CASE PRESENTATION

OZA BIJAL, PATIL AKASH, POTE SONALI

General Data: Ocampo Baby Girl, NB, Filipino, Roman

Catholic, residing at Bulaon, was admitted for the 1st time at our institution on Nov. 4, 2010

Informant - father Reliability - fair

Chief Complaint:Difficulty of breathing

History of Present IllnessPreterm baby girl, born to a 23y/o

G2P2(0201)mother via NSD at home assisted by midwife, AS ?, MT 30 -32 wks, AGA .

At 2nd hr of life ptn had difficulty of breathing At 3rd hr of life patient was brought to our

institution because of increased severity of DOB and was admitted.

Maternal History Antenatal: Mother is a 22 yr old,G2P2(0201),

LMP- 1st week April 2010, EDC 2nd week Jan, 2010, with no medical illnesses, had her regular prenatal check ups every 2 mo at Bulaon hospital and took vit C and FeSO4 daily.

Mother is a non smoker, non alcoholic beverage drinker, no hx of drug use or abuse, no exposure to radiation, during the gestational period.

Hx of 2 UTZ, one in 1st trimester and other one day before delivery, with unknown results

Perinatal: born premature by NSD, AS ?, BW- 1.2 kg, home delivery, MF assisted, no complications at birth like PPROM

Post natal: on NPO

Family History

(-) Asthma (-) HPN(-) DM(-)Allergies(-)Mental retardation(-)Congenital anomalies

Sibling ,born on 7th month of AOG, died at 6 month of life 2* to pneumonia

Review of Systems

Not applicable

9

Physical Exam

General Survey – patient is awake, hypoactive, pale, no physical deformities or asymmetry, in respiratory distress

Vital Signs- PR – 162 bpm, RR – 66 cpm, T – 36.8 C Anthropometry- Wt –1.2 kg(10th percentile) , length- 43 cm(50th percentile), HC-30cm(50th per.) , CC-27cm , AC-28cm NMR- 30-32 weeks

SIGNSCORE

SIGN SCORE-1 0 1 2 3 4 5

SkinSticky, friable,

transparentgelatinous, red,

translucent smooth pink, visible

veinssuperficial peeling

&/or rash, few veinscracking, pale areas,

rare veinsparchment, deep

cracking, no vesselsleathery, cracked,

wrinkled   

Lanugo 

none sparse abundant thinning bald areas mostly bald    

Plantar Surface heel-toe

40-50mm: -1 <40mm: -2

>50 mmno crease

faint red marksanterior

transverse crease onlycreases ant. 2/3

creases over entire sole

 

Breast imperceptable barely perceptableflat areola

no budstippled areola1-2 mm bud

raised areola3-4 mm bud

full areola5-10 mm bud

 

Eye / Earlids fusedloosely: -1tightly: -2

lids openpinna flat

stays folded

sl. curved pinna; soft; slow recoil

well-curved pinna; soft but ready recoil

formed & firminstant recoil

thick cartilageear stiff

   

Genitals (Male) scrotum flat, smoothscrotum empty,

faint rugaetestes in upper canal,

rare rugaetestes descending,

few rugaetestes down,good rugae

testes pendulous,deep rugae

   

Genitals (Female)clitoris

prominent & labia flat

prominentclitoris & small labia

minora

prominentclitoris & enlarging

minora

majora & minora equally prominent

majora large,minora small

majora cover clitoris & minora

   

TOTAL PHYSICAL MATURITY SCORE  

7

9

TOTAL SCORE  (NEUROMUSCULAR + PHYSICAL)

WEEKS

-10 20

-5 22

0 24

5 26

10 28

15 30

20 32

25 34

30 36

35 38

40 40

45 42

50 44

MATURITY RATING

Skin – pale , milia on nose, cheek, forehead, (-)cyanosis

HEENT – Normocephalic, no bulging of ant. fontanelle, anicteric sclera, pink palpebral conjunctiva, pupils equally reactive to light, normally set and symmetric ears,(+) nasal flaring, no cleft lip/palate, symmetric neck, no clavicular fractures.

Chest and Lungs – symmetrical chest expansion, w/ subcostal retractions, tachypneic, audible expiratory grunting

Heart –(+)pallor, adynamic precordium, normal rate and rhythm, no murmur

Abdomen- globular, no distension, no masses, 2 arteries ,1 vein in umbilical cord, NABS

Genitalia – grossly female, prominent clitoris, enlarging minora, no discharge

Anus: patent

Extremities – (-) edema, (-) deformities, no cyanosis Spine- no defects

Physical Exam

CN OBSERVATIONS

2,3,4,6 (+)blink reflex,

5 (+)rooting,(+) sucking reflex

7 Full facial movements and symmetry

8 (+) acoustic blink reflex

9,10,12 Could not assess

Salient features

Subjective - PT, BG- Severe DOB

Objective - MT 30-32 wks- Wt : 1.2 kg- G2P2(0201)- Grunting(expiratory)- Subcostal

retractions- Tachypnea- Pallor- Alar flaring- Hypoactive

Initial Diagnosis :Preterm baby girl, born to a 23y/o G2P2(0201)mother via NSD at home assisted by midwife, AS ?, MT 30 -32 wks, AGA .T/C RDS type 1

Differential Diagnosis

Condition Rule in Rule out

Pneumonia (+)DOB, (+)tachypnea, (+)retractions,(+)alar flaring

(-)Diffuse homogenous & linear radiating densities

Condition Rule in Rule out

Transient tachypnea of newborn

(+)tachypnea,(+) grunting,(+/-)retractions

(+)whiteout lung fields(+) severe DOB

Early onset sepsis (+)prematurity(+)LBW,(+)hypoactive(+)tachypnea,(+) grunting,(+)retractions

(-)UTI (+)normothermic(-) PROM

Cyanotic heart disease

(+)DOB,(+) pallor (-)murmurs,(-)cyanosisx ray findings,(-) drug use/abuse,(-) hx of heart dis in siblings

Condition Rule in Rule out

Respiratory Distress syndrome

MT 30- 32 wks,wt 1.2 kg, G2P2(0201),Severe DOB(+) pallor (+)tachypnea, (+)alar flaring (+)subcostal retractions, (+)grunting(+)whiteout lung fields, cardiac borders not visible, cardiothymic shadow upto lung periphery

Approach to DX

Premature, 30-32 wk, wt:1.2 kg DOB, grunting , tachypnea, subcostal retractions, alar flaring given o2 support no improvementX-ray, CBCX-ray revealing: whiteout lungs, cardiothymic borders at lung periphery, cardiac borders not visibleCBC: blood type o +ve Hb- 121 Hct- 0.36 WBC- 7.2 Neutrophills-0.37 Lymphocytes- 0.57 Platelet-266 Blood GS,CS : awaiting

Course in the Ward

Patient’s condition

Diagnostics Therapeutics

uponAdmission

(+) expiratory grunting(+)tachypnea

(+)subcostal retractions

HR- 162RR- 66T-36.8C

Hgb-121Hct- 0.36WBC count- 7.2Neutrophils- 0.37Lymphocytes- 0.57Platelets- 266Typing – O+CXR APL

D10 water 93.6ccCa Gluc 2.4 cc so 96cc in soluset for 24 hrs at 4 ugtts/min

Ampicillin 60mg/iv q 12Amikacin 20mg/iv ODAminophylline 6mg/iv (2.2cc)+0.7cc DW as LD then 2mg/iv(0.1cc)+0.3cc DW q 8.Vit k 0.5mg/imErythromycin eye ointmenton both eyes

Patient’s condition

Diagnostics Therapeutics

2 hours after admission

(+) Apnea (+)bradycardia

(+)subcostal retractions

HR- 110RR- 0

CXR APL Intubated the patientHooked to continuous ambubagging at 10 lpmDiscontinued aminophylline

Patient’s condition

Diagnostics Therapeutics

(+) Apnea

No cardiac rate

HR- 0RR- 0

CXR APL

Final diagnosisRDS 4

RESPIRATORY DISTRESS SYNDROME

INCIDENCE

Incidence inversely related to gestational age and birthweight .

60–80% of infants less than 28 wk of gestational age, 15–30% in 32 and 36 wk, 5% beyond 37 wk

Risk increases with maternal diabetes, multiple births, CS delivery, precipitous delivery, asphyxia, cold stress, and Hx of previously affected infants.

Highest in preterm male or white infants.

Risk reduced in pregnancies with chronic or pregnancy-associated hypertension, maternal heroin use, prolonged rupture of membranes, and antenatal corticosteroid prophylaxis

INCIDENCE

ETIOLOGY AND PATHOPHYSIOLOGY

Surfactant deficiency, primary cause

The failure to attain an adequate FRC and the tendency of affected lungs to become atelectatic correlate with high surface tension and the absence of pulmonary surfactant.

Constituents: dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), and cholesterol

With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells.

The amounts produced, insufficient to meet postnatal demands because of immaturity.

Surfactant is present in high concentrations in fetal lung homogenates by 20 wk of gestation.

Appears in the amniotic fluid between 28 and 32 wk.

Mature levels of pulmonary surfactant are usually present after 35 wk.

Abnormalities in surfactant protein B , C genes ,ABC transporter 3 [ABCA3] are associated with severe and often lethal familial respiratory disease.

Other familial causes of respiratory distress include alveolar capillary dysplasia, acinar dysplasia, pulmonary lymphangiectasia, and mucopolysaccharidosis.

Deficient synthesis or release of surfactant, together with small respiratory units and a compliant chest wall, produces atelectasis.

Results in perfused but not ventilated alveoli, which causes hypoxia.

Decreased lung compliance, small tidal volumes, increased physiologic dead space, increased work of breathing, and insufficient alveolar ventilation eventually result in hypercapnia.

Severity Grade Reticulogram pattern

Cardio thymic shadow

Air bronchogram

Mild 1 Mild,hazy generalized

Clearly defined Perihilar, w/i CT shadow

2 Mod, generalized

Just past CT borders

Moderate 3 Heavier and more confluent

Hazy,barely discernible

Past 2/3 of lung

Severe 4 White-out lungs

Upto lung periphery

Cardiac border no longer visible

Risk Factors

Increased Risk Decreased risk

PrematurityMale genderFamilial predisposition Cesarean section without labor Perinatal asphyxiaCaucasian race Maternal diabetesMultiple gestation Chorioamnionitis

Chronic intrauterine stressProlonged ruptured of membranesMaternal hypertensionNarcotic/cocaine useIUGR/ SGACorticosteroidsThyroid hormonesTocolytic agents

CLINICAL MANIFESTATIONS

Tachypnea,

Prominent (often audible) grunting,

Intercostal and subcostal retractions,

Nasal flaring, and duskiness

Cyanosis increases and is often relatively unresponsive to oxygen administration.

Breath sounds,normal or diminished with a harsh tubular quality and, on deep inspiration, fine rales may be heard

If the condition is inadequately treated, blood pressure may fall; fatigue, cyanosis, and pallor increase, and grunting decreases or disappears as the condition worsens.

Apnea and irregular respirations occur as infants tire and are ominous signs requiring immediate intervention.

Patients may also have a mixed respiratory-metabolic acidosis, edema, ileus, and oliguria

CLINICAL MANIFESTATIONS

DIAGNOSIS:

CXR : not pathognomonic appearance that includes a fine reticular granularity of the parenchyma and air bronchograms, which are often more prominent early in the left lower lobe because of superimposition of the cardiac shadow

Blood gas and acid-base values

The initial roentgenogram is occasionally normal, with the typical pattern developing at 6–12 hr.

PREVENTION

Avoidance of poorly timed cesarean section, appropriate management of high-risk pregnancy and labor, and prediction and possible in utero acceleration of pulmonary immaturity .

In timing cesarean section or induction of labor, estimation of fetal head circumference by ultrasonography and determination of the lecithin concentration in amniotic fluid by the lecithin: sphingomyelin ratio decrease the likelihood of delivering a premature infant.

PREVENTION

Antenatal and intrapartum fetal monitoring may similarly decrease the risk of fetal asphyxia; asphyxia is associated with an increased incidence and severity of RDS.

Administration of betamethasone to women 48 hr before the delivery of fetuses between 24 and 34 wk of gestation significantly reduces the incidence, mortality, and morbidity of RDS.

Corticosteroid administration is recommended for all women in preterm labor .

Prenatal glucocorticoid therapy decreases the severity of RDS and reduces the incidence of other complications of prematurity, such as IVH, patent ductus arteriosus (PDA), pneumothorax, and necrotizing enterocolitis.

Administration of a 1st dose of surfactant into the trachea of symptomatic premature infants immediately after birth (prophylactic) or during the 1st few hours of life (early rescue) reduces air leak and mortality from RDS.

Treatment Secure the airway and listen for breath sounds

over all lung fields. Obtain chest x-ray. Give supplemental oxygen. Intubation and ventilation for respiratory

failure (arterial oxygen <60 mm Hg with inspired oxygen concentration of >60%) or apnea.

Umbilical artery catheterization allows repeated evaluations of PaO2.

Give ampicillin and gentamycin IV for presumed pneumonia.

sepsis until diagnosis is clarified

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