HS8116: Case Study 1bOur 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 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.

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 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

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 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)

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

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

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

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)

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

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

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

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 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

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

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

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

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).