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Neonatal Diseases. RC 290. Respiratory Distress Syndrome (RDS). Also known as Hyaline Membrane Disease (HMD). Occurrence. 1-2% of all births 10% of all premature births Greatest occurrence is in the premature and low birth weight infant. Etiology & Predisposing Factors. Prematurity

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Neonatal diseases l.jpg

Neonatal Diseases

RC 290


Respiratory distress syndrome rds l.jpg

Respiratory Distress Syndrome(RDS)

Also known as Hyaline Membrane Disease

(HMD)


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Occurrence

  • 1-2% of all births

  • 10% of all premature births

    • Greatest occurrence is in the premature and low birth weight infant


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Etiology & Predisposing Factors

  • Prematurity

    • Immature lung architecture and surfactant deficiency

  • Fetal asphyxia & hypoxia

  • Maternal diabetes

    • Increased chance of premature birth

    • Possible periods of reflex hypoglycemia in the fetus causing impaired surfactant production


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Pathophysiology

Surfactant deficiency

  • Decreased FRC

  • Atelectasis

  • Increased R-L shunt

  • Increased W.O.B.

  • Hypoxemia and eventually hypercapnia because of V/Q mismatch


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Pathophysiology (cont.)

Atelectasis keeps PVR high

  • Increased PAP

  • Lung hypoperfusion

  • R-L shunting may re-occur across the Ductus Arteriosus and the Foramen Ovale


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Hypoxia/hypoxemia results in anaerobic metabolism and lactic acidosis

This damages the alveolar-capillary membrane causing formation of hyaline membranes. Hyaline membranes perpetuate all of the problems in the lung


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The cycle continues until surfactant levels are adequate to stabilize the lung

  • Symptoms usually appear 2-6 hours after birth

    • Why not immediately?

  • Disease peaks at 48-72 hours

  • Recovery usually occurs 5-7 days after birth


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Tachypnea (60 BPM or >)

Retractions

Nasal flaring

Expiratory grunting

Helps generate autoPEEP

Decreased breath sounds with crackles

Cyanosis on room air

Hypothermia

Hypotension

Clinical findings: Physical


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Clinical Findings: Lab

  • ABGs: initially respiratory alkalosis and hypoxemia that progresses to profound hypoxemia and combined acidosis

  • Increased Bilirubin

  • Hypoglycemia

  • Possibly decreased hematocrit


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CXR: Normal


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RDS CXR: Ground Glass Effect


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RDS CXR: Air Bronchograms & Hilar Densities


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Time constant is decreased since elastic resistance is so high

Increased elastic resistance means decreased compliance!


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RDS Treatment: Primarily supportive until lung stabilizes

  • NTE, maintain perfusion, maintain ventilation and oxygenation

  • O2 therapy, CPAP or mechanical ventilation

    • May require inverse I:E ratios if oxygenation can not be achieved with normal I:E ratio

  • Surfactant instillation!!!

    • May cause a sudden drop in elastic resistance!


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Prognosis/Complications

Prognosis is good once infant makes it past the peak (48-72 hours)

Complications possible are:

  • Intracranial Bleed

  • BPD (Bronchopulmonary Dysplasia)

  • PDA (Patent Ductus Arteriosus)


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Transient Tachypnea of the Newborn (TTN)

Also known as Type II RDS or Retained Lung Fluid


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Occurrence: Similar to RDS

More common in term infants!


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Etiology & Predisposing Factors

  • C-section

    • These infants do not have the fluid expelled from their airways as occurs in vaginal delivery

  • Maternal Diabetes

    • Increased chance of C-section due to LGA

  • Cord Compression

  • Anesthesia


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TTN Pathophysiology

Primary problem = retained lung fluid

  • Fluid not expelled from airways because of C-section

  • Poor absorption of remaining fluid by pulmonary capillaries and lymphatics

  • If retained fluid is in interstitial spaces, compliance and TC are decreased

  • If retained fluid is in airways,airway resistance and TC are increased

  • TTN can be restrictive , obstructive, or both!

  • Fluid usually clears by itself after 24-48 hours after birth


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Clinical Signs

  • Tachypnea (usually rate is greater than seen in RDS)

  • Minimal (if any) nasal flaring or expiratory grunting

  • ABG’s: mild hypoxemia. PaCO2 depends on whether problem is restrictive or obstructive


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TTN CXR

  • Coarse peri-hilar streaks

  • Prominent lung vasculature

  • Flattened diaphragms if fluid is causing obstruction/air-trapping


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TTN Treatment: Like RDS, it is primarily supportive

  • Monitoring and O2 therapy

  • Possibly CPAP or mechanical ventilation


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Prognosis/Complications

  • Prognosis is very good

  • Main complication is pneumonia

    • Often initial diagnosis


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Lab Time!


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Patent Ductus Arteriosus-PDA_

Failure of the D.A. to close at birth or a re-opening of the D.A. after birth. Allows shunting between the pulmonary artery and the aorta


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Occurrence

  • 1 per 2000 term babies

  • 30-50% of RDS babies


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Etiology & Predisposing Factors

  • Prematurity

    • D.A. not as sensitive to increasing PaO2

  • Hypoxia

    • Decreasing PaO2 allows it to re-open for up to three weeks after birth

  • Thus, a PDA can occur in a premature infant who is NOT hypoxic or in a term baby who is hypoxic

    • Worst case is a premature infant who is hypoxic!


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Pathophysiology

  • D.A. fails to close or it re-opens

  • Then shunting occurs between the pulmonary artery and the aorta

  • The direction of the shunt depends on which vessel has the higher pressure

    • A PDA can cause L-R shunting or R-L shunting!

  • Clinically, most PDA’s refer to a L-R shunt


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Clinical Signs

  • Tachypnea, bounding pulses, hyperactive pre-cordium

  • Decreased breath sounds and possibly some crackles

  • Possible murmur over left sternal border

    • Murmur is loudest when D.A. just starts opening or when it is almost closed


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Clinical Signs (cont.)

  • ABGs – hypoxemia with respiratory acidosis

  • If R-L shunting, the PaO2 in the upper extremities, ie pre-ductal, will be greater than the PaO2 in the umbilical artery, ie post-ductal!

  • TC – decreased if L-R shunting causes pulmonary edema; increased if fluid spills into airways and increases airway resistance

  • CXR – if L-R shunt, butterfly pattern of pulmonary edema with possible cardiomegaly


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PDA Treatment

  • Basic – NTE, O2, may require CMV if not already on the ventilator

  • Medical

    • L-R shunt that fails to close: Indomethacin (Indocin)

    • R-L shunt: Priscoline (Tolazoline) to decrease PVR; also nitric oxide

  • Surgical –if medical treatment fails, the PDA may be surgically ligated


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Prognosis/Complications

Good prognosis when baby responds to medical treatment

May develop :

  • Shock

  • CHF

  • Necrotizing Enterocolitis (NEC)


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Meconium Aspiration Syndrome-MAS-

Syndrome of respiratory distress that occurs when meconium is aspirated prior to or during birth


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Occurrence

  • 10-20% of ALL births show meconium staining

    • 10-50% of stained babies may be symptomatic

  • More common in term and post-term babies


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Etiology & Predisposing Factors

  • Intra-uterine hypoxic or asphyxic episode

  • Post-term

  • Cord compression


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Pathophysiology: Check Valve Effect

Causes gas trapping (obstruction)

If complete obstruction, then eventually atelectasis occurs

Irritating to airways, so edema and bronchospasm

Good culture ground for bacteria, so pneumonia possible


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Pathophysiology (cont.)

  • V/Q mismatch leads to hypoxia and acidosis which increases PVR

  • TC increases because it increases airway resistance

  • Meconium is usually absorbed in 24-48 hours; there are still many possible complications


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Respiratory depression or distress at birth

Hyperinflation

Pallor

Meconium stained body

Possible cyanosis on room air

Moist crackles

ABGs – hypoxemia with combined acidosis

CXR – coarse, patchy infiltrates with areas of atelectasis and areas of hyperinflation

May see flattened diaphragms if obstruction is severe

Clinical Signs


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Amnioinfusion – artificial amniotic fluid infused into uterus to dilute meconium

Proper resuscitation at birth(clear meconium from trachea before stimulating respiration)

Oro-gastric tube

NTE

O2

NaHCO3 if severe metabolic acidosis

Broad spectrum antibiotics

Bronchial hygiene

May need mechanical ventilation

Slow rates and wide I:E ratios because of increased TC

Low level of PEEP may help prevent check valve effect

May need HFO

M.A.S. Treatment


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Prognosis & Complications

Good prognosis if there are no complications

Complications:

Pneumonia

Pulmonary baro/volutrauma

Persistent Pulmonary Hypertension (PPHN)


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Persistent Pulmonary Hypertension-PPHN-

Also known as Persistent Fetal Circulation

-PFC-


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Failure to make the transition from fetal to neonatal circulation or a reversion back to the condition where pulmonary artery pressure exceeds aortic pressure

Results in R-L shunting across the D.A. and the Foramen Ovale


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Occurrence

  • Usually term and post-term babies

  • Females more often than males

  • Symptoms may take 12-24 hours after birth to develop


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Etiology & Predisposing Factors

  • M.A.S – most common

  • Hypoxia and /or acidosis, eg RDS

  • Any condition that causes PVR to increase


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Pathophysiology

  • Primary problem is pulmonary artery hypertension

    • Infants arterial walls are thicker and they are more prone to vasospasm

  • If pulmonary artery pressure gets high enough, blood will shunt R-L across the D.A. and Foramen Ovale

    • Remember, conditions that drive up PAP usually make the D.A. open

  • Lung is hypoperfused resulting in refractory hypoxemia and hypercapnia


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Clinical Signs

  • Refractory hypoxemia and cyanosis

  • Shock and tachypnea

  • Murmur possible

  • Pre-ductal PaO2 > post-ductal PaO2

    • Hypoxemia with combined acidosis

  • CXR usually OK when compared to infants condition


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PPHN Treatment

  • NTE and O2

  • Nitric Oxide

    • Often in conjunction with HFO

  • Priscoline, Indocin may also be used

  • If completely unresponsive to therapy ECMO may be tried


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Prognosis & Complications

Prognosis depends on how well infant responds to treatment

Complications

  • Shock

  • Intracranial bleed

  • Internal bleeding

    • Especially a problem if Priscoline is used


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Wilson – Mikity Syndrome-Pulmonary Dysmaturity-

Respiratory distress that develops after the first week of life and presents with definite CXR changes


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Occurrence

  • Usually in <36 weeks gestational age and birth weight <1500 grams

  • After first week of life

    • No prior symptoms


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Etiology & Predisposing Factors

  • Exact etiology unknown

  • Appears to be due to immature lung and airways trying to function

  • Not due to O2 toxicity or mechanical ventilation!


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Pathology

  • Immature alveoli and T-B tree causes V/Q mismatch

  • Areas of atelectasis and hyperinflation develop


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Pathology (cont.)

3 Stages

  • Stage 1

    • 1-5 weeks after birth

    • Diffuse areas of atelectasis and hyperinflation

  • Stage 2

    • 1-5 months after birth

    • Cystic (hyperinflated) areas coalesce and cause flattening of the diaphragms

  • Stage 3

    • 5-24 months after birth

    • Cystic areas start to clear up


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Clinical Signs

  • Tachypnea

  • Cyanosis on room air

  • Some retractions and/or nasal flaring

  • Decreased breath sounds with crackles

  • ABGs – respiratory acidosis with hypoxemia

  • CXR consistent with the stage of the disease


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Wilson – Mikity Treatment

  • Is purely supportive-there is no medicinal or surgical treatment

  • O2 and NTE

    • Some cases require mechanical ventilation

  • Maintain fluids/electrolytes and caloric intake

  • Watch for infection


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Prognosis & Complications

Prognosis good if infant survives stage 2

Complications

  • PDA

  • Cor Pulmonale

  • CNS damage


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Bronchopulmonary Dysplasia-BPD-

A result of RDS and/or its treatment that results in areas of fibrosis, atelectasis, and hyperinflation


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Etiology & Predisposing Factors

  • RDS and prematurity

  • Triad of O2, ET tube, and mechanical ventilation


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Stage 1

Acute phase of RDS

Stage 2

4-10 days after the onset of RDS

Areas of atelectasis and hyperinflation

Stage 3

2-3 weeks after RDS

Hyperinflated areas start to coalesce

Fibrosis starts to develop

Stage 4

1 month after the onset of RDS

Diaphragms start to flatten

Interstitial fibrosis evident on CXR

PPHN may start to develop

O2 dependency develops

Pathology: 4 Stages


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Clinical Signs

  • Tachypnea

  • Persistent retractions

  • A-B spells

  • Cyanosis on room air

  • Decreased breath sounds with crackles

  • ABGs – respiratory acidosis (may be compensated) with hypoxemia

  • CXR – consistent with stage of disease


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BPD: Stage 4 CXR

Interstitial fibrosis and flattened diaphragms


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BPD Treatment

  • Prevention is best! Use the least amount of intervention for the least amount of time!

  • Supportive care

    • O2, NTE, bronchial hygiene, maintain fluids/electrolytes

    • Diuretics if needed to prevent fluid overload and heart failure

  • Possibly vitamin E


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Prognosis & Complications

Good if infant survives to age 2

  • 50% mortality if PPHN develops

    Complications

  • PHTN

  • Cor Pulmonale

  • Respiratory Infections

  • CNS damage


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    Diaphragmatic Hernia

    Congenital malformation of the diaphragm that allows abdominal viscera into the thorax


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    Occurrence

    • 1 per 2200 births


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    Etiology & Predisposing Factors

    • Exact unknown but may be related to vitamin A deficiency


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    Pathology

    • Usually occurs during the 8-10th week of gestation

    • 80% occur on the left at the Foramen of Bochdalek

    • Abdominal viscera enters thorax and compresses developing lung

    • As baby attempts to breathe after birth, the stomach and bowel fill with air and cause further compression of the lung

      • Severe restriction!


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    Clinical Signs

    • Cyanosis

    • Severe respiratory distress with retractions and nasal flaring

    • Bowel sounds in chest

    • Uneven chest expansion

    • Decreased breath sounds on affected side

    • ABGs – profound hypoxemia with combined acidosis

    • CXR – loops of bowel in chest with shift of thoracic structures towards unaffected side, eg dextrocardia


    Diaphragmatic hernia cxr l.jpg

    Diaphragmatic Hernia CXR


    Diaphragmatic hernia treatment l.jpg

    Diaphragmatic Hernia Treatment

    • Immediate ET tube and NG tube

      • No BVM – it will make things worse!

    • Surgical repair

    • Post operative ECMO and/or HFO

      • May need NO with HFO


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    Prognosis & Complications

    50% mortality

    Complications

    • Pneumothorax

    • PDA

    • Hypoplastic lung


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    Pulmonary Barotrauma& Air Leak Syndromes


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    4 Main Types

    • Pneumothorax

    • Pneumomediastinum

    • Pneumopericardium

    • PIE (Pulmonary Interstitial Emphysema)

      • Gas from ruptured alveoli dissects along perivascular and interstitial spaces

      • Causes airway compression (obstruction) and alveolar compression (restriction)

      • May lead to pneumothorax, pneumomediastinum, or pneumopericardium


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    Occurrence

    1-2% of all births

    (not all are symptomatic)


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    Etiology & Predisposing Factors

    • Positive pressure ventilation

    • Increased airway resistance/airway obstruction

    • RDS


    Clinical signs77 l.jpg

    Sudden cyanosis (except with PIE)

    Respiratory distress

    Mediastinal shift

    Sudden hypotension (except with PIE)

    Crepitus (if sub-Q emphysema develops)

    Unequal chest expansion

    Decreased breath sounds and hyperressonance

    ABGs – hypoxemia with respiratory acidosis

    Transillumination

    Clinical Signs


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    Transillumination

    Small Pneumothorax


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    Transillumination

    Big Pneumothorax


    Cxr pneumothorax l.jpg

    CXR: Pneumothorax


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    CXR: Pneumomediastinum

    Note how air does NOT outline the apex of the heart


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    CXR: Pneumopericardium

    Note how air completely outlines the heart


    Cxr pie l.jpg

    CXR: PIE


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    Air Leak Syndrome Treatment

    • Prevention! Use the least amount of intervention for the shortest time possible!

    • Chest tube for pneumothorax

    • HFO may help prevent and/or resolve PIE


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    Prognosis and Complications

    • Good as long as shock and/or cardiac tamponade does NOT occur

    • PIE puts infant at risk for BPD


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    Necrotizing Enterocolitis-NEC-

    Necrosis of the intestinal mucosa


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    Occurrence

    • 20% of all premature births

    • Males = Females

    • Most common in low birth weight babies who experience perinatal distress


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    Etiology & Predisposing Factors

    Exact cause unknown but seen with the following:

    • Intestinal ischemia

    • Bacterial colonization

    • Early formula feeding


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    Pathology

    • Intestinal ischemia due to hypoperfusion, eg shock, or vascular occlusion, eg, clot from umbilical artery catheter

    • Bacterial colonization after ischemia starts necrosis

    • Early formula feeding may provide substrate needed for further bacterial growth and further necrosis


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    Clinical Signs

    • Abdominal distention

    • Poor feeding

    • Blood in fecal material

    • Lethargy

    • Hypotension

    • Apnea

    • Decreased urine output

    • Bile stained emesis

    • CXR – bubbles in intestinal wall


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    NEC Treatment

    • NPO and NG suction

    • IV hydration and hyperalimentation

    • Broad spectrum antibiotics

      • Ampicillin, Gentamycin

    • Minimum pressure on abdomen

      • No diapers or prone positioning

    • Monitor for/treat sepsis

    • Necrotic bowel may need surgical resection


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    Prognosis & Complications

    • Mortality is 20-75%

      • Best prognosis if infant does NOT require any surgery

    • Main complication is sepsis

    • Infants who have bowel resection may develop malabsorption syndrome


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    Congenital Cardiac Anomalies


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    Tetralogy of Fallot

    • VSD

    • Over-riding aorta

    • Pulmonary valve stenosis

    • Right ventricular hypertrophy

    • Significant cyanosis because of R-L shunt


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    Complete Transposition of the Great Vessels

    • Pulmonary artery arises from left ventricle and Aorta arises from right ventricle

    • R-L shunt through PDA, ASD, or VSD needs to be present for infant to survive until corrective surgery

      • Balloon septostomy during cardiac catheterization


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    Truncus Arteriosus

    • Aorta and pulmonary artery are the same vessel

    • Large VSD

    • Requires MAJOR surgical repair

    • Mortality is 40-50%


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    Case Study Time


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    Never Stop Being Inquisitive!


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