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HS8116: Case Study 1bOur group members are:
Zhao Xinmei Khong Huilin
Juliana Bt Jumahat Ang Nancy
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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
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Case studyBaby 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.
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Diagnosis
Bronchopulmonary Dysplasia(BPD)
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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).
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Diagnostic Criteria for Bronchopulmonary Dysplasia
Gestational age
<32 week ≥ 32 week
Time point of assessment
36 weeks PMA or discharge to home, whichever comes first >28 days but <56 days postnatal age or discharge to home, 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 comes first
Breathing room air by 56 days postnatal age or discharge, whichever comes first
Moderate BPD Need* for <30 percent oxygen at 36 weeks PMA or discharge, whichever comes first
Need* for <30 percent oxygen at 56 days postnatal age or discharge, 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
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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
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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
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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
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(Monte et al., 2007)
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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
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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
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Clinical features
• Chest retraction• Crepitation • Rhonchi Bronchospasm• Tachypnoea hypoxia, hypercapnia• Cor pulmonale ascites, pedal edema ECG RVH • CXR changes• ABG respiratory acidosis
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Medical Management
Management of infants with bronchopulmonary dysplasia is aimed at maintaining adequate gas exchange while limiting the progression of the disease.
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Mechanical ventilationMechanical 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)
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Mechanical VentilationWeaning in ventilators-dependent infants with BPDis difficult, so it must be accomplishedgradually.
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
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Mechanical ventilation
Optimal levels are:
• pH 7.25-7.40• pCO2 45-65 mmHg• pO2 50-70 mmHg• Oxygen saturation at 88-94%
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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
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Medications
• Diuretics• Bronchodilators• Corticosteroids• Vasodilators
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DiureticsFurosemide (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
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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
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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)
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BronchodilatorsCaffeine 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/IVMaintenance dose: 5 mg/kg/d PO/IV
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BronchodilatorsTheophylline• systemic bronchodilator • improve contractility of skeletal muscle and
decrease diaphragmatic fatigue in infants
Loading dose: 3-5 mg/kg PO/IVMaintenance dose: 1-3 mg/kg/d PO/IV q8-12h
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CorticosteroidsDexamethasone• 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
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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
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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
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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
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Nursing managementPrevention 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
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Nursing managementMechanical 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
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Nursing ManagementNutrition• 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
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Nursing managementInfant 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
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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.
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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.
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Cardiac Function
• Pulmonary hypertension
• Congestive heart failure from Cor pulmonale.
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Infection
• Increased susceptibility to infection• Respiratory syncytial virus (RSV) is a
major pathogen.
Recurrent infections• Pneumonia• Upper respiratory tract infection• Otitis media
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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
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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.
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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.
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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).