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PHONGTHORN TUNTIVARARUT PRESENTER URAROM PANTUMAPOL ADVISOR Respiratory Distress Syndrome
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Respiratory distress syndrome

Jun 12, 2015

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Page 1: Respiratory distress syndrome

PHONGTHORN TUNTIVARARUTPRESENTER

URAROM PANTUMAPOLADVISOR

Respiratory Distress Syndrome

Page 2: Respiratory distress syndrome

Respiratory Distress Syndrome (RDS)

Also known as Hyaline Membrane Disease (HMD)

RDS occurs primarily in premature infants; its incidence is inversely related to gestational age and birthweight

Gestational age

Percentages

Less than 28 wks

60-80%

32-36 wks 15-30%

37-39 wk 5%

Term RareNelson Textbook of Pediatrics, 18th Ed.

Page 3: Respiratory distress syndrome

Incidence of RDS

The risk of developing RDS increases with : Maternal diabetes, multiple births, cesarean section

delivery, perinatal asphyxia, cold stress, and a history of previously affected infants

The risk of RDS is reduced in pregnancies with : Chronic or pregnancy-associated hypertension,

maternal heroin use, prolonged rupture of membranes, and antenatal corticosteroid prophylaxis

Page 4: Respiratory distress syndrome

Etiology & Pathophysiology

Surfactant deficiency (decreased production and secretion) is the primary cause of RDS The failure to attain an adequate FRC and the

tendency of affected lungs to become atelectatic correlate with high surface tension and the absence of pulmonary surfactant

The major constituents of surfactant Dipalmitoyl phosphatidylcholine (lecithin) <- Major

component Phosphatidylglycerol Apoproteins (surfactant proteins SP-A, -B, -C, -D) Cholesterol

Page 5: Respiratory distress syndrome

Nelson Textbook of Pediatrics, 18th Ed.

Page 6: Respiratory distress syndrome

Etiology & Pathophysiology

Surfactant is produced by Type II pneumocytes (Great alveolar cells) and present in high concentrations in fetal lung by 20 wk of gestation, but it does not reach the surface of the lungs

Surfactant appears in amniotic fluid between 28 and 32 wk of gestation

Mature levels of pulmonary surfactant are usually present after 35 wk (L/S ratio = 2:1)

Page 7: Respiratory distress syndrome

Etiology & Pathophysiology

Advancing gestational age

Increasing amounts of phospholipids are synthesized and stored in type II alveolar cells

Surface-active agents are released into the alveoli (Air-Liquid Interface)

Reduce surface tension of the water and help maintain alveolar stability by preventing the collapse of small air spaces at end-expiration

Page 8: Respiratory distress syndrome

Etiology & Pathophysiology

Genetic disorders may contribute to respiratory distress : Abnormalities in surfactant protein B and C genes Abnormalities in gene responsible for transporting

surfactant across membranes (ABC transporter 3 [ABCA3])

Page 9: Respiratory distress syndrome

Fetal rat lung, day 20 (term, day 22)

showing developing type II cells, stored glycogen (pale areas), secreted lamellar bodies, and tubular myelin

Nelson Textbook of Pediatrics, 18th Ed.

Page 10: Respiratory distress syndrome

Etiology & Pathophysiology

Synthesis of surfactant depends in part on Normal pH Temperature Perfusion

The epithelial lining of the lungs may also be injured by high oxygen concentrations and the effects of respirator management, thereby resulting in a further reduction in surfactant

Page 11: Respiratory distress syndrome

Etiology & Pathophysiology

The highly compliant chest wall of preterm infants offers less resistance to the natural tendency of the lungs to collapse

At end-expiration, the volume of the thorax and lungs tends to approach residual volume, and atelectasis may develop

Page 12: Respiratory distress syndrome
Page 13: Respiratory distress syndrome

Etiology & Pathophysiology

Deficient synthesis or release of surfactant Atelectasis and

results in perfused but not ventilated

alveoli

Hypoxia

Small respiratory units and a

compliant chest wall

Page 14: Respiratory distress syndrome

Nelson Textbook of Pediatrics, 18th Ed.

Page 15: Respiratory distress syndrome

Pathology

The lungs appear deep purplish red and are liver-like in consistency

Extensive atelectasis with engorgement of the interalveolar capillaries and lymphatics

Page 16: Respiratory distress syndrome

Liver-like consistency of the

lungs

Page 17: Respiratory distress syndrome

Clinical manifestations

Characteristically, tachypnea, prominent (often audible) grunting, intercostal and subcostal retractions, nasal flaring, and duskiness are noted

Signs of RDS usually appear within minutes of birth, although they may not be recognized for several hours in larger premature infants until rapid, shallow respirations have increased to 60/min or greater

Page 18: Respiratory distress syndrome

Clinical manifestations

Breath sounds may be normal or diminished with a harsh tubular quality

Fine rales may be heard, especially posteriorly over the lung bases

Apnea and irregular respirations occur as infants tire and are ominous signs requiring immediate intervention

Page 19: Respiratory distress syndrome

Clinical manifestations

In most cases, the symptoms and signs reach a peak within 3 days, after which improvement is gradual

Death is rare on the 1st day of illness, usually occurs between days 2 and 7 associated with alveolar air leaks (interstitial emphysema,

pneumothorax), pulmonary hemorrhage, or IVH.

Mortality may be delayed weeks or months if BPD develops in mechanically ventilated infants with severe RDS

Page 20: Respiratory distress syndrome

Clinical diagnosis

On X-ray, the lungs may have a characteristic, but not pathognomonic appearance Fine reticular granularity of the parenchyma Air bronchograms More prominent early in the left lower lobe because of

superimposition of the cardiac shadowTypical pattern developing at 6–12 hr.Laboratory findings are initially

characterized by hypoxemia and later by progressive hypoxemia, hypercapnia, and variable metabolic acidosis

Page 21: Respiratory distress syndrome

Infant with respiratory distress syndrome. Note the granular lungs, air bronchogram, and air-filled esophagus. ( A is the endotracheal tube; B is the umbilical venous catheter at the junction of the umbilical vein, ductus venosus, and portal vein; C is the umbilical artery

catheter passed up the aorta to T12)Nelson Textbook of Pediatrics, 18th Ed.

Page 22: Respiratory distress syndrome

Ground glass appearance

• Fine reticulogranular• Air bronchogram

Page 23: Respiratory distress syndrome

Progression of the disease

Acute phase First 48-72 hr. after birth, newborn begins to have

tachypnea, chest tightness The sign and symptoms are peak on day 1-2 Patients may death if they did not receive adequate

treatment

Recovery phase Started on day 3-5 Type II Pneumocytes are regenerated Decreased oxygen requirement

Page 24: Respiratory distress syndrome

Differential diagnosis

Group B streptococcal pneumoniaTransient tachypnea of the newborn (TTNB)Diaphragmatic hernia

More common in term newbornTotal anomalous pulmonary venous return

(TAPVR)

Page 25: Respiratory distress syndrome

Treatments

Because most cases of RDS are self-limited, the goal of treatment is to minimize abnormal physiologic variations and superimposed iatrogenic problems

There are 4 main treatments for RDS : Supportive treatments Oxygen therapy Mechanical ventilation Surfactant replacement therapy

Page 26: Respiratory distress syndrome

Supportive treatment

Body temporature Scheduled “touch times” to avoid hypothermia and

minimize oxygen consumption Placed in an isolette or radiant warmer to maintaine

core temperature between 37 ± 0.5 °C

Page 27: Respiratory distress syndrome

Supportive treatment

Nutritional support For the 1st 24 hr, 10%DW should be infused through

a peripheral vein at a rate of 65–75 mL/kg/day For VLBW and ELBW, TPN should be added Day 2-3, Na 3-4 mEq/kg/day and K 2-3 mEq/kg/day

should be added (TV not more than 90 ml/kg/day) Excessive fluids (>140 cc/kg/day) contribute to the

development of PDA and BPD

On day 1, if good clinical, step feed by started at 0.5-1 ml/kg x 8 feeds drip in 1-2 hr with TPN (TV 80-100)

Page 28: Respiratory distress syndrome

Supportive treatment

Others Give a blood transfer when Hct is less than 40% (*

Protocol)

Page 29: Respiratory distress syndrome

Hgb RESPIRATORY SUPPORT AND/OR SYMPTOMS TRANSFUSION VOLUME

Hct ≤ 35/ Hgb ≤ 11

Infants requiring moderate or significant mechanical ventilation (MAP > 8 cm H2O and Fio2 > 0.4)

15 mL/kg PRBCs[*] over period of 2–4 hr

Hct ≤ 30/ Hgb ≤ 10

Infants requiring minimal respiratory support (any mechanical ventilation or endotracheal/nasal CPAP > 6 cm H2O and Fio2 ≤ 0.4)

15 mL/kg PRBCs over period of 2–4 hr

Hct ≤ 25/ Hgb ≤ 8

Infants not requiring mechanical ventilation but who are receiving supplemental O2 or CPAP with an Fio2 ≤ 0.4 and in whom 1 or more of the following is present:

20 mL/kg PRBCs over period of 2–4 hr (divide into 2–10 mL/kg volumes if fluid sensitive)

 

• ≤24 hr of tachycardia (HR > 180) or tachypnea (RR > 80)

 

• An increased oxygen requirement from the previous 48 hr, defined as a ≥4-fold increase in nasal canula flow (i.e., 0.25 to 1 L/min) or an increase in nasal CPAP ≥ 20% from the previous 48 hr (i.e., 5 to 6 cm H2O)

• Weight gain <10 g/kg/day over the previous 4 days while receiving ≥100 kcal/kg/day

• An increase in episodes of apnea and bradycardia (>9 episodes in a 24-hr period or ≥2 episodes in 24 hr requiring bag and mask ventilation) while receiving therapeutic doses of methylxanthines

• Undergoing surgery

Hct ≤ 20/ Hgb ≤ 7

Asymptomatic and an absolute reticulocyte count <100,000 cells/μL

20 mL/kg PRBCs over period of 2–4 hr (2–10 mL/kg volumes)* RBC should be irradiated prior to

transfusionNelson Textbook of Pediatrics, 18th Ed.

Page 30: Respiratory distress syndrome

Oxygen therapy

Warm humidified oxygen should be provided at a concentration initially sufficient to keep PaO2 50-80 mmHg, pH 7.25-7.45, PaCO2 40-50 mmHg and SpO2 90–95% to maintain normal tissue oxygenation while

minimizing the risk of oxygen toxicity

O2 box is not recommended for newborn with VLBW and ELBW because of high concentration of O2 may increase risk of ROP

Page 31: Respiratory distress syndrome

Oxygen therapy

If the PaO2 cannot be maintained above 50 mmHg at inspired oxygen concentrations of 60% or greater, applying CPAP at a pressure of 5–10 cm H2O by nasal prongs CPAP prevents collapse of surfactant-deficient alveoli,

improves FRC, and improves ventilation-perfusion matching

The amount of CPAP required usually decreases abruptly at about 72 hr of age, and infants can be weaned from CPAP shortly thereafter

Page 32: Respiratory distress syndrome

Mechanical ventilation

Continue positive airway pressure (CPAP) is being use with 4-8 cm·H2O To make Functional residual capacity (FRC) for the

lung to prevent atelectasis Usually started with 5 cm·H2O and increased by 1

cm·H2O in subsequent with increase oxygen by 10% Routes of administration

Nasal prongs Nasopharyngeal tube

Page 33: Respiratory distress syndrome

Mechanical ventilation

Indication for ventilator Apnea with no improvement Cyanosis or PaO2 ≤ 40 mmHg (when using CPAP and

high oxygen concentration) Signs of Respiratory failure

PaCO2 > 60 mmHg Metabolic acidosis

Page 34: Respiratory distress syndrome

Surfactant replacement therapy

Surfactant replacement therapy can reduce mortality and incidence of Chronic pulmonary disease

There are 2 types of surfactant :1. Natural surfactant extract

Bovine(Survanta), Porcine(Curosurf), Surfacten, Alveofact and Calf (Infasurf)

2. Synthetic surfactant Exosurf and ALEC (Artificial Lung Expanding Compound)

Page 35: Respiratory distress syndrome

Surfactant replacement therapy

Natural surfactants appear to be superior, perhaps because of their surfactant-associated protein content

Natural surfactants have a more rapid onset and are associated with a lower risk of pneumothorax and improved survival

Page 36: Respiratory distress syndrome

Surfactant replacement therapy

The 2 main indications : Prophylactic treatment

Being use for infant delivered during 23-29 wk of gestation and birth weight 600-1250 g

Results : Improve dyspnea in first 48-72 hr of life (Decrease O2

requirement, ventilation improved) Decreased incidence of pneumothorax and BPD Not affect the incidence of IVH and PDA Decrease mortality

Page 37: Respiratory distress syndrome

Surfactant replacement therapy

The 2 main indications : Therapeutic or Rescue treatment

Initiated as soon as possible in the 1st 24 hr of life Repeated dosing is given via the endotracheal tube every

6–12 hr for a total of 2 to 4 doses, depending on the preparation

Results : Clinical improved (Decrease O2 requirement) Decreased incidence of pneumothorax Not affect the incidence of BPD, IVH and PDA Decrease mortality

There is no significantly difference between single dose and multiple dose of surfactant replacement therapy (Dunn et al. and

Speer et al.)

Page 38: Respiratory distress syndrome
Page 39: Respiratory distress syndrome

Complication

Bronchopulmonary dyaplasia (BPD) Result of lung injury in infants requiring mechanical

ventilation and supplemental oxygen disease of more mature preterm infants with RDS treated

with positive pressure ventilation and oxygen

BPD is usually defined as a need for supplemental oxygen at 36 wk after conception Another definition of BPD is based on the severity of

disease Neonates on positive pressure support or receiving

>30% supplemental oxygen are diagnosed with BPD

Page 40: Respiratory distress syndrome

GA <32 WK ≥32 WK

Time point of assessment

36 wk PMA or discharge home

Treatment with >21% oxygen for at least 28 days plus

> 28 days but < 56 days postnatal age or discharge home

Treatment with 21% oxygen for at least 28 days plus

Mild BPD Breathing room air at 36 wk PMA or discharge

Breathing room air by 56 days postnatal age or discharge

Moderate BPD

Need[*] for < 30% oxygen at 36 wk PMA or discharge

Need[*] for < 30% oxygen at 56 days postnatal age or discharge

Severe BPD Need[*] for ≥ 30% oxygen and/or positive pressure (PPV or NCPAP) at 36 wk PMA or discharge

Need[*] for ≥ 30% oxygen and/or positive pressure (PPV or NCPAP) at 56 days' postnatal age or discharge

* A physiologic test confirming that the oxygen requirement at the assessment time point remains to be defined.

Nelson Textbook of Pediatrics, 18th Ed.

Page 41: Respiratory distress syndrome

Complication

Physiologic test Those receiving 30% oxygen or less undergo a

stepwise 2% reduction in supplemental oxygen to room air while under continuous observation and oxygen saturation monitoring.

Outcomes are “no BPD” (saturations 88% or greater for 60 min) or “BPD” (saturation <88%)

This test is highly reliable and correlated with discharge home in oxygen, length of hospital stay, and hospital readmissions in the 1st yr of life

Page 42: Respiratory distress syndrome

Complication

Patent ductus arteriosus (PDA) Delayed closure of the PDA is associated with hypoxia,

acidosis, increased pulmonary pressure secondary to vasoconstriction, systemic hypotension, immaturity, and local release of prostaglandins, which dilate the ductus

As RDS resolves, pulmonary vascular resistance decreases, and left-to-right shunting may occur and lead to left ventricular volume overload and pulmonary edema

Page 43: Respiratory distress syndrome

Complication

Patent ductus arteriosus (PDA) Manifestations of PDA may include :

Apnea for unexplained reasons in an infant recovering from RDS

Hyperdynamic precordium, bounding peripheral pulses, wide pulse pressure, and a continuous or systolic murmur with or without extension into diastole or an apical diastolic murmur, multiple clicks resembling the shaking of dice

Carbon dioxide retention Increasing oxygen dependence X-ray evidence of cardiomegaly and increased pulmonary

vascular markings Hepatomegaly

Page 44: Respiratory distress syndrome

Complication

Intraventricular hemorrhage (IVH) Commonly occurs on day 3-4 in preterm newborn with

low birth weight and severe RDS Can be detected by Brain ultrasonography

Page 45: Respiratory distress syndrome

Complication

Intraventricular hemorrhage (IVH)

Grading of IVH Grade 1 - bleeding occurs just in a small area of the

ventricles Grade 2 - bleeding also occurs inside the ventricles Grade 3 - ventricles are enlarged by the blood Grade 4 - bleeding into the brain tissues around the

ventricles

Page 46: Respiratory distress syndrome

Prevention

Avoidance of preterm laborAvoidance of unnecessary cesarean sectionEvaluation of L/S ratio for lung maturity

L/S ratio = 2:1 in mature lungFoam test (Shake test)Administration of corticosteroid before labor

Page 47: Respiratory distress syndrome

Prevention

Corticosteroid administration is recommended for all women in preterm labor (24–34 wk gestation) who are likely to deliver a fetus within 1 wk

Betamethasone 12 mg IM q 24 hr for 2 doses Repeated weekly doses of betamethasone until 32 wk

Dexamethasone 6 mg IM q 12 hr for 4 doses

Page 48: Respiratory distress syndrome

Prevention

Prenatal dexamethasone may be associated with a higher incidence of periventricular leukomalacia than betamethasone

The relative risk of RDS, IVH and death is higher with antenatal dexamethasone treatment when compared with betamethasone

Page 49: Respiratory distress syndrome

Prevention

Administration of a 1st dose of surfactant into the trachea of symptomatic premature infants immediately after birth (prophylactic) or during the 1st few hours of life (early rescue) reduces air leak and mortality from RDS

Page 50: Respiratory distress syndrome

References

Robert M. Kliegman, Richard E. Behrman, Hal B. Jenson, Bonita M.D. Stanton. Nelson Textbook of Pediatrics. Saunders; 18th edition, 2007:

พิ�มลรั�ตน์ ไทยธรัรัมยาน์น์ท. การัดู�แลทารักแรักเก�ดู. ชั�ยเจรั�ญ, 2554: 149-157

Page 51: Respiratory distress syndrome

…Thank you…