Respiratory distress syndrome
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Transcript of Respiratory distress syndrome
PHONGTHORN TUNTIVARARUTPRESENTER
URAROM PANTUMAPOLADVISOR
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.
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
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
Nelson Textbook of Pediatrics, 18th Ed.
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)
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
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])
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.
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
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
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
Nelson Textbook of Pediatrics, 18th Ed.
Pathology
The lungs appear deep purplish red and are liver-like in consistency
Extensive atelectasis with engorgement of the interalveolar capillaries and lymphatics
Liver-like consistency of the
lungs
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
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
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
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
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.
Ground glass appearance
• Fine reticulogranular• Air bronchogram
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
Differential diagnosis
Group B streptococcal pneumoniaTransient tachypnea of the newborn (TTNB)Diaphragmatic hernia
More common in term newbornTotal anomalous pulmonary venous return
(TAPVR)
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
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
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)
Supportive treatment
Others Give a blood transfer when Hct is less than 40% (*
Protocol)
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.
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
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
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
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
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)
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
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
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.)
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
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.
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
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
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
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
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
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
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
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
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
References
Robert M. Kliegman, Richard E. Behrman, Hal B. Jenson, Bonita M.D. Stanton. Nelson Textbook of Pediatrics. Saunders; 18th edition, 2007:
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