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 Illness
Preterm 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
 SCORE
SIGN SIGN SCORE
-1 0 1 2 3 4 5

Sticky, friable, gelatinous, red, smooth pink, visible superficial peeling cracking, pale areas, parchment, deep leathery, cracked,
Skin    
transparent translucent  veins &/or rash, few veins rare veins cracking, no vessels wrinkled

Lanugo none sparse abundant thinning bald areas mostly bald    

 

 heel-toe
>50 mm anterior creases over entire
Plantar Surface 40-50mm: -1 faint red marks creases ant. 2/3  
no crease transverse crease only sole
<40mm: -2

flat areola stippled areola raised areola full areola

Breast imperceptable barely perceptable  
no bud 1-2 mm bud 3-4 mm bud 5-10 mm bud

lids fused lids open

sl. curved pinna; soft; well-curved pinna; formed & firm thick cartilage
Eye / Ear loosely: -1 pinna flat    
slow recoil soft but ready recoil instant recoil ear stiff
tightly: -2 stays folded

scrotum empty, testes in upper canal, testes descending, testes down, testes pendulous,
Genitals (Male) scrotum flat, smooth    
faint rugae rare rugae few rugae good rugae deep rugae

7
clitoris prominent prominent
majora & minora majora large, majora cover clitoris
Genitals (Female) prominent & labia clitoris & small labia clitoris & enlarging    
equally prominent minora small & minora
flat minora minora

TOTAL PHYSICAL MATURITY SCORE  

9
TOTAL SCORE  
(NEUROMUSCULAR + WEEKS
PHYSICAL)

-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
 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.
 Physical Exam

 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
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

 Objective
 Subjective
- MT 30-32 wks
- PT, BG
- Severe DOB
- 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, (-)Diffuse homogenous &

(+)retractions,(+)alar linear radiating densities
flaring
Condition Rule in Rule out
Transient tachypnea (+)tachypnea,(+) (+)whiteout lung
of newborn grunting, fields
(+/-)retractions (+) severe DOB

Early onset sepsis (+)prematurity (-)UTI

(+)LBW, (+)normothermic
(+)hypoactive (-) PROM
(+)tachypnea,
(+) grunting,
(+)retractions

Cyanotic heart disease (+)DOB,(+) pallor (-)murmurs,

(-)cyanosis
x ray findings,(-) drug
use/abuse,(-) hx of
heart dis in siblings
Condition Rule in Rule out
Respiratory Distress MT 30- 32 wks,wt 1.2
syndrome 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 improvement
X-ray, CBC
X-ray revealing: whiteout lungs, cardiothymic borders at lung
periphery, cardiac borders not visible
CBC: 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 Diagnostics Therapeutics
condition

upon (+) expiratory Hgb-121 D10 water 93.6cc

Admission grunting Hct- 0.36
HR- 162 Ca Gluc 2.4 cc so 96cc in
WBC count- 7.2
(+)tachypnea RR- 66 soluset for 24 hrs at 4
Neutrophils-
(+)subcostal T-36.8C 0.37 ugtts/min
Lymphocytes-
retractions 0.57
Ampicillin 60mg/iv q 12
Platelets- 266
Typing – O+
Amikacin 20mg/iv OD
CXR APL Aminophylline 6mg/iv
(2.2cc)+0.7cc DW as LD
then 2mg/iv(0.1cc)+0.3cc
DW q 8.
Vit k 0.5mg/im
Erythromycin eye
ointmenton both eyes
 Patient’s Diagnostics Therapeutics
condition

(+) Apnea CXR APL Intubated the patient

2 hours
after (+)bradycardia HR- 110 Hooked to continuous
admission ambubagging at 10 lpm
(+)subcostal RR- 0
retractions Discontinued
aminophylline
Patient’s Diagnostics Therapeutics
condition

(+) Apnea CXR APL

No cardiac HR- 0
rate RR- 0
Final diagnosis
RDS 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.
 INCIDENCE

 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
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.

 Surfactantis 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.

 Resultsin 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 Cardio thymic Air bronchogram
pattern shadow

Mild 1 Mild,hazy Clearly defined Perihilar, w/i CT

generalized shadow

2 Mod, generalized Just past CT

borders

Moderate 3 Heavier and more Hazy,barely Past 2/3 of lung

confluent discernible

Severe 4 White-out lungs Upto lung Cardiac border no

periphery longer visible
 Risk Factors

Increased Risk Decreased risk

Prematurity Chronic intrauterine stress

Male gender Prolonged ruptured of membranes
Familial predisposition Maternal hypertension
Cesarean section without labor Narcotic/cocaine use
Perinatal asphyxia IUGR/ SGA
Caucasian race Corticosteroids
Maternal diabetes Thyroid hormones
Multiple gestation Tocolytic agents
Chorioamnionitis
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
CLINICAL
MANIFESTATIONS
 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
 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 .

 Prenatalglucocorticoid 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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