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PRESENTED BY, MS.L.SOUNDARYA M.SC.NURSING (PEDIATRICS) BRONCHO-PULMONARY DYSPLASIA

broncho pulmonary dysplasia

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Page 1: broncho pulmonary  dysplasia

PRESENTED BY, MS.L.SOUNDARYAM.SC.NURSING (PEDIATRICS)

BRONCHO-PULMONARY DYSPLASIA

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•Broncho-pulmonary dysplasia is chronic lung disease of the neonate that typically is caused by prolonged ventilation and is further defined by age of prematurity and extent of O 2

requirement.(OR)

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•A progressive chronic pulmonary condition characterized by pulmonary edema and a prolonged requirement of oxygen in infants who have been treated for respiratory distress syndrome.

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CAUSES Significant risk factors include•Prolonged mechanical ventilation•High concentrations of inspired O 2

•Infection (eg, chorio-amnionitis or sepsis)

•Degree of prematurity

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Additional risk factors include

•Pulmonary interstitial emphysema

•High peak inspiratory pressures

•Large end-tidal volumes

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•Repeated alveolar collapse•Increased airway resistance•Increased pulmonary artery pressures

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pathophysiology 4-pathological changes:STAGE –I (MILD): Clinically identical to IRDS lasts from 2-3 days during this time, there are profuse hyaline membrane,

patchy mucosal cilia and slight edema of the interstitium but no necrosis of alveolar cells.

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STAGE-II (MODERATE): it last from 4-10 days, during this time, there are hyaline membrane present, but

extensive loss of cilia,Some focci of atelectasisSmall amount of esino-philic exudates in the brochioles,

Wide spread edema of the interstitium

Necrosis of alveolar cells are evident.

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STAGE-III (SEVERE): Lasts from 10-20 days.Increased of alveolar

cells and bronchiolar mucosa

Wide spread alveolar collapse

Increased interstitial fibrosis

Hypertensive changes occur in arterioles and arteries

Oxygenation is difficult.

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STAGE-IV (ADVANCE CHRONIC):

Lasts for a monthWide spread necrosis, interstitial fibrosis

Emphysema presentPulmonary failure cardiomegaly with cor-pulmonale

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ASSESSMENT IT is evident when there is increased need of oxygen

Crepitant rales and diminished breathing sounds

Barrel shape chest appearanceEmphysema Oxygenation difficult and carbon dioxide retention

Respiratory acidosis occurs

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DIAGNOSTIC EVALUATIONHistory collectionPhysical examinationRadiological findingsBlood investigations for o2 tension, and acidosis

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TREATMENT•Nutrition supplementation

•Fluid restriction•Diuretics•O 2 supplementation as needed

•Respiratory syncytial virus (RSV) monoclonal antibody

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NURSING MANAGEMENT

•Oxygen therapy can be provided

•Supportive measurements- *Nutritional supplementation,*Fluid restriction, diuretics, * Bronchodilators.

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PREVENTION•Use of antenatal corticosteroids•Prophylactic use of exogenous surfactant in selected high-risk infants (eg, weighing < 1000 g and requiring ventilator support)

•Early therapeutic continuous positive airway pressure

•Early use of surfactant for treatment of RDS

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•Prophylactic use of methylxanthines (eg, caffeine 5 to 10 mg/kg po once/day), particularly when birth weight is < 1.250 kg

•Permissive hypercarbia and hypoxemia to achieve low ventilator pressures, volumes, or both

•Prophylactic use of vitamin A (5000 units IM 3 times/wk for a total of 12 doses) for infants with birth weight < 1000 g

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PROGNOSIS•Prognosis varies with severity.

•Infants who still depend on mechanical ventilation at 36 wk gestation have a 20 to 30% mortality rate in infancy.

•1/3rd of affected infants die by 7-8 months of age.

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•If the child is survive –corpulmonary function can be expected by 5-6 years.

•Infants are at increased risk of lower respiratory tract infections (particularly viral pneumonia or bronchiolitis) and may quickly develop respiratory decompensation if pulmonary infection occurs.

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