DR RAGHAVENDRA .FELLOW IN NEONATOLOGY

CASE PRESENTATION ONRESPIRATORY DISTRESS SYNDROME

B/o rashmi natraj

B/O RASHMI NATRAJDOB:5/2/2015DOA:6/2/2015

BIRTH WT :1.2 KG SINGLE LIVE PRETERM (30-32WKS) DELIVERED BY NORMAL VAGINAL DELIVARY INDICATION WAS PROLONGED RUPTURE OF MEMBRANE >18HRS IN HAVERI PRIVATE HOSPITAL,BABY CRIED IMMEDIATELY AFTER BIRTH.

WAS REFFERED FROM HAVERI IN VIEW OF PRETERM CARE AND RESPIRATORY DISTRESS.

FAMILY HISTORY: MARRIED LIFE 8 YEARS, G3P2L2A0 ,1ST CHILD 6YRS MALE CHILD, 2ND CHILD FEMALE 2 YRS,3RD PRESENT ONE.

OBSTETRIC HISTORY:REGULAR ANC DONE ANTENATAL 3 SCAN DONE ,TAKEN 2 DOSE OF TT.SHE HAD LEAKING PV SINCE MORNING OF 4/02/15.NO ANTENATAL STERIOD TAKEN.

SOCIAL HISTORY:JOINT FAMILY 8 MEMBER, FATHER BUSINESSMAN,MOTHER IS HW.

HEART RATE 145/M RESPIRATORY RATE 64/M ICR+SCR+ SPO2 68% CRT >3. PALE ,HYPOTHERMIC. PERIPHERAL PULSE ARE WEAK. CRY, TONE ,ACTIVITY ARE WEAK.

EXAMINATION ON ADMISSION

HEIGHT :39CM.

HEAD CIRCUMFERENCE :29CM.

WEIGHT:1.2 KG

PONDREL INDEX:2.02

ANTROPOMETRY

HEAD TO TOE EXAMINATION NORMAL.

RS: AEBE NVBS ICR +SCR+ OCCASIONAL GRUNTING.

CVS :S1 S2 NORMAL.WEAK PULSES CRT>3. P/A : SCAPHOID ABDOMEN,SOFT LIVER 3 CM

SPLEEN NOT PALPABLE. CNS MORO’S INCOMPLETE.

ON ADMISSION CORRECTION BOLOUS WERE GIVEN ,TREATED FOR SHOCK, PUT ON CPAP.

SINCE DOWNES SCORE MORE THAN 6 DUE TO IMPENDING RESPIRATORY FAILURE BABY WAS ELECTIVELY INTUBATED AT 12 HOL.

SINCE X RAY SUGGESTIVE OF HYALINE MEMBERANE DISEASE PLANNED FOR SURFACTANT.

XRAY CHEST POST INTUBATION

The diffuse reticular-granular opacification, air bronchograms and decreased lung volumes in the chest radiograph film indicate respiratory distress syndrome.

AT 15 HOL 6 ML OF SURFACTANT GIVEN BY INSURE METHOD AND CONNECTED TO VENTILATOR WITH FIO2 80% PIP 14 PEEP 4 RR 40/M WITH 2.5MM ET TUBE.

STARTED ON SECOND LINE ANTIBIOTICS AND CALCIUM SUPPLEMENT.

AT 24 HOL VENTILATOR SETTING WERE REDUCED TO MINIMUM SHIFTED TO SIMV MODE.PLANNED WEANING FOR NEXT 24 HR.

AT 48HOL BABY WAS EXTUBATED AND KEPT OXYGEN HOOD WITH FIO2 40%.

Post extubation

HB:15.4GM/DL TLC:7210 PLT:1.09LAAKH/CUMM N:64% LYM:27 EOS:1 CRP 3MG/DL NUCLEATED RBC 4550 CELLS/CUMM SERUM CALCIUM:9.2MG/DL TSB:8MG/DL AT 48HRS

INVESTIGATION :

BABY WAS PUT ON DOUBLE SURFACE FOR PHOTOTHERAPY AT 48 HRS WITH MAX TSB OF 8MG /DL

OXYGEN IS SLOWLY WEANED OFF FOR NEXT 24 HR.

PLANNED FOR SMALL INCREMENT OF RYLE TUBE FEED AND SHIFT TO INCUBATOR FOR FURTHER MANAGEMENT.

SINGLE LIVE PRETEM MALE CHID DELIVERED VIA NATURALIS WITH BT WT OF 1.2KG ADMITTED I/V/O RESPIRATORY DISTRESS AND LOW BIRTH WEIGHT REQUIRING PRETEM CARE. SURFACTANT THERAPY AND VENTILATORY SUPPORT FOR 48 HRS .SEPTIC SCREENING NEGATIVE.PHOTOTHERAPY FOR WAS GIVEN FOR HYPERBILIRUBENEMIA .

FINAL DIAGNOSIS

The primary cause of RDS(hyaline membrane disease) is due to inadequate pulmonary surfactant.

Preterm birth is the important etiological factor.

Important cause of neonatal mortality and morbidity.

Prenatal diagnosis of infants at risk, administration of glucocorticosteriods improve prenatal and neonatal care .

Respiratory distress syndrome

HMD occurs primarily in Premature infant,

◦ Infants less than 28 wk of GA: 60-80%.

◦ Infants between 28 and 32 wk: 60%.

◦ Infants between 32 and 36wk of GA: 15-30%.

◦ Infants beyond 37 wk of GA: 5%.

Epidemiology

Perinatal risk factors

Factors that affect state of lung development,

prematurity ,maternal diabetes,genetic factor,sthoracic malformations -diaph.hernia,Gene defect : Def.of surfactant.

Perinatal risk factors

Factors that may acutely impair surfactant

production, release or function.

Perinatal asphyxia in Prematures

APH

Second born twins

Cesarean section without Labor

Surfactant decreases surface tension in the alveolus helps

in maintaining a functional residual capacity.

Lack of pulmonary surfactant leads to progressive atelectasis, loss of functional residual capacity, alterations in ventilation-perfusion ratio, and uneven distribution of ventilation.

The increased surface tension in the alveolus results in poor lung compliance, Edema and cell injury. decreased tidal volumes increased physiologic dead space Poor lung distensibility Poor alveolar stability.

Pathophysiology

weak respiratory muscles and the compliant chest wall of the premature infant, impair alveolar ventilation.

Diminished oxygenation, cyanosis , respiratory and metabolic acidosis contribute to increased pulmonary vascular resistance (PVR).

Right-to-left shunting through the ductus arteriosus, foramen ovale, and intrapulmonary ventilation-perfusion mismatch further exacerbate hypoxemia.

Extensive lung atelectasis .

Injury to epithelial cells .

Pulmanory vascular congestion and edema .

Lung hemorrhage.

Hyaline membranes contains fibrin and cellular products

Pathology

Perinatal prediction Done by Lung maturity tests.

Prophylactic maternal glucocorticoid .

◦ pregnancies shorter than 34 wk

◦ those with documented lung immaturity

◦ optimal benefit begins 24 hr after initiation of treatment

◦ Contraindications : Amnionitis

Lecithin /sphingomyelin ratio:it is performed by thin layer chromatography.the risk of RDS is low if L/S ratio >2 .

TDx-FLM II it measure sufactant to albumin ratio by flurorescent polarization technique.

A valve of > 55mg correlates with lung maturity.

Assessment of fetal lung maturity.

Lamellar body count in amniotic fliud determine FLM. increase numbers with advancing gestational age

. Phosphatidyl glycerol determine FLM appear

late in maturation process.it appears late in maturation process of lung.

Foam stability index predicts FLM based on formation of stable foam. when amniotic fliud is shaken with ethanol in test tube.

Assessing of vitals ,retractions ,grunt, air entry, saturation ,inspired oxygen concentration and blood gases.

Two important scores for assessing RDS are

1)DOWNES SCORE.2) SILVERMAN SCORE.

Assess ment for severity of RDS

Hourly vitals.Downes and silverman scoreContinuous saturation monitoringABG & xrayFluid and electrolyte status Blood sugarSepsis workupechocardiogram

MONITORING

Onset near the time of birth or within 4-6 hr after birth. poor feeding.

Rapid, shallow respirations ≥ 60/ min.

Intercostal and sub costal retractions and progressive respiratory distress.

Flaring of nasal alae

Expiratory grunt.

Cyanosis or pallor.

Xray suggestive of classic ground glass appearance low volume lungs with diffuse reticulogranular pattern and air bronchograms.

Diagnosis:

Most common cause: Transient tachypnea of newborn. Me conium aspiration syndrome

Less common but significant cause: Delayed transition Infection Non pulmonary causes Persistent pulmonary hyper tension pneumothorax

Differential diagnosis

Management Prevent hypoxia and acidosis to optimize fluid management to reduce metabolic demands to prevent worsening atelectasis and

pulmonary edema to minimize lung injury due to barotrauma

or oxygen

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