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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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