holistic approach to children with cld revised[2][1] [โหมด ... · holistic approach to...
TRANSCRIPT
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Holistic Approach to ChildrenHolistic Approach to Children
ith Ch i L Diwith Chronic Lung Disease
Suchada Sritippayawan, MD.
Div. Pulmonology & Crit Care
Wanida Pao-in, MD.
Div. Pulmonology & Crit Care gy
Dept. Pediatrics,
Faculty of Medicine
gy
Dept. Pediatrics,
Faculty of Medicine
Chulalongkorn UniversityThammasart University
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Case illustration
• Triplet, GA 25 weeks
• Triplet A (male) 635 g, triplet B (female) 720 g, triplet C (female) 605 gtriplet C (female) 605 g
• APGAR: A-2,7, B-1,7, C-1,7• Surfactant, on mechanical ventilator,
antibiotics since birthantibiotics since birth• Triplet B died at DOL 2 because of pulmonary
hemorrhage
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Case illustration
Triplet C• BW 605 g, HC 21 cm, Ht 30, APGAR 1,7• Ventilator support: conventional mode• Ventilator support: conventional mode
Initial setting: Conventional mode PIP 15 cmH2O, PEEP 4 cmH2O, IMV rate 60/min, T 0 34 sec FiO 0 8TI 0.34 sec, FiO2 0.8
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Case illustration
• Antibiotics, antifungal• Dopamine to maintain BP
PRC furosemide• PRC, furosemide• Monitor fluid, electrolytes • Indomethacin for PDA closure• PPN • Enteral feeding: start at DOL 3, full feed at te a eed g sta t at O 3, u eed at
DOL 13
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Chest x-ray at DOL 1
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Triplet C at DOL 28
• BW 670 g• Ventilator support: PIP 19 cmH2O, PEEP 4
cmH O IMV rate 70/min T 0 34 sec FiO 0 8cmH2O, IMV rate 70/min, TI 0.34 sec, FiO2 0.8 • PE: active, PR 130, RR 79, BP 50/28, BT 36.7
Heart: normal S1S2, no murmur, no hyperactive precordiumhyperactive precordiumLung: subcostal retraction, occ. coarse crepitations and wheezing Others: unremarkableOthers: unremarkable
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Triplet C at DOL 28
Labs • CBG: pH 7.23, PCO2 70, PO2 43, HCO3 28
BUN 25 Cr 1 5• BUN 25, Cr 1.5• Eye exam: no ROP• U/S: no IVH
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Chest x-ray at DOL 28
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Problem lists
• Premie 25 weeks• Ventilator dependent since birth• PDA (S/P close with indomethacin)• PDA (S/P close with indomethacin)• Bacterial / fungal infection• Renal insufficiency
Poor weight gain• Poor weight gain
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Questions
Q1: Does this patient have CLD?Q2: What are respiratory problems and their
pathophysiology?pathophysiology?Q3: How can we treat respiratory problems?Q4: What are other comorbids and their
pathophysiology?pathophysiology?Q5: How can we treat these comorbids?Q6: Is there any long term sequelae and
how to follow up?how to follow up?
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Problem lists
• Premie (GA 25 weeks)• Ventilator dependent since birth• PDA (S/P close with indomethacin)PDA (S/P close with indomethacin)• Bacterial / fungal infection • Renal insufficiency• Poor weight gain• Poor weight gain
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Respiratory problems
• Premie (GA 25 weeks)• Ventilator dependent
at DOL 28at DOL 28• CBG: CBG: pH 7.23,
PCO2 70, PO2 43, HCO3 28C f• CXR: Bilateral hyperinflation, radiolucent areas plus strands of radiodensity ad o uce t a eas p us st a ds o ad ode s ty
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Q1: Does this patient
have CLD?
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What is chronic lung disease?
• Bronchopulmonary
dysplasia
P l d MV• Prolonged MV use
• Chronic aspirationChronic aspiration
• Chronic infection
• BronchiectasisChronic ILD• Chronic ILD
• Asthma, etc.,
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Chronic lung disease
AJRCCM 2003;168:356-96
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Definition of BPD
Old definition (Bancalari’s criteria)• MV at least 3 days in neonate plus• Oxygen dependent at DOL 28 plus• Oxygen dependent at DOL 28 plus• Radiologic changes
Clin Pediatr (Phila) 2002;41:77-85
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Definition of BPD
Old definition (Bancalari’s criteria)• Radiologic changes
- RDS (D1-3)RDS (D1 3)- Opacification of both lungs (D4-10) - Small rounded areas of radiolucency in both lungs (D10-20)both lungs (D10 20)
- Enlarged radiolucent areas + strands of radiodensity
Clin Pediatr (Phila)2002;41:77-85
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Definition of BPD
New definition (NIH consensus)• Time point of assessment
GA < 32 wk : 36 wk PMA or D/C homeGA < 32 wk : 36 wk PMA or D/C homeGA > 32 wk : > 28 d but < 56 d of postnatal age or D/C home
• Treatment with oxygen > 21% for at least 28Treatment with oxygen 21% for at least 28 days plus
Clin Pediatr (Phila)2002;41:77-85
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Definition of BPD
New definition (NIH consensus)• Severity of BPD
Mild BPDMild BPDGA < 32 wk : Breathing RA at 36 wk PMA or D/C homeGA > 32 wk : Breathing RA at 56 d of postnatalGA 32 wk : Breathing RA at 56 d of postnatal age or D/C home
Clin Pediatr (Phila)2002;41:77-85
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Definition of BPD
New definition (NIH consensus)• Severity of BPD
Moderate BPDModerate BPDGA < 32 wk : Need FiO2 ≥ 0.3 and/or positive pressure at 36 wk PMA or D/C homeGA > 32 wk : Need FiO2 ≥ 0.3 and/or positiveGA 32 wk : Need FiO2 ≥ 0.3 and/or positive pressure at 56 d of postnatal age or D/C home
Clin Pediatr (Phila) 2002;41:77-85
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Definition of BPD
New definition (NIH consensus)• Lung parenchymal disease plus• Clinical features of respiratory distress plusClinical features of respiratory distress plus• Not acute event
Clin Pediatr (Phila) 2002;41:77-85
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Q2: What are respiratory problems
d h i h h i l ?and their pathophysiology?
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Pulmonary system
Abnormal lung Abnormal AbnormalAbnormal lung parenchyma &
chest wall
Abnormal airway
Abnormal cardiorespiratory
control duringchest wall control during sleep
Other bid
Abnormal gas
comorbids
gexchange and lung
function during gawake and sleep
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Chronic lung disease: BPD
• Age at the onset
• Types and severity of
respiratory insults
• DurationSeverity of
BPDDuration
• Body responseBPD
• Treatment
• Genetics
Pediatr Respir Rev 2003;4:28-39.
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Pulmonary system
Abnormal lung Abnormal AbnormalAbnormal lung parenchyma &
chest wall
Abnormal airway
Abnormal cardiorespiratory
control duringchest wall control during sleep
Other bid
Abnormal gas
comorbids
gexchange and lung
function during gawake and sleep
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Pathogenesis of CLD• Oxygen free radical
↓ ti id tAcute lung injury • Ventilator-induced
PDA l l d• ↓ antioxidant
enzymes system Recruitment of
• PDA, vol. overload
• Infections
inflammatory cells
• Age at the onset
• Types, severity,
Acute inflammatory reactions
yp y
duration of
respiratory insults
Resolved Persistent inflammation
respiratory insults
• Body response
• Treatment
No CLDLung destruction & damage
• Treatment
• Genetics
No CLDCLD
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Pathogenesis of BPD
N Engl J Med 2007; 357:1946-55
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Old BPD vs. New BPD
Old BPD New BPD
• Alternating atelectasis
with hyperinflation
• Less regional heterogeneity
of lung diseasewith hyperinflation
• Severe airway epithelial
of lung disease
• Rare airway epithelial
lesions
• Marked airway smooth
lesions
• Mild airway smoothMarked airway smooth
muscle hyperplasia
y
muscle thickening
• Extensive diffuse fibroproliferation
• Rare fibroproliferative changes
Lancet 2006;367:1421-31
p
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Old BPD vs. New BPD
Old BPD New BPD
• Hypertensive remodeling
of pulmonary arteries
• Fewer arteries but
dysmorphicof pulmonary arteries
• Decreased alveolarisation
dysmorphic
• Fewer, larger and and surface area simplified alveoli
Lancet 2006;367:1421-31
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Pulmonary system
Abnormal lung Abnormal AbnormalAbnormal lung parenchyma &
chest wall
Abnormal airway
Abnormal cardiorespiratory
control duringchest wall control during sleep
Other bid
Abnormal gas
comorbids
gexchange and lung
function during gawake and sleep
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Airway abnormalities in CLD
• Prolonged intubation, PPV
• Cyanotic spell
• Inappropriate intubation,
suctioning Cyanotic spell
• Wheezing not respond
g• Concomitant infections
Central & upper airway obstruction
to bronchodilator
• Recurrent atelectasis
• Lobar emphysema• Glottic and subglottic stenosis
• Tracheobronchial stenosis • Failed extubation• Ventilator dependent
Tracheobronchial stenosis
• Granuloma formation
AJRCCM 2003;168:356-96
• Tracheobronchomalacia
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Abnormal lung function in CLD
CLD
Abnormal Abnormal lungAbnormal Other co-morbid
airway Abnormal lung parenchyma chest wall
mechanics
Other co morbid
• RAD
• GER• etc.
Ob t ti d f t• Hypoxemia • Obstructive defect
• Restrictive defect
• Hypoxemia
• Hypercarbia Can persist • Diffusion defect• BHR
until adult• O2 dependent
• BHR• MV dependent
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Pulmonary system
Abnormal lung Abnormal AbnormalAbnormal lung parenchyma &
chest wall
Abnormal airway
Abnormal cardiorespiratory
control duringchest wall control during sleep
Other bid
Abnormal gas
comorbids
gexchange and lung
function during gawake and sleep
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Cardiorespiratory control during sleep in CLDsleep in CLD
CLD
Abnormal Abnormal lung AbnormalOther co-morbid
airway Abnormal lung mechanics
Abnormal chest wall mechanics
• RAD• GERGER
Sleep-related hypoxemia, hypercarbia
Abnormal hypoxic ventilatory and arousal
• Poor RV function
response during sleep
AJRCCM 2003;168:356-96
Poor RV function• Abnormal autonomic control of HR
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Q3: How can we treat
respiratory problems?p y p
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Management of Respiratory ProblemRespiratory Problem
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Ventilatory strategiesVentilatory strategies
After Birth
• Early initiation of nasal CPAP
After Birth
Early initiation of nasal CPAP• Nasal intermittent positive pressure
ventilation (NIPPV)ventilation (NIPPV)• Patient-triggered ventilation (SIMV, assist-
control, and pressure support ventilation)control, and pressure support ventilation)• High-frequency ventilation (HFV)• Volume targeted ventilation:• Volume targeted ventilation:• Permissive hypercapnia
P i i h i• Permissive hypoxemia
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Ventilatory strategies
Established CLD
• Minimizing ventilatory support (e.g. nCPAP, NIPPV whenever possible)
• Tolerating higher PaCO (55-60 mm Hg• Tolerating higher PaCO2 (55-60 mm Hg provided pH >7.25)
• Target SpO2 : 89-94%• If on IMV: consider using PTV• If on IMV: consider using PTV • Oxygen therapy to maintain SpO2 > 92-93%
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Other strategiesg
• Methylxanthines• Steroids: considered in infants after 10-14Steroids: considered in infants after 10 14
days of age• Diuretics for features of pulmonary edema • Bronchodilators for bronchospasmBronchodilators for bronchospasm • Sedation and muscle relaxation for ‘BPD
spells’
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Wheezing in CLDI
• Airway hyperresponsiveness• Airway inflammation
A t i l d f t b l tti t i• Anatomical defect: subglottic stenosis, airway malacia
• Interstitial edemaH t f il• Heart failure
• Aspiration syndromep y• Infection
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Q4: What are other comorbidsQ4: What are other comorbids
and their pathophysiology?and their pathophysiology?
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Chronic lung diseases
Multidisciplinary (Holistic)(Holistic)
approach and follow-up isfollow-up is
required
AJRCCM 2003;168:356-96
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Comorbids in CLD
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Abnormal CVS in CLD
• PHT, Cor pulmonale
• LVH, LVF
• Systemic HT
• ↑systemic-to-pulmonary collateral circulation• ↑systemic-to-pulmonary collateral circulation
Lancet 2006; 367:1421-31
AJRCCM 2003;168:356-96
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Pathophysiology of PHT in CLD• Hypoxemia
H bi ↓ Al l• Premie
• Hypercarbia
• MetabolicPulmonary
vasoconstriction↓ Alveolar
development• Hypoxemia
• HYperoxiaacidosis
Vascular remodeling
• Intrauterineinfection
↓ Pulmonary vascular Endothelial
ll i j developmentcell injury
I ti lIntimal proliferation
Pulmonary hypertension RHF
Lancet 2006; 367:1421-31
AJRCCM 2003;168:356-96
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Pathophysiology of HT & LVH in CLD• Hypoxemia
H bi ↑ R i ↑ N ti• Hypercarbia
• Metabolic
↑ Renin-angiotensin
activity
↑ WOB↑ Negative intrathoracic pressure
acidosis
↑↓ ↑ LV afterload↓ Pulmonary endothelial
function
↑ PVR
SystemicLVH↓ Clearance of
norepinephrine Systemic HT
norepinephrine
AJRCCM 2003;168:356-96
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Pathophysiology of GER in CLD
• ↑ intrathoracic –ve
pressure
• Low, flat diaphragmLow, flat diaphragm
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Abnormal KUB function in CLD
↑ PVR Prolonged loop diuretic use
• Hypoxia
↑ RAP
diuretic use• Hypotension
• Nephrotoxic
• ↑ ANP
• Hypercalciuria
• Nephrocalcinosis
pdrug
• ↑ Vasopressin
p
• Hyperphosphaturia
↓ M K
• ↑ water retention
• ↓ Mg, K
• Metabolic alkalosisTubular injury
• ↓ Na
Clin Pediatr 2002; 41:77-85.
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Other comorbids in CLD
• ↑REE
• ↓ intake
• Drugs
• Other comorbids
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Q5: How can we treat
these comorbids?
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Management of Oth C bidOther Comorbids
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Management of ComorbidsManagement of Comorbids
• PHT
• GERDOxygen GERD
• KUB
Calcium channel blockersProstacyclin Phosphodiesterase inhibitor: sildenafil• KUB
N t iti
Phosphodiesterase inhibitor: sildenafil Endothelin receptor antagonists: bosentan
• Nutrition
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GERDGERD
• Feeding• Drugs: - prokineticsDrugs: prokinetics• - H2-receptor antagonists• - proton-pump inhibitors
• FundoplicationFundoplication
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nutritionnutrition
– Calorie intake to 120 to 150 Kcal/kg/d– Breast milk fortified with HMF– Fat supplementation (e.g. MCT oil) – Multivitamin to meet RDA Multivitamin to meet RDA
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Q6: Is there any long term
sequelae and how to seque ae a d o to
follow up?follow up?
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Abnormal lung function in CLD
CLD
Abnormal Abnormal lungAbnormal Other co-morbid
airway Abnormal lung parenchyma chest wall
mechanics
Other co morbid
• RAD
• GER• etc.
Ob t ti d f tH i • Obstructive defect
• Restrictive defect
• Hypoxemia
• Hypercarbia Can persist • Diffusion defect• BHR
• Exerciseintolerance
until adult
• BHRintolerance
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Long term sequelae
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Management of Long Term SequelaeLong Term Sequelae
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Management of Long Term SequelaeManagement of Long Term Sequelae
• Respiratory system• Infection prevention• Infection prevention• Neurologic/developmentalg p• Hearing/vision• Growth• Other
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Triplet C at DOL 1 - 4.5 months
• NSS neb, chest PT• On nasal CPAP at age 2 months• Seretide® Ventolin® MDI at age 2 months• Seretide®, Ventolin® MDI at age 2 months
(2 weeks) • O2box/cannula at age 2.5 months (36 wk PMA)
Discharge at age 4 5 mo (corrected age 1 mo)• Discharge at age 4.5 mo (corrected age 1 mo)– BW 2,700 g, HC 35 cm, length 48 cm – Home med: MTV, FeSO4
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Triplet C at DOL 9 months
Age 9 mo (corrected age 6 mo)• 5.6 kg, HC 39.5 cm, length 61 cm
• spastic diplegia • DENVER II: PS 6 mo FM 4 mo L 4 mo• DENVER II: PS 6 mo, FM 4 mo, L 4 mo,
GM 6 mo