Bpd

HS8116: Case Study 1b Our group members are: Zhao Xinmei

Juliana Bt Jumahat

Khong Huilin

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

Time point of assessment

<32 week

≥ 32 week

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

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 •

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Pulmonary system development

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

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 1518cmH2O) • 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, ventilationperfusion 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.

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Driscoll, W. and Davis, J. (2007). Bronchopulmonary Dysplasia. eMedicine. (On-line), Available:http://www.emedicine.com/ped/TOPIC289.HTM

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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

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Greenough, A. and Milner, A.D. (Ed) (2003). Neonatal Respiratory Disorders. (2nd ed.). London: Arnold.

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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.

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Kenner, C., Brueggemeyer, A. and Gunderson, L.P. (1993). Comprehensive Neonatal Nursing: A Physiologic Perspective. Philadelphia: W.B. Saunders Company.

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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.

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Monte, L.F.V., Filho, L.V.F.S, Miyoshi, M.H., Rozor, T. (2005). Bronchoplumonary Dysplasia. Jornal de Pediatria. 82(2).