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Perinatal Lung Disea

RCP 214 Unit 1 Perinatal lung disease and other problems of prematurity

Chronic Lung Disease encompasses Wilson-Mikity Syndrome Pulmonary Insufficiency in prematurity Classic BPD The "new" BPD
Other complications of neonatal respiratory care include Retinopathy of Prematurity (ROP) Intraventricular Hemorrhage (IVH)
Chronic Lung disease presents as prematurity need for ventilation/oxygenation
In chronic lung disease diagnosis is required oxygen or mechanical ventilation. Required oxygen at 36wks gestational age.
The pathophysiology of chronic lung disease includes surfactant deficiency/inactivation oxidative stress (o2 toxicity) inflammation/infection mechanical ventilation barotrauma Barotrauma and air block syndromes
The treatment for chronic lung disease is temperature oxygenation surfactant replacement resusscitation and ventilation
Wilson-Mikity Syndrome is also know as pulmonary dysmaturity
Wilson-Mikity syndrome is a disease of functional and structural pulmonary changes seen in premature neonates with no apparent underlying lung disease
The etiology of wilson-mikity syndrome is unkown and linked to low birth weight (<1500g), lung immaturity, maternal bleeding and asphyxia
The pathosphysiology of wilson-mikity syndrome presents similar to stage 3 and 4 CBD except the neonate has not been ventilated.
The early signs and symptoms of Wilson-Mikity Syndrome appear by the end of the first week and are hyperpnea expiratory grunting, nasal flaring, retractions hypoxemia transient cyanosis (comes and goes)
The acute phase of wilson-mikity syndrome appears after the first week and presents like RDS poor feeding and vomiting CXR: similar to stage 3 and 4 CBD changes
The treatment of wilson-mikity syndrome is support treat like bpd
What is the prognosis of Wilson-Mikity Syndrome? 2/3s of neonates survive and recover by age 2
Pulmonary insufficiency in prematurity includes premature infants <1200gms normal lung function in 1st 2 days Lung function deterioration by day 7
CPIP (CHronic pulmonary insufficiency of prematurity) Required supplemental 02 with apneas but normal CXR findings
The mortality of CPIP in the 1970's was 20%
The mortality of CPIP today is 0% with current standards of Care
CBD classic bronchopulmonary displasia "aka" the old bronchopulmonary displasia etiology is unknown but most incidences follow treatment of RDS with mechanical ventilation and oxygen
The pathophysiology of BPD is characterized by thickening of the alveolar membrane, necrosis of the alveolar tissues, and fibrotic changes in the interstitial spaces
air bronchograms appear as fluid filled tubes
CBD Stage 1 (Days 2-3) granular pattern, air bronchograms, small volume
CBD stage 2 (4-10) opacification
CBD Stage 3 (10-20) small areas of lucency, alternating w/areas of irregular density small cyst formation, visible cardiac sillhouette
Stage 4(<30 days) large cysts, hyperinflation, interstitial fibrosis, and cardiomegaly.
The New BPD clinical presentation of hyperinflation cystic emphysema persistent oxygen requirements may suffer complications from PDA/Sepsis
The pathosphysiology of the new BPD is linked to 5 factors surfactant deficiency/inactivation oxidative stress (oxygen toxicity) inflammation/infection mechanical ventilation (barotrauma) Barotrauma and air block syndromes
In BPD the ABG will show chronic respiratory failure and hypoxemia
BPD signs/symptoms cor pulmonale (right vent. hypertrophy) pulmonary functions: increased minute ventilation requirement, increased airway resistance, decreased lung compliance
The criteria of BPD diagnosis include 36 weeks corrected gestational age need for supplemental 02 or 8wks since birth and still requires supplemental 02
What is the tx of BPD prevention ventilatory support long term, low flow oxygen airway clearance bronchodilator therapy neoprofen; higher incidence of cld maintain fluid and nutrition status vitamen e therapy- increased risk of sepsis/NEC
What is the prognosis of BPD? increased risk of asthma and growth suppression.
Retinopathy of prematurity is also known as Retrolental fibroplasia (RLP) (ROP)
ROP is defined as disordered vascularization and fibrovascular changes in retinas or preterm infants
With ROP scar tissue forms behind the lens of the eye
What is the etiology of ROP? Primary factor: 02 use/hyperoxia it occurs in <36% if 501-1500gm birth weight
What is the pathophysiology of ROP? High Pa02 leads to constriction of retinal vessels. Constriction leads to necrosis of vessels; called vaso-obliteration vessels hemorrhage which leads to scar formation
What are some factors associated with ROP? Preterm birth, RDS, Mechanical ventilation, Chorioamnionitis, apnea, hypercarbia, surfactant deficiency, pneumonia, sepsis, CLD
How is ROP diagnosed? It develops in 5 stages opthalmologic exam
How is ROP treated? Prevention Indirect laser therapy
Intraventricular Hemorrhage is also known as periventricular leukomalacia (PLV)
IVH occurs in 26% in babies with 501-1500gm BW
What are the type of bleeds with IVH? Subdural or subarachnoid bleeding or cerebeller tissue bleeds
In subdural or subarachnoid bleeding it can be caused by trauma or asphyxiation
In cerebeller tissue bleeds it is associated with prematurity
What is the pathosphysiology of IVH? Autoregulation (temperature) absent, puts brain at risk of hemorrhage
What are the signs/symptoms of IVH? Severe, rapid deterioration, apnea, hypotension, decreased hematocrit, flaccidity, bulging fontanelles and posturing
How is IVH diagnosed? CT scan or ultrasound
How is IVH classified? Grade 1 to Grade 4 severe to most severe
What is the tx of IVH? supportive: monitor for hyperbilirubinemia, avoid hypotension, monitor icp Correct blood loss/hypoxemia: administer osmotic agents (volume expander) Possible shunt placement
IVH complications: depends on severity of the bleed neurodevelopmental disability (MR) Posthemorrhagic hydrocephalus (CSF) Vision/Hearing loss contralater himparesis (cerebral palsy) Death
How can IVH be prevented avoid wide fluctuations in BP, Oxygenation, and pH Avoid trendelenburg position
Respiratory distress syndrome is also known as hyaline membrane disease
RDS etiology prematurity of the lung/surfactant deficiency infants <37 weeks gestation
What is the pathosphysiology of RDS? Atelectasis leads to v/q mismatch and low FRC. Results in respiratory failure further hinders surfactant production Worsening atelectasis
RDS complications can be associated with ventilator support (Development of BPD, IVH,ROP, Air leaks, development of reactive airway Disease (RAD), infection, patient ductus arteriosus (PDA), DIC, necrotizing enterocolitis (NEC)
What are RDS signs and symptoms RR > 60 bpm expiratory grunting, nasal flaring, and retractions cyanosis ABG-low pa02, combined acidosis Other-hypothermia, flaccid muscle tone, pallor skin, severe edema (kidneys shut down)
In RDS CXR is a definitive diagnosis
IN RDS the CXR will show underaerated bilaterally, ground glass appearance, air bronchograms, stages 1-4 according to increased severity of disease
What is the treatment of RDS? Prevention:maternal steroid therapy Surfactant replacement CPAP Mechanical ventilation
CPAP (nasal prongs) neonates are obligate nose breathers 4-6 cmh20; if > 40% fi02 is needed intubation is indicated for surfactant tx, extubation within 10 minutes
Mechanical ventilation pac02 40-50 mmhg, ph >7.25, sa02 88-94% VMS allows permissive hypercapnia; 85%-93%
Transient Tachypnea of the Newborn (TTN) is also known as Type II RDS & Wet lung syndrome
TTN is more common in boys and infants with perinatal asphyxia; also common in C-section delivery
The etiology of TTN is unkown, associated with delayed clearing of fetal lung fluid
TTN Clinical presentation tachypnea, breath sounds-rales, cyanosis, grunting, retractions, nasal flairing
In TTN the ABG will read as mild-moderate hypoxemia, hypercapnia, respiratory acidosis
With TTN the CXR will present as pulmonary vascular congestion, perihilar streaking, hyperexpansion, flat diaphragm, mild cardiomegaly, mild pleural effusions, mimics RDS, except better aeration and clears within 24-48 hours)
How is TTN diagnosed R/O other conditions (RDS, Group B strep pneumonia, PPHN) Lab to R/O infection- would see increased WBC w/ infection
What is the treatment of TTN? oxygen therapy and CPAP 02 hood <40%(warmed); 3-5 cmh20 cpap with increased fio2 is required mechanical ventilation antibiotics until infection is ruled out
Created by: kparkerlehman
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