physiologic basis for the management of acute respiratory disorders in the newborn marc collin, md...
TRANSCRIPT
Physiologic Basis for the Management of Acute
Respiratory Disorders in the Newborn
Marc Collin, MD18 November 2003
Developmental Anatomy
• Alveoli-developed by 25th week -increase in # until 8 yr. -from 20 to 300 million -surface area: 2.8 m2 @ birth 32 m2 @ 8 yr.
75 m2 @ adulthood -diameter: 150- 300 um(NB-Adult)
Developmental Anatomy
• Airways- cartilaginous - relatively weak in infancy - dynamic compression - bronchiolitis (RSV)
- RAD - crying!
Developmental Anatomy
– airways enlarge in diameter/length– distal airways lag in first 5 yr.– high peripheral resistance in infancy
– Resistance = 1/R4
Pulmonary Physiology
• Compliance = Change in Volume Change in Pressure
Static Lung Volumes
Mechanics of Infant v. Adult Lung
Pulmonary Physiology
• Alveoli at birth• fluid-filled v. air-filled v. air-liquid interface
• pressures up to 80 cm H2O @ birth
• alveolar rupture
Pressure-Volume Curves after Air v. Liquid Lung Expansion
Pulmonary Physiology
LaPlace relationship:
P = 2T/R
P= distending pressure
T= wall tension
R= radius (alveolar)
Pressure-Volume Curves of First 3 Breaths
Developmental Biochemistry of Alveoli
• History: Avery & Mead-1959 - RDS secondary to surfactant deficiency - Treatment: CPAP
Surfactant
• Phospholipids - phosphatidylcholine
- phosphatidylglycerol
• Surfactant proteins - A, B, C
Surfactant Components
Surfactant
• Type II alveolar epithelial cells-responsible for synthesis,
storage, secretion, and reuptake
• Lamellar bodies -intracellular storage form of surfactant -secreted via exocytosis -forms tubular myelin in extracellular space
Surfactant and Type II Cells
Surfactant
• Inactivation by: - alveolar-capillary leak - pulmonary edema - hemorrhage (hemoglobin) - alveolar cell injury - meconium
Surfactant
• Recycling - spent forms taken up/reused by Type II cells. - process facilitated by SP-A, B, and C - half-life = 3.5 days
RDS
• US incidence: 30,000/yr.
• Inversely related to gestational age
• Onset-shortly after birth
• Signs-grunting, flaring,retracting
• Duration-1 week
RDS
RDS
• Progressive atelectasis
• V/Q mismatch
• Decreased FRC
• Impaired ventilation (weak respiratory m’s, compliant chest wall)
• Increased PVR due to hypoxia, acidosis
RDS
• Right to left shunting leading to further hypoxemia
• Left to right shunting leading to pulmonary edema
Exogenous Surfactants
• Replacement therapy/Fujiwara, Japan, 1980
• Human (from C/S)
• Artificial (Exosurf)
• Bovine (Survanta)
• Calf (Infasurf)
• Pig (Curosurf)
Compliance Before and After Surfactant
Before surfactant
After surfactant
VOLUME
PRESSURE
Air Leaks
• Pulmonary interstitial emphysema (PIE)
• Pneumomediastinum
• Pneumothorax
• Pneumopericardium
• Pneumoperitoneum
Subtle left pneumothorax
Left pneumothorax now more obvious
Left pneumothorax?
pneumothorax
Transillumination of left pneumothorax
pneumomediastinum
Pneumopericardium (note air under heart)
Air Leaks
• initiating factor: PIE (alveolar rupture into perivascular and peribronchial spaces)
• dissection into mediastinum
• further dissection into pleural, pericardial space
• rupture from surface blebs
• direct lung rupture-VERY rare
Air Leak Risk Factors
• RDS: 12-26%
• MAS/other aspirations
• Spontaneous
Air Leak Management
• early recognition (esp. in preterms)
• nitrogen wash-out (term/near-term)
• needle aspiration v. tube thoracotomy
• limit barotrauma
• HFOV
• positioning
• selective ET intubation
Meconium Aspiration Syndrome (MAS)
• GI secretions, cellular debris, bile, pancreatic juice, mucus, lanugo hairs, vernix; blood.
• incidence: ~15% (30% @ >42 wks)
• cause v. result of ‘asphyxia’
MAS
• Asphyxia intestinal ischemia
anal sphincter relaxation
meconium passage
MAS
• Asphyxia fetal gasping
enhanced meconium entry into respiratory tract
MAS-Presentation
• Respiratory distress
- tachypnea
- prolonged expiratory phase - hypoxemia
• Increased A-P diameter (‘barrel’ chest)
• Pulmonary hypertension
MAS-Radiographic Findings
• coarse alveolar infiltrates
• consolidation/hyperaeration
• pleural effusion (30%)
• pneumothorax/pneumomediastinum
Meconium aspiration syndrome
Meconium aspiration syndrome
MAS-Pathophysiology
• Acute small airway obstruction -increased expiratory resistance -increased FRC -regional atelectasis -V/Q mismatching
MAS-Pathophysiology
• Surfactant inactivation -decreased compliance -hypoxia
• Pulmonary hypertension
MAS-Treatment
• Intubation/tracheal suction @ delivery
• Saline lavage?
• Surfactant therapy
MAS-Ventilatory Support
• CPAP/PEEP (be careful)
• Air leak due to ball-valve phenomenon
• Decreased I/E ratio (more E time)
• Hyperventilation (CMV)
• HFOV
• iNO
• ECMO
Persistent Pulmonary Hypertension of the Newborn
(PPHN)
• Etiology: Primary v. Secondary
• Failure of transition from high to low PVR after birth
• PFO and PDA rightleft shunting
• Intrapulmonary shunting, esp. w/ pulmonary parenchymal disease
PPHN
• PVR decreases secondary to:
• -mechanical distention of pulmonary vascular bed
• improved oxygenation of pulmonary vascular bed
• prostacyclin and NO production
PPHN
• Remodeling of pulmonary vascular musculature
• Normally, fully muscularized preacinar arteries extend to terminal bronchiolar level.
• Muscularization begins to decrease w/in days, complete w/in months.
• Regression process delayed by hypoxia
• Chronic hypoxia stimulates further muscularization
PPHN
• Differential Diagnosis:
- Primary (chronic hypoxia) - Parenchymal disease (MAS, pneumonia, RDS, hemorrhage) - Cyanotic heart disease (TGV, critical PS, HLHS, severe coarctation) - Pulmonary hypoplasia (Potter’s S., Oligohydramnios, CDH, CCAM)
Congenital cystic adenomatoid malformation
Congenital diaphragmatic hernia
Thoracic hypoplasia
Hypoplastic right lung
Hypoplastic lungs
PPHN-Treatment/Medical
• Intravascular volume
• Correct metabolic acidosis
• Pressors (be careful!)
• Sedation (for lability) v. paralysis
PPHN-Treatment/Respiratory
• induction of respiratory alkalosis
• pressure support/barotrauma risk depending on etiology (compliance)
• very labile….SLOW wean (maintain relative HYPERoxia, if possible)
• iNO
• ECMO