CLD Flashcards

1
Q

CLD

A

The term “chronic lung disease” (CLD), used to
describe the aftermath of prematurity and its
treatment on the respiratory system.

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2
Q

term bronchopulmonary dysplasia (BPD)

A

• The term bronchopulmonary dysplasia (BPD) ALSO
describes chronic lung disease subsequent to oxygen
and/or ventilator therapy for respiratory distress
syndrome (RDS) in preterm newborns.

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3
Q

BPD in full term?

A

Some full-term newborns can have BPD subsequent
to mechanical ventilation for other neonatal
respiratory conditions.

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4
Q

CLDP

A
# Chronic lung disease of prematurity (CLDP) is
sometimes used interchangeably with BPD 

, but this
term is best reserved for other chronic lung diseases
of the preterm infant that can arise after an initial
period without an oxygen or ventilatory requirement.

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5
Q

NICHD : national institute of child health and human development

A

• Patients who are <32 weeks GA are assessed at 36
weeks postmenstrual age (PMA) or when discharged
home, whichever comes first.
• Patients who are ≥32 weeks GA are assessed between
29 to 55 days of age or when discharged home,
whichever comes first

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6
Q

RISK FACTORS

• Prematurity

A

The lung appears to be most susceptible to damage during the saccular
stage of development from 23 to 32 weeks gestation.

At this stage, the premature lung has poorly developed airway
supporting structures, surfactant deficiency, decreased compliance,
underdeveloped antioxidant mechanisms, and inadequate fluid
clearance.
The premature lung’s structural and functional immaturity increases the
risk of injury and disruption of normal pulmonary microvascular and
alveolar development from external antenatal and postnatal insults.

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7
Q

Post-surfactant “New”

A

Saccular stage (23-32w) antenatal insults result in developmental arrests or delay in pulmonary maturation

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8
Q

Pre-surfactant “Old”

A

Post-natal insults causing structural pulmonary injuries

Alveolar stage 36-40 ( delivery)

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9
Q

2nd RF Mechanical ventilation
1-volutrauma
2-Barotrauma

A

Injury caused by mechanical ventilation primarily is due to large tidal
volumes (volutrauma) that overdistend airways and airspaces, rather than
increased airway pressures
Mechanical ventilation (Barotrauma)
Positive pressure ventilation typically induces bronchiolar lesions

~$$$$$The risk of BPD increases with decreasing arterial carbon dioxide
tension (PCO2) as a measure of more aggressive ventilation that includes large tidal volumes.

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10
Q

Wt is RF of BPD “

A

Infants with birth weight (BW) <1250 g
account for 97 percent of the cases of BPD
BW from 1251 to 1500: 6 percent BW from 1001 to 1240: 14 percent BW from 751 to 1000: 33 percent BW from 501 to 750: 46 percent

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11
Q

RISK FACTORS

• Oxygen toxicity

A

Cellular damage is caused by the overproduction of cytotoxic
reactive oxygen metabolites: superoxide free radical hydrogen peroxide hydroxyl free radical singlet oxygen
which overwhelm the neonate’s immature antioxidant system

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12
Q

Oxygen toxicity

A

Preterm infants have inadequate antioxidant defenses because of: •Nutrient deficiencies: (vitamins A and E, iron, copper, zinc, and selenium) •Immature antioxidant enzyme systems

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13
Q

RISK FACTORS

• Infection

A

Sepsis is associated with an increased risk of BPD.

Infants with candidemia had the highest risk of developing BPD

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14
Q

Chorioamnionitis

A

The presence of chorioamnionitis has been reported to be
protective against the development of RDS but is a significant
risk factor for the development of CLD and also of cerebral
palsy.

The chorioamnionitis has been known to protect against respiratory distress syndrome (RDS). The beneficial effect of chorio­ amnionitis on the incidence of RDS has been shown under the exposure to antena tal corticosteroid

Chorioamnionitis is an inflammation in the fetal membranes or placenta. When chorioamnionitis de­ velops, fetal lungs are exposed to inflammatory cytokines and mediators via amniotic fluid. Because inflammation plays a pivotal role in the development of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, fetal lung inflammation induced by chorioamnionitis has been considered to be one of the major pathogenetic factors for BPD.

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15
Q

Rf

A

An increased incidence of CLD has been reported in infants
from families with atopy.

Patent ductus arteriosus (PDA) was associated with increased
risk

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16
Q

Physical examination

A

Infants usually are tachypneic.
May have mild to severe retractions, and scattered rales may be audible.
Intermittent expiratory wheezing may be present in infants with airway narrowing from scar formation, constriction, mucus retention, collapse, and/or edema.

17
Q

Radiograph

A

• Radiologic manifestation of mild BPD usually appears
normal or mild haziness lung field.
• Moderate to severe BPD may show hyperinflation, lobar
or segmental atelectasis, gas trapping with pulmonary
interstitial emphysema (PIE) and increased lung
streaking.
• Fibrosis and enlarg

18
Q

Management

A

• RESPIRATORY SUPPORT . • NUTRITION • FLUID RESTRICTION • DIURETICS • BRONCHODILATORS • CORTICOSTEROIDS

19
Q

RESPIRATORY SUPPORT

• Mechanical ventilation

A

Mechanical ventilation • Small tidal volumes to avoid additional mechanical less than 6ml/kg
injury. • PaCO2 levels between 55 and 65 mmHg are
tolerated as long as pH remains in the normal range #premissive hypercapnea
• In general, maintaining a PEEP of 5 to 7 cm H2O
may minimize atelectasis, and counter the
development of pulmonary edema.
PEEP: positive end expiratory pr

20
Q

RESPIRATORY SUPPORT

• Oxygen

A

Supplemental oxygen is used to ensure adequate tissue
oxygenation and avoid alveolar hypoxia which increases pulmonary vascular resistance, potentially leading to the development of cor-pulmonale.
However, increases in inspired oxygen concentrations
have increasing the risk of retinopathy of
prematurity or exacerbating pulmonary
inflammation or pulmonary edema.

21
Q

NUTRITION

A

Total energy needs in some infants may increase
to 150 kcal/kg per day, and protein intake of 3-4
g/kg per day is needed.

22
Q

FLUID RESTRICTION

A
Based upon clinical experience, current
bronchopulmonary dysplasia (BPD) management
recommend  restricting fluid intake to avoid
pulmonary edema and improve pulmonary function • Most infants can be managed with modest fluid
restriction of 140 to 150 mL/kg per day
23
Q

DIURETICS

A

The two classes of diuretic agents used in infants
with BPD are:
• Thiazide diuretics • Loop diuretics - furosemide
Furosemide increases calcium excretion, sometimes leading to nephrocalcinosis and/or nephrolithiasis and potentially ototoxic.

24
Q

SYSTEMIC CORTICOSTEROIDS

A

The benefits of early postnatal corticosteroid treatment (= 7 days), particularly dexamethasone, may not outweigh the known or potential adverse effects of this treatment.
Early (<8 days) postnatal corticosteroids for preventing chronic lung disease in preterm infants.Halliday HL, Ehrenkranz RA, Doyle LW Cochrane Database Syst Rev. 2009.
•Although early corticosteroid treatment facilitates extubation and reduces the risk of chronic lung disease and patent ductus arteriosus, •it causes short-term adverse effects including gastrointestinal bleeding, intestinal perforation, hyperglycaemia, hypertension, hypertrophic cardiomyopathy and growth failure

25
Q

Prevention of RSV infection

A

• Severe respiratory failure may occur in patients with
BPD who develop infection with respiratory syncytial
virus (RSV).
• Prophylaxis should be provided with palivizumab for
infants younger than two years of age who have
required medical therapy for BPD within six
months of the RSV season
Mid oct the mid march