Respiratory distress in newborn Dr. Mahmood Noori-Shadkam

Respiratory distress in newborn

• Dr.Mahmood Noori-Shadkam

• Neonatologist

Neonatal Respiratory Distress Signs and symptoms

• Tachypnea (RR > 60/min)

• Nasal flaring

• Retraction

• Grunting

• Delayed or decreased air entry

• +/- Cyanosis

• +/- Desaturation

Neonatal Respiratory Distress Etiologies

• Pulmonary

• causes

• RDS

• Pneumonia

• TTN

• MAS

• Other aspiration syndrome

• Air leak syndrome

• Lung hemorrhage

• Lung hypoplasia

• Congenital malformations

Neonatal Respiratory Distress Algorithm

• Respiratory

• Distress

• (tachypnoea, retractions, grunt)

• Preterm Term

• < 6hrs old > 6hrs old < 6hrs old > 6hrs old

• Respiratory Distress Syndrome

Introduction

• The most frequent cause of respiratory distress in premature infants.

• 60-80% of <28wk GA ; 15-30% of 32-36wk GA ; 5% of 37wk-term.

• Classic presentation of grunting, retractions, increasing O2 requirement, reticulogranular pattern and air bronchograms on CXR and onset < 6hrs age

Pathogenesis

• Prematurity Prenatal asphyxia

• Reduced surfactant synthesis, storage, release

• Increased alveolar surface tension

• Progressive atelectasis Diffusion

• Uneven V/Q Hypoventilation gradient

• Hypoxemia CO2 retention

• Acidosis

• Pulmonary vasoconstriction Hypoperfusion

• Capillary endothelial damage

• Plasma leak Fibrin

Pathology

• Gross : Lung firm, red, liverlike

• Microscopic : Diffuse atelectasis, pink membrane lining alveoli & alveolar ducts. Pulmonary arterioles with thick muscular coat, small lumen. Distended lymphatics

• Electron microscopic : Damage / loss of alveolar epithelial cells, disappearance of lamellar inclusion bodies, swelling of capillary endothelial cells

Pathology (contd.)

• Biophysical :

• Deficient / absent surfactant
• Abnormal pressure volume curve
• Normal
• Vol
• RDS
• Pressure
• Severely reduced arterial bed with blockage near pulmonary arterioles

Pathology (contd.)

• Biochemical :

• Diminished surface-active phospholipid (phosphatidylcholine)
• Diminished apoprotein content ( SP-A, B, C, D)

Pathophysiology

• Reduced lung compliance (1/5th -1/10th)

• Poor lung perfusion ( 50-60% not perfused), decreased capillary blood flow

• R--> L shunting ( 30-60% )

• Alveolar ventilation decreased

• Lung volume reduced

• Increased work of breathing

• Hypoxemia, hypercapnia, acidosis

Physiologic abnormalities

• Lung compliance 10-20% of norm

• Atelectasis…areas not ventilated

• Areas not perfused

• Decrease alveolar ventilation

• Reduce lung volume

Risk factor

• Prematurity

• Acidosis

• Hypoxia

• Hypercapnia

• Hypothermia

• C/S

• Asphyxia and stress

• Male

• Familial

• DM mother

signs

• tachypnea

• retraction

• grunting

• Nasal flaring

• apneic episode

• cyanosis

• extremities puffy or swollen

Ground glass appearance

• Ground glass appearance

• Reticulogranular

• With air bronchograms

Treatment

• Surfactant

• Prevention
• rescue

• Supportive

• Thermal
• Fluid and nutrition
• oxygen

• Mechanical ventilation

complications

• Pneumothorax

• PDA

• Infection

• Line problems

• ROP

• Chronic lung disease

• Meconium aspiration

M .A .S

• آسپيريشن مايع آمنيوتيك آغشته به مكونيوم ممكن است منجر به سندرم آسپيريشن مكونيوم گردد كه مربيديتي و مورتاليتي قابل ملاحظه اي دارد بنابراين مديريت زايمان با مايع آمنيوتيك آغشته به مكونيوم براي پيشگيري از آسپيراسيون اهميت زيادي دارد

تركيب مكونيوم

• Cellular particle

• Bile pigment

• Lango

• Mocus

• Vernix

• Pancreatic secretion

• One gr meconium = one mg Billirubin

Incidence

• دفع مكونيوم 8 تا 20 درصد كل زايمانها ( متوسط 12 %)

• مكونيوم آسپيريشن در 4 درصد مكونيومي ها دیده می شود

• وجود دارد. SGA و Post maturityعمدتا

فيزيوپاتولوژي

• اگر چه فيزيوپاتولوژي كامل آن و علت دفع مكونيوم كاملا شناخته نشده اما اين پديده بندرت قبل از هفته 34 ديده مي شود

• بسياري از مكونيوم دفع كرده ها علامتي دال بر مشكل تنفسي يا دپرسيون نداشته اند و عده اي هم بعلت آسفيكسي مكونيوم دفع كرده اند

علت دفع مكونيوم

• 1) پديده فيزيولوژيك : تكامل عصبي پاراسمپاتيك و برقراري پريستالتيسم روده اي در پاسخ به تكامل جنين (شيوع در ترم ها و نادر بودن در نوزادان نارس )

• 2) هيپوكسي : مي تواند باعث افزايش پريستالتيسم روده ها و كاهش تو ن اسفنكترآنال شود (البته اكثر نوزادان با مايع آمنيوتيك مكونيال آپگار پايين و اسيدوز ندارند )

Alarm of MAS

• 1- Thick meconium

• 2-Fetal tachycardia

• 3- lack of increase heart rate during intra partum monitoring

• 4-Low cord PH

پاتوژنز

MAS complication

• Partial obstruction o

• complete obstruction :

• Surfactant destruction

• Chemical pneumonitis &Bacterial pneumonia

• Asphyxia

• PPHN

Clinical sign

• Classic sign: Post maturity nail, skin , umblical cord are heavily stained with a yellowish pigment

• Early sign (resp . Distress) : grunting & cyanosis & nasal flaring & retraction & marked tachypnea

• Characteristic sign : chest overinflation and Rale

Radiography of M.A.S

• Coarse , nodular , irregular pulmonary densities with areas of diminished aeration or consolidation.

• Hyperinflation of the chest .

• Atelectasis

• Flattening of diaphragm

• Cardiomegally

• (manifestation of the underlying prenatal hypoxia)

Meconium Aspiration Syndrome

Meconium Aspiration Syndrome

ABG in M.A.S

• شواهدي از يك آلكالوز تنفسي

• هيپوكسي

• در مواقع شديد اسيدوز تنفسي و اسيدوز متابوليك

• شواهدي از شنت راست به چپ

Management of M.A.S

• حضور مكونيوم در مايع آمنيوتيك دليل بردیسترس جنینی نيست وچنانچه ضربان قلب جنین و پی-اچ بند ناف طبيعي باشد پيش آگهي خوب است

• آميخته شدن مكونيوم با مايع آمنيوتيك باضافه ضربان قلب نا مناسب نويد دهنده يك آسفيكسي مي باشد

Intra partum

• در اين گونه مواقع وقتي سر بيرون آمد در روي پرينه بايد ساكشن دهان وبيني و فارنكس با كاتتر نمره 12 يا 14 انجام شود (قبل از اينكه توراكس بيرون بيايد و نوزاد بخواهد تنفس كند )

• اولين ارزيابي نوزاد متولد شده : vigorous or depress

Criteria of vigorous

• 1) Heart rate greater than 100 beat /min

• 2) Good muscle tone

• 3) regular breathing

• Infections

Pneumonia & Sepsis have various manifestations including typical signs of distress as well as temperature instability.

• Pneumonia & Sepsis have various manifestations including typical signs of distress as well as temperature instability.

• Common pathogen- Group B Streptococcus, Staph aureus, Streptococcus Pneumonia,Gm neg. rods

Risk factors- prolonged rupture of membranes, prematurity,& maternal fever.

• Risk factors- prolonged rupture of membranes, prematurity,& maternal fever.

• CXR- bilateral infiltrates suggesting in utero infection.

Congenital pneumonia

• Sepsis risk factors

• PROM
• Prematurity
• Maternal fever, discharge, abdominal pain, leukocytosis
• Colonization with GBS

• Same signs of RDS

• X-ray

Most common cause of respiratory distress.

• Most common cause of respiratory distress.

• Residual fluid in fetal lung tissues.

• Risk factors- maternal asthma, c- section, male sex, macrosomia, maternal diabetes

Tachypnea immediately after birth or within two hours, with other predictable signs of respiratory distress.

• Tachypnea immediately after birth or within two hours, with other predictable signs of respiratory distress.

• Symptoms can last few hours to two days.

• Chest radiography shows diffuse parenchymal infiltrates, a “ wet silhouette” around heart, or intralobar fluid accumulation

Transient tachypnea of newborn

• Term

• Cesarian delivery

• Usually tachypnea without O2 requirment

• Resolve in 48-72 houres

• Lung fluid

• X-ray

Congenital malformations-Pulmonary hypoplasia, congenital emphysema, esophageal atresia & diaphragmatic hernia.

• Congenital malformations-Pulmonary hypoplasia, congenital emphysema, esophageal atresia & diaphragmatic hernia.

• Neurological causes- hydrocephalus & intracranial hemorrhage.

• Metabolic derangements-hypoglycemia, hypocalcemia, polycythemia.

Cyanotic Heart Disease-

• Cyanotic Heart Disease-

• Tetralogy of fallot- ( VSD, Pulmonary stenosis, overriding aorta, RVH)

• Tricuspid atresia

• Transposition of great vessel

• Total anomalous pul. venous return

• Truncus arteriosus.

Obtain ABG–> Then place the patient on 100% O2 for 10 minutes then repeat ABG , If the cyanosis is pulmonary , the PaO2 should be increased by 30 mm of Hg. If the cause is cardiac , there will be minimal improvement in PaO2.

• Obtain ABG–> Then place the patient on 100% O2 for 10 minutes then repeat ABG , If the cyanosis is pulmonary , the PaO2 should be increased by 30 mm of Hg. If the cause is cardiac , there will be minimal improvement in PaO2.