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HS8116: Case Study 1b

Our group members are:


Zhao Xinmei Khong Huilin

Juliana Bt Jumahat Ang Nancy


Objectives
• Discuss the pathophysiology of BPD
• Discuss the possible causes for (BPD)
• Describe the clinical features of BPD
• Discuss the medical and nursing
management of baby Sam
• List the likely complications for baby Sam
Case study
Baby Sam was born prematurely at 26
weeks of gestation and required
mechanical ventilation for the past 6
weeks. The doctors are having difficulty
in weaning baby Sam off the ventilator.
Diagnosis

Bronchopulmonary Dysplasia
(BPD)
Definition of Bronchopulmonary
dysplasia
• Also known as chronic lung disease (CLD)
• Dysplasia: abnormal development
• An infant who are oxygen dependent at 1
month of age or 36 weeks postmenstrual
age, and associated with an abnormal chest
radiograph appearance
(Genen & Davis, 2007).
Diagnostic Criteria for
Bronchopulmonary Dysplasia
Gestational age

<32 week ≥ 32 week

Time point of 36 weeks PMA or discharge to home, whichever comes first >28 days but <56 days postnatal age or discharge to home,
assessment whichever comes first

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

Mild BPD Breathing room air at 36 weeks PMA or discharge, whichever Breathing room air by 56 days postnatal age or discharge, whichever
comes first comes first

Moderate BPD Need* for <30 percent oxygen at 36 weeks PMA or discharge, Need* for <30 percent oxygen at 56 days postnatal age or discharge,
whichever comes first whichever comes first

Severe BPD Need* for ≥30 percent oxygen and/or positive pressure (PPV or
NCPAP) at 36 weeks PMA or discharge, whichever comes first Need* for ≥ 30 percent oxygen and/or positive pressure (PPV or
NCPAP) at 56 days postnatal age or discharge, whichever comes
first

NCPAP: nasal continuous positive airway pressure; PMA: postmenstrual age; PPV: positive-pressure ventilation.

National Institute of Child Health and Human Development (NICHD), USA,2007


Alveolar Sac
• Type I pneumocytes: for
gas exchange.
• Type II cells: produce
surfactant (keep alveoli
partially open)
• Macrophage: respond for
inflammation.
• Epithelial (type I cells)
and endothelia (Capillary)
junctions: gas exchange
region
• Alveolar development: in
36 gestation week
Pathophysiology
• Prematural newborn:
- Immaturity of the pulmonary
paranchyma
- Surfactant deficiency
- Immaturity of endothelial and
epithelial junctions
- V/Q mismatch
- Noncompliant stiff lungs
• Lead to hypoxia, hypercarbia:
- Treated with assisted
ventilation and O2

Pulmonary system development


Pathophysiology
• Continued positive pressure and oxygen:
- Immature Antioxidant
- Free oxygen radicals: toxic
- Alveolar-capillary membrane damage: fluids and
proteins leak
• Damage lead to inflammatory response
- Influx of fluid, protein and enzymes
- causes inactivation of surfactant
- loss of ciliary clearance
- pulmonary interstitial fibrosis and edema
- Atelectasis and emphysema
(Monte et al., 2007)
Causes
•Lower birth weight / premature
a) Lung:
surfactant deficiency absence α-ATP,
vital elastin fibers that offer structural
support are destroyed
b) Heart:
PDA prostocyclin being produce
shunt from aorta to PA↑ PAP
• Positive pressure support Barotrauma
Causes
• Oxygen toxicity
less antioxidant enzyme unable help to prevent
injuries from free O2 radicals
• Air leak
air dissection into false air spaces create dead space
for ventilation ↑in size & compress lung tissue
• Infection
barotrauma & O2 toxicity  Neutrophils release
inflammatory mediators pulmonary fibrosis &
edema
Clinical features
• Chest retraction
• Crepitation
• Rhonchi  Bronchospasm
• Tachypnoea  hypoxia, hypercapnia
• Cor pulmonale  ascites, pedal edema
ECG RVH
• CXR changes
• ABG  respiratory acidosis
Medical Management
Management of infants with
bronchopulmonary dysplasia is aimed at
maintaining adequate gas exchange while
limiting the progression of the disease.
Mechanical ventilation
Mechanical ventilation should be used as
short possible, to reduce risk of
volutrauma and infection

• Lowest peak pressure (lower than 15-


18cmH2O)
• Fio2 lower than 0.3-0.4L/min
• Inspiratory times between 0.3-0.5 secs
• PEEP between 4-6 cmH2O
• Ventilator rate is gradually reduced (10-15
bpm)
Mechanical Ventilation
Weaning in ventilators-dependent infants with BPD
is difficult, so it must be accomplished
gradually.

Oxygen therapy

• Reduce FiO2 to avoid oxygen toxicity


• Maintain saturation between 88%-94%
• PaO2 50-70 mmHg
• Infant with BPD may have increased metabolic
demands associated with low oxygen tension
Mechanical ventilation

Optimal levels are:

• pH 7.25-7.40
• pCO2 45-65 mmHg
• pO2 50-70 mmHg
• Oxygen saturation at 88-94%
Fluid Management
• Infants with BPD tolerate excessive or even
normal amounts of fluid intake poorly
• Tendency to accumulate excessive interstitial
fluid in the lung which causes pulmonary
edema and congestive heart failure
• Water and salt must be limited to minimum
required
• Diuretics therapy
Medications
• Diuretics
• Bronchodilators
• Corticosteroids
• Vasodilators
Diuretics
Furosemide (loop diuretics)
• Improves clinical pulmonary status and function
• Decrease pulmonary vascular resistance
• Facilitate weaning from positive pressure
ventilators and oxygenation

Dosage:0.5-2mg/kg/dose, PO/IV, bd-qds


Bronchodilators
Albuterol (Ventolin)
• improve lung compliance by decreasing airway
resistance by relaxing smooth muscle cell.

Dosage: 0.1-0.2 mg (0.02-0.04 mL of 0.5%


solution diluted with 1-2 mL 0.45-0.9% NaCl) per
kg/dose inhaled by nebulizer
Bronchodilators
Ipratropium bromide (Atrovent)
• Muscarinic antagonist with potent
bronchodilating effects
• improve pulmonary mechanics

Dosage: 0.025-0.08 mg/kg inhaled by nebulizer


q6h (dilute in 1.5-2 mL 0.9% NaCl)
Bronchodilators
Caffeine citrate
• CNS and respiratory stimulant used to treat
apnea of prematurity and infants with BPD
• Improve respiratory muscle and contractility
• Caffeine facilitate weaning from ventilator.

Loading dose: 20 mg/kg PO/IV


Maintenance dose: 5 mg/kg/d PO/IV
Bronchodilators
Theophylline
• systemic bronchodilator
• improve contractility of skeletal muscle and
decrease diaphragmatic fatigue in infants

Loading dose: 3-5 mg/kg PO/IV


Maintenance dose: 1-3 mg/kg/d PO/IV q8-12h
Corticosteroids
Dexamethasone
• Enhanced production of surfactant and
antioxidant enzymes
• Decreased bronchospasm,
• Decreased pulmonary and bronchial edema
and fibrosis
• Reduction in pulmonary inflammation
mediators

Dosage: 0.15-0.25 mg/kg/d PO/IV divided bid;


wean over 5-7 days
Pulmonary Vasodilators
Inhaled NO (iNO)
• short-acting gas that relaxes the pulmonary
vasculature
• act as an anti-inflammatory agent at low
concentrations
• Improve ventilation-perfusion matching
• Prolonged use of high concentrations of iNO;
hyperoxia may be associated with increased
oxidant injury
Nutrition
• Promote normal lung growth and development
• To compensate for the increased oxygen and
caloric consumption
• Supplements of protein, calcium, phosphorus
and zinc can be used to maximize calories
intake
• Calories should be adequate to meet their
metabolic needs and growth
Nutrition
• Supplement formula or breast milk with
medium chain triglyceride (MCT) oil, glucose
polymer or rice cereal
• TPN with glucose, amino acids and fat should
be subtituted until the GI tract again becomes
functional
Nursing management
Prevention of infection

• Strict handwashing
• Strict adherence to sterile technique in assessing
line and invasive procedures
• Periodic collection of tracheal secretions for c/s,
obtain FBC, bld c/s, and chest x-ray if pneumonia
suspected
Nursing management
Mechanical ventilation

• Chest physio and gentle suctioning to be done


only when its benefits the patient as to
minimized stress
• Organize care
• Monitor arterial blood gas for adequate gas
exchange and electrolytes imbalances
• Monitor vital signs
• Change ventilators tubing as per protocol
Nursing Management
Nutrition
• Encourage mother to express breast
milk as it provides the best nutrition
• Infants may require 110-150 kcal/kg/day
to produce a weight gain of 15-30g/day
• Adequacy of nutrition should be closely
monitored
Nursing management
Infant stimulation and parental support

• Infant stimulation incl. PT,OT and speech


therapy
• Encourage parents visit and be involved in the
routine care
• Answer parents question
Complications
• Most neonates who develop BPD ultimately
achieve normal lung function.
• However , this group of neonates is at higher
risk of dying in the first year of life or
developing significant long-term complications.
• Complications may occur during infancy or
later in the childhood.
• Therefore, required careful follow-up.
Pulmonary Function
• Increased airway resistance and reactivity.
Decreased lung compliance, ventilation-
perfusion mismatch and blood gas
abnormalities.
• Residual volumes were increased and forced
expiratory volumes were reduced.
• Inability to wean of ventilator.
Cardiac Function
• Pulmonary hypertension

• Congestive heart failure from Cor


pulmonale.
Infection
• Increased susceptibility to infection
• Respiratory syncytial virus (RSV) is a
major pathogen.
Recurrent infections
• Pneumonia
• Upper respiratory tract infection
• Otitis media
Growth and Neurological
Development
• Increased risk for growth failure and
abnormal neuro-developmental outcome.
Due to:
• Use of long term steriods
• Inadequate caloric intake
• Inadequate oxygenation
Conclusion
• BPD remains one of the most significant costs of
survival for premature infants.
• It is a complex and multifactorial disorder which
many of the causes or inciting events had been
identified.
• Therefore, with comprehensive and effective
management, prevention or reduction of BPD
can be achieved.
References
• Donn, S.M. and Sinha, S.K. (2006). Manual of Neonatal
Respiratory Care. (2nd ed.). Philadelpia: Mosby Elsevier.

• Driscoll, W. and Davis, J. (2007). Bronchopulmonary Dysplasia.


eMedicine. (On-line),
Available:http://www.emedicine.com/ped/TOPIC289.HTM

• Genen, L., & Davis, J. M.(2007). Chronic lung disease: etiology


and pathogenesis. In S.M. Down, & S.K. Sinha (Eds.), Manual of
neonatal respiratory care (2nd ed.). Philadelphia: Mosby

• Greenough, A. and Milner, A.D. (Ed) (2003). Neonatal


Respiratory Disorders. (2nd ed.). London: Arnold.

• Ho, L.Y. (2002). Bronchopulmonary Dysplasia and Chronic Lung


Disease of Infancy: Strategies for Prevention and Management.
Annuals Academy of Medicine Singapore,31(1), 119-130.
References
• Jobe, AH. and Bancalari, E. (2001). Bronchopulmonary
dysplasia. American Journal of Respiratory in Critical Care
Medicine,163:1723.

• Kenner, C., Brueggemeyer, A. and Gunderson, L.P. (1993).


Comprehensive Neonatal Nursing: A Physiologic Perspective.
Philadelphia: W.B. Saunders Company.

• Martin, R.J., Fanaroff, A.A. and Walsh, M.C. (2006). Fanaroff and
Marti’s Neonatal-Perinatal Medicine: Disease of the Fetus and
Infant. (8th ed.). Philadelphia: Mosby Elsevier.

• Monte, L.F.V., Filho, L.V.F.S, Miyoshi, M.H., Rozor, T. (2005).


Bronchoplumonary Dysplasia. Jornal de Pediatria. 82(2).