HYALINE MEMBRANE DISEASEWilliam 2001

Hyaline membrane disease Retinopathy of prematurity Respiratory distress in term

infants Meconium aspiration

HYALINE MEMBRANE DISEASE

Fetal lungs at birth: ↓ fluid ( expressed or absorbed ) ↑ air ↑ blood

Type II pneumocytes surfactantSurfactant ↓ surface tension

↓surfactant collapse of the alveoli at the end of expiration + hyaline membrane in alveoli and distal bronchioles

Corticosteroid therapy ↓ HMDHMD ↑ in boys – blacksPreeclampsia and PROM no ↓ HMDClinical 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 shuntHyaline 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 PO2 < 40mmHg give the

lowest level sufficient to treat hypoxia and acidosis = PO2 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:1st report in 1980 by FujiwaraHelpful in LBW = 500 – 750 gm

= 23 – 26 weeks ↓mortality by 20 – 25%

It’s rule in older fetuses debateTypes :Biological (animal-human)–synthetic

Complications: Bronchopulmonary dysplasia Pulmonary HTN Retinopathy

Bronchopulmonary dysplasia : =O2 toxicity lung disease

Alveolar and bronchiolar epithelialdamage hypoxia + hypercarbia

+O2 dependence peribronchial and interstitial fibrosis P HTN

Prevention:Avoid elective preterm labor:

Estimate GA Confirm lung maturity

Then weigh risks of maternal diseaseagainst risks of prematurityAmniocentesis to confirm fetal lung maturity:

TESTS OF 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 ½2 – 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 – TDx – 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 1st line before L/S4 - Shake test:

1972

Contamination↑ false –ve results Used as screening test by some

5 – Lumadex – FSI: reliable6 -- Fluorescent polarization:

reliable simple rapid expensive

7 – AF absorbance at 650 - nm wavelength = L/S R

8 - Lamellar body count: Simple – rapid – accurate

≥35000/mL = 100% lung mature9 -

Dipalmitoylphosphatidylcholine ( DPPC test) :

sensitivity = 100% specificity = 96%

RETINOPATHY OF PREMATURITY

<1950 = largest single cause of blindness >1950 = ↓due to avoiding ↑ O2 therapy

-The retina vascularizes centrifugally from the optic nerve starting at the 4th month

until after birth . During this period it is easily damaged

-↑O2 mostly damage the temporal portion of the retina

-↑O2 severe VC endothelial damage and vessel obliteration hypoxia -↓O2 hypoxia neovascularization Hg and proteinaceous material adhesions retinal detachment

Prevention: -↓O2 to 40% of the inhaled air ( may not be sufficient for very immature fetus)

-Large dose of vit E ( controversial )

RESPIRATORY DISTRESS IN THE TERM INFANT

Much less frequentCauses:

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 pulmonaryHTN pulmonary VD with no systemic VD

↓ fetal death ↓ need for extracorporeal

membrane oxygenation ( ECMO )But not useful < 34 weeks

MECONIUM ASPIRATION

Severe pulmonary disease characterizedby:

Chemical pneumonitis Mechanical obstruction

Resulting from: Peripartum inhalation of meconium

- stained AF inflammation + hypoxia Free fatty acids remove the surfactantIn severe cases pulmonary HTN deathor long – term neurological sequelae

% =20 of pregnancies at termIn the past MA = fetal distressNow = normal GIT maturation

or vagal stimulation by UC compressionBut still considered a marker of :

adverse perinatal outcomeIn healthy fetuses + normal AFV clearedNot 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 acidosisUseful 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 mouthStudy:

-Both are equally efficacious -Carful suction 5% MA in moderate

to thick meconium

- If the infant is depressed or + thick particulate meconium:Suction under visualizationIntubation + tracheal suctionStomach suction

-In thin meconium tracheal suction is controversial

-Efficacy is unknown skillful suction carry little risk of harm