pulmonary function

Intrapartum events initiating the meconium passage may cause the infant to have long-term neurologic deficits: CNS damage, seizures, mental retardation, and cerebral palsy.

HYPERBILIRUBINEMIA

HYPERBILIRUBINEMIA Yellow color usually results from

accumulation of unconjugated, nonpolar, lipid-soluble bilirubin pigment in the skin

May be due in part to deposition of pigment from conjugated bilirubin

Elevated levels of indirect, unconjugated bilirubin potentially neurotoxic

HYPERBILIRUBINEMIA Unconjugated hyperbilirubinemia factors: Increase load of bilirubin to be metabolized

by liverHemolytic anemia, polycythemia, shortened red

cell life, increased enterohepatic circulation, infection

Damaged or reduced the activity of the transferase enzyme or other related enzymesGenetic deficiency, hypoxia, infection, thyroid

deficiency Blocked transferase enzyme Absence or decreased amounts of enzyme or

reduced bilirubin uptake by liver cellsGenetic defect, prematurity

HYPERBILIRUBINEMIA Jaundice appearing after the 3rd day

and within the 1st week suggests bacterial sepsis or urinary tract infection

Other causes: syphilis, toxoplasmosis, CMV, enterovirus

HYPERBILIRUBINEMIA Regardless of the cause, goal of

therapy is to prevent indirect-reacting bilirubin related neurotoxicity

Tx: phototherapy and exchange therapy

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