William 2001

 Hyaline membrane disease  Retinopathy of prematurity  Respiratory distress in term infants  Meconium aspiration

Fetal lungs at birth :  ↓ fluid ( expressed or absorbed )  ↑ air  ↑ blood Type II pneumocytes  surfactant Surfactant  ↓ surface tension ↓ surfactant  collapse of the alveoli at the end of expiration + hyaline membrane in alveoli and distal bronchioles

Corticosteroid therapy  ↓ HMD HMD ↑ in  boys – blacks Preeclampsia and PROM  no ↓ HMD Clinical picture:  Tachypnea  Retraction of chest wall  Grunting – flaring Progressive shunting of blood through

nonventilated areas   Hypoxemia  Acidosis ( respiratory – metabolic )  Hypotension ( systemic – peripheral ) X ray:  Diffuse reticulogranular infiltrate  Air – filled tracheobronchial tree ( air bronchogram )

Other causes of respiratory insufficiency:  Sepsis  Meconium aspiration  Pneumonia  Pneumothorax  Diaphragmatic hernia  Persistent fetal circulation  HF

Common causes of cardiac decompensation in neonates:  PDA  CHD Pathology: Hypotension and hypoxemia  Epithelial tissue necrosis  Pulmonary HTN + relative R to L shunt

O2 therapy   damage to the lungs & retina  reversal of the shunt Hyaline membrane =  fibrin rich protein  cellular debris  necrotic tissue below it Gross appearance = liver - like

Histologically:  Collapsed alveoli  Some widely dilated alveoli  Vacuolated duct epithelium Treatment:  ICU  If arterial PO 2 < 40mmHg  give the lowest level sufficient to treat hypoxia and acidosis = PO 2 50 – 70 mmHg

Continuous +ve airway pressure (CPAP): - Prevent alveolar collapse  ↓mortality - Disadvantages:  ↓ VR  Possible barotrauma  Brochopulmonary dysplasia High frequency oscillatory ventilation ± NO for severe pulmonary HTN:  Pulmonary VD with no systemic VD

Surfactant: 1 st report in 1980 by Fujiwara Helpful in LBW = 500 – 750 gm = 23 – 26 weeks ↓ mortality by 20 – 25% It’s rule in older fetuses  debate Types: Biological (animal-human)–synthetic

Complications :  Bronchopulmonary dysplasia  Pulmonary HTN  Retinopathy Bronchopulmonary dysplasia: = O 2 toxicity lung disease Alveolar and bronchiolar epithelial damage  hypoxia + hypercarbia + O 2 dependence  peribronchial and interstitial fibrosis  P HTN

Prevention: Avoid elective preterm labor:  Estimate GA  Confirm lung maturity Then weigh risks of maternal disease against risks of prematurity Amniocentesis to confirm fetal lung maturity:

1 – Lecithin-to-sphingomyelin ratio: < 34 weeks L/S R = < 2 ≥ 34 weeks L/S R = ≥ 2 RDS ↑ if L/S R = < 2 ↓ if L/S R = ≥ 2 Blood contamination  ↑↓ L/S Meconium  ↓L/S

Studies on L/S Ratio :  ↓ L/S R is more predictive of the need for ventilatory support # ↓ GA & BW  Some maternal diseases  RDS with L/S R ≥ 2 espatially DM  Metabolic and respiratory acidosis in severe DM  RDS  Lung maturation not delayed in DM  Delayed lung maturation is associated with poor glucose control

 No RDS in blacks if L/S ratio is > 1 ½ 2 – Phosphatidylglycerol:  Enhance surface active properties  Not detected in blood, meconium or vaginal secretions  For more assurance that RDS will not develop  It’s absent does not mean that RDS will develop after delivery  Some do not deliver DM except if it is +ve

3 – TD x – FLM: - Measures surfactant/albumen R - rapid  ½ hour - ≥ 50  100% lung maturity - Equal or superior to L/S R, shake and phosphatidylglycerol tests - Some use it as 1 st line before L/S 4 - Shake test: 1972

Contamination  ↑ false –ve results Used as screening test by some 5 – Lumadex – FSI: reliable 6 -- Fluorescent polarization: reliable simple rapid expensive 7 – AF absorbance at nm wavelength = L/S R

8 - Lamellar body count: Simple – rapid – accurate ≥ 35000/mL = 100% lung mature 9 - Dipalmitoylphosphatidylcholine ( DPPC test ): sensitivity = 100% specificity = 96%

< 1950 = largest single cause of blindness > 1950 = ↓ due to avoiding ↑ O 2 therapy - The retina vascularizes centrifugally from the optic nerve starting at the 4 th month until after birth. During this period it is easily damaged - ↑ O 2  mostly damage the temporal portion of the retina

- ↑ O 2  severe VC  endothelial damage and vessel obliteration  hypoxia - ↓ O 2  hypoxia  neovascularization  Hg and proteinaceous material  adhesions  retinal detachment Prevention: - ↓ O 2 to 40% of the inhaled air ( may not be sufficient for very immature fetus ) - Large dose of vit E ( controversial )

Much less frequent Causes:  Sepsis  Meconium aspiration  Intrauterine pneumonia  Persistent pulmonary HTN  Pulmonary Hg Sepsis  septicemia mostly due to group - B streptococcus disease

Meconium is usually associated with:  Oligohydramnios  Uteroplacental insufficiency  Fetal distress Persistent pulmonary HTN may follow:  Elective CS  Premature closure of ductus arteriosus

Treatment: Similar to hyaline membrane disease: High frequency oscillatory ventilation + nitric oxide inhalation in severe pulmonary HTN  pulmonary VD with no systemic VD  ↓ fetal death  ↓ need for extracorporeal membrane oxygenation ( ECMO ) But not useful < 34 weeks

Severe pulmonary disease characterized by: Chemical pneumonitis Mechanical obstruction Resulting from: Peripartum inhalation of meconium - stained AF  inflammation + hypoxia Free fatty acids  remove the surfactant In severe cases  pulmonary HTN  death or long – term neurological sequelae

= % 20 of pregnancies at term In the past MA = fetal distress Now = normal GIT maturation or vagal stimulation by UC compression But still considered a marker of: adverse perinatal outcome In healthy fetuses + normal AFV  cleared Not cleared mostly in thick meconium with: Postterm - FGR

Risk factors:  ↓ AFV  Cord compression  Uteroplacental insufficiancy MA ↑ in:  Thick meconium  Abnormal FHR Transient episodes of cord compression may  MA in cases of oligohydramnios

MA can not be predicted: - = 20% of normal pregnancies - CS for meconium and abnormal FHR  no alteration of % of meconium beneath the cords - Aggressive peripartum airway management did not prevent fetal death

Prevention: Carson 1976  - Oropharyngeal suction of the infant before delivery of the chest - Laryngoscope visualization: If meconium is visualized  additional suctioning of the trachea

Studies: - This procedure  2.1% MA = still occur = not caused by delivery - Routine tracheal suction of nondepressed infants with meconium stained AF  ↑ morbidity # no suction - MA is caused by chronic antenatal insult  abnormal muscularization of interacinar arteries - MA in baboon model  no death or long – term neurological sequence

- MA is caused by chronic fetal asphyxia  pathological changes:  Pulmonary vascular damage  Persistent fetal circulation  Pulmonary HTN - Markers of acute asphyxia are not ↑: pH - lactates - hypoxanthine - 1 Marker of chronic asphyxia is ↑: erythropoietin

Amnioinfusion: Used to relief variable decelerations during labor:  ↓ VD & cord compression  ↓ MA & meconium below the cords  ↓ Operative delivery  Neonatal acidosis Useful for healthy fetus with thick meconium Not useful for chronic asphyxia

Management of MA: - Suction before delivery of the shoulders by:  Suction bulb  DeLee trap connected to wall suction and not suctioned by mouth Study: - Both are equally efficacious - Carful suction  5% MA in moderate to thick meconium

- If the infant is depressed or + thick particulate meconium: Suction under visualization Intubation + tracheal suction Stomach suction - In thin meconium  tracheal suction is controversial - Efficacy is unknown  skillful suction carry little risk of harm