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Lower airway disease in children and neonates PowerPoint Presentation

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Description : Check out this medical titled "Lower airway disease in children and neonates".

This medical talks about Lower airway disease which refers to conditions that affect the airways and lungs, including the bronchi and bronchioles. In children and neonates, lower airway disease can be caused by various factors, including infections, allergies, asthma, and congenital abnormalities.

Some common lower airway diseases in children and neonates include Bronchiolitis, Asthma, Croup, Bronchopulmonary dysplasia (BPD), and Congenital anomalies, etc.

Treatment for lower airway disease in children and neonates may involve medication, oxygen therapy, breathing treatments, and in severe cases, mechanical ventilation. Prevention measures, such as avoiding exposure to allergens or quitting smoking during pregnancy, may also be helpful in reducing the risk of lower airway disease in children and neonates.

Tags : Lower airway disease in children and neonates, Bronchiolitis, Asthma, Croup, Bronchopulmonary dysplasia (BPD), Congenital anomalies, Emergency Medicine, Emergency Medicine

Published on : Apr 14, 2023 | Views : 1004 | Downloads : 0

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Slide 1-

1) Typical features of neonatal and pediatric lung disease 2) Pediatric mechanical ventilation: Anything special to know? Conventional vs high frequency ventilation Lower airway disease in children and neonates
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pump failure neuromuscular diseases central nervous system disease lung failure primary lung disease (inflammatory) of various etiology IRDS (infant) / ARDS (adult = acute) elevated PaCO2 minimal intrapulmonary shunting easily managed with conventional ventilation settings diffuse atelectasis, permeability oedema low lung compliance, and intrapulmonary shunting (hypoxemia) Acute respiratory failure in childhoood
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Typical features of neonatal and pediatric lung disease: Infant respiratory distress syndrome Acute hypoxic respiratory failure (incl. ARDS) Bronchiolitis (RSV-Bronchopneumonia)
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Clinical characteristics of infant RDS Polypnea resp. freq. > 60 / Min Intercostal Retractions use of accessory muscles Grunting glottis closure at end-expiration Cyanosis intra pulmonary shunting
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HMD wet lung congenital pneumonia meconial aspiration
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LUNG IMMATURITY Surfactant deficit Preterm infant ASPHYXIE, SHOCK, ACIDOSIS Neonate at near-term or term
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Normal lung aereation, thin septa Generalized atelectasis, leukocyte infiltration, thick septa, hyaline membranes
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1950 1960 1970 1980 1990 O2 Mechanical Ventilation Antenatal steroids Exogeneous Surfactant Mortality Medical developments in the treatment of infant RDS CPAP In the year 2000: Incidence of BPD = 26% < 1500g Lee, Canadian Network, Pediatrics 2000
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Treatment-Concept No 1: Lung-Maturation
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Airway pressure (cmH2O) Volume (l) (surfactant depleted lung) Normal lung ALI RDS at birth severe (A)RDS Reduced pulmonary compliance: C = D V D P
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Concept No 2: Open the lung and keep it open T --> Surfactant
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Surfactant as a recruitment agent PEEP PIP PEEP PIP pre post Volume Pressure Kelly E Pediatr Pulmonol 1993;15:225-30
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Soll RF (Cochrane Database) 2002 Mortality Bronchopulmonary dysplasia
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4-day-old, 26-week gestation infant 2-day-old, 38-week gestation infant MRI signal intensity from non-dependent to dependent regions The water burden of the lung makes the lung of the preterm infant, despite surfactant treatment,vulnerable to VILI Adams EW AJRCCM 2002; 166:397–402
Slide 16-

Concept No 2: Open the lung and keep it open T --> Surfactant P --> positive airway pressures: - CPAP - CMV / HFO
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VILI prevention: Avoidance of shear, overdistension, cyclic stress and high intrathoracic pressures
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Acute respiratory failure in childhoood Preterm infant Hyaline membrane disease = infant RDS Lung immaturity Congenital pneumonia acquired lung diseases: nosocomial pneumonia bronchiolitis sepsis Newborn (at term) Congenital pneumonia Meconium aspiration Malformations: Lung hypoplasia, CDH acquired lung diseases: nosocomial pneumonia bronchiolitis sepsis
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Acute respiratory failure in childhoood Infant (1- 12 months) sepsis-syndrome infectious pneumonia (RSV-bronchiolitis) non infectious pneumonia - inhalational injury circulatory arrest Preschool age sepsis-syndrome infectious pneumonia (RSV-bronchiolitis) non infectious pneumonia - foreign body aspiration - inhalational injury - drowning trauma circulatory arrest
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Neonatal period: group B beta-hemolytic streptococci (GBS) gram negative enteric bacilli (E.coli) Infants and viral (especially RSV) small children: bacterial: Streptococcus pneumoniae mixed infections (e.g., viral-bacterial) can occur in 16-34% of patients Common pathogens for respiratory infections:
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Acute viral bronchiolitis Primo-infection during the first year of life: 70% At the age of 2 years: 100%. Transmission: surface, droplets Variations: seasonal and biannual (?) Respiratory syncytial virus (RSV) in > 80 % of all cases Parainfluenza I et III, Adenovirus, Rhinovirus
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Acute Bronchiolitis: Epidemiology Classical resp. tract infection of the infant (up to 2 years) Hospitalisation required in: 1-3% normal infants 10-25% infants prematurely born Prematurity = single most important risk factor for both hypoxemia and respiratory failure in RSV bronchiolitis 15-25% infants with cardiac malformations 15-45 % infnats with bronchopulmonary dysplasia Prevention: Passiv Immunization Maternal antibodies Monoclonal antibodies: Palivizumab (Synagis) 15mg/Kg im q 1 month
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Cellular (lymphocytic) infiltration + edema Normal bronchioli
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Bronchiolitis: Physiopathology Edema + infiltration increased resistance + mucus +/- cellular debris ~ 1/R 4 Insp. resist. < exp. resist. Insp. retractions Polypnea Exp. wheezing Hyperinflation Respiratory fatigue Insuffisance respiratoire The child will try to maintain normal minute ventilation Hypercapny (= first warning sign) Hypoxemia occurs later (= vital warning sign) ·
Slide 25-

Typical hyperinflation in bronchiolitis
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Hyperinflation and atelectasis in bronchiolitis
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Humidification O2 Surveillance and respiratory monitoring Bronchodilators b-mimetics +/- ipratropium bromide inhaled adrenaline Antiviral therapy Ribavarin - acute effect ?, - longterm benefit + Chest 2002; 122:935-9 Antiinflammatory tx: Steroides - acute phase: shortens length of hospital stay but not duration of ICU-stay or mechanical ventilation Thorax 1997; 52:634-7 - not effective on long term outcome Pediatr Pulmonol 2000; 30:92-96 CPAP, non-invasive ventilation, intubation + ev. HFO Acute Bronchiolitis: Treatment
Slide 28-

1) Typical features of neonatal and pediatric lung disease 2) Pediatric mechanical ventilation: Anything special to know? Conventional vs high frequency ventilation
Slide 29-

From the newborn to the adult: Physiology Chest wall compliance FRC Elastic Recoil Rib cage distortion Pleural pressure distortion
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From the newborn to the adult: Crs chest wall chest wall lung lung Newborn Adult Agostini J Appl Physiol 1959; 14: 909-913
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From the newborn to the adult: FRC chest wall chest wall lung lung Newborn Adult Agostini J Appl Physiol 1959; 14: 909-913
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To maintain a reasonable EELV the neonate closes his glottis at the end of expiration (to avoid lung unit closure) Therefore: An intubated neonate or infant is always ventilated with PEEP
Slide 34-

From the newborn to the adult: Paw effect chest wall chest wall lung lung Newborn Adult Agostini J Appl Physiol 1959; 14: 909-913 EELV above FRC EELV above FRC
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decreased lung compliance normal lung compliance
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How much pressure in small children?
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Adults and children: Acute respiratory distress syndrome (ARDS) Newborn: Infant respiratory distress syndrome (iRDS) Mortality: 25 - 35% CLD: 15 - 25% Ventilator induced lung injury Mechanical ventilation Oxygenation Lung volumes Pulm. compliance
Slide 38-

Airway pressure (cmH2O) Volume (l) (surfactant depleted lung) Normal lung ALI severe (A)RDS Allowable Vt and disease severity
Slide 39-

1) Typical features of neonatal and pediatric lung disease 2) Pediatric mechanical ventilation: Anything special to know? Conventional vs high frequency ventilation
Slide 40-

HFOV uses very small VTs. This allows the use of higher EELVs to achieve greater levels of lung recruitment while avoiding injury from excessive EILV. CMV HFOV CMV HFOV Rationale for HFOV-based lung protective strategies 2. Respiratory rates with HFOV are much higher than with CV. This allows the maintenance of normal or near-normal PaCO2 levels, even with very small Vts.
Slide 41-

Suzuki H Acta Pediatr Japan 1992; 34:494-500 The concept of volume recruitment during HFO
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Favors HFO Favors CMV Elective HFOV vs CMV in preterm infants: Outcome 28 days With volume recruitment All trials
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0.0006 # Survival and CLD Morbidity all patients HFO (n=32) CMV (n=39) p - value survivors to 30 days HFO (n=27) CMV (n=35) Ventilation (days) 5 (3-6) 14 (6-23) 0.0004 * Oxygen dependency (FiO2 > 0.21) (days) 12 (4-17) 51 (20-60) <0.0001 * Oxygen at 28 d, no (%) 6 (22) 22 (63) 0.002 # survivors to 36 weeks PCA HFO (n=27) CMV (n=34) CLD; Oxygen > 36 weeks PCA, no (%) 0 (0) 12 (35) Values are given as the median (95% CI) or the number (percentage) of patients; * Mantel-Cox log-rank; # Fisher's exact Rimensberger PC et al. Pediatrics 2000; 105:1202-1208 First Intention HFO with early lung volume recruitment Retrospective study with historical cohort in preterm infants with RDS, mean GA = 27.7 (± 1.9), < 32 w / mean BW = 970 (± 250), < 1200 g
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MOAT II: Overall Survival CV HFOV HFOV CV N 75 73 P/F 114 (37) 111 (42) Derdak S Am J Respir Crit Care Med 2002; 166:801–808 30d p=0.057 90d p=0.078
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MOAT II: Survival - PIP  38 cmH20 (post-hoc) CV 30d p=0.019 90d p=0.026 HFOV European HFV-Meeting 2001
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Conclusions Although there exist some special respiratory pathologies in early childhood, treatment concepts are not to much different from the one in adult patients. However, it is important to recognize early signs of respiratory distress in infants and small children, because this patients are at high risk for a sudden cardiac arrest.