Respiratory distress

Five stages of lung development

Embryonic development: weeks one through five
pseudo-glandular.: Weeks five through 17
canalicular: week 17 through 24- formation of gas exchanging units
terminal sac.: Weeks 24 through 37- produced surfactant but not in sufficient quantities to maintain

Surfactant

Phospholipids line terminal air sacs to maintain alveolar stability by reducing surface tension
surfactant is a mixture of at least six phospholipids and for proteins
surfactant reduces surface tension forces in the alveoli that are capable of producing c

FLM fetal lung maturity

Measures ratio of surfactant to albumin
sample should be free of blood and meconium
less than 50 = immaturity; 5270 = borderline maturity; greater than 70 = mature lungs

LS ratio

Has been used to assess fetal lung maturity
in L/S ratio greater than 2:1 is considered to indicate fetal lung maturity
an infant of a diabetic mother may develop RDS even with mature L/S ratio
chronic fetal stress will tend to accelerate surfactant produ

Role of antenatal steroids

Affect along with maturation and present strategy for preventing morbidity
steroids accelerate the normal pattern lung growth by increasing the rate of glycogen depletion and glyceride oh phospholipid biosynthesis

Treatment with steroids is recommended for

Maternal risk of preterm delivery between 34 and 24 weeks
premature rupture of membranes at less than 30 to 32 weeks without chorioamnionitis, because of the risk of interest vascular hemorrhage
associated with decreased mortality, RDS, and IVH it should

Respiratory distress syndrome

Developmental disorder starting at or soon after birth and occurring most frequently in infants with immature lungs
increasing respiratory difficulty in the first 3 to 6 hours, leading to the hypoxia and hypo ventilation
progressive atelectasis

Etiology of respiratory distress syndrome

Surfactant deficiency
pulmonary hypoperfusion
anatomic immaturity
Precipitating factors associated with incidence or severity of RDS
prematurity
cesarean delivery without labor
maternal diabetes
acute antepartum hemorrhage
asphyxia at birth
multi-parity n

Pathophysiology of respiratory distress

Production of surfactant is in adequate
serum proteins which inhibit surfactant function leak into the alveoli
is still logic findings of the presence of hyaline membranes

Clinical presentation of RDS

Almost exclusively in premature infants
increasing respiratory difficulty related to progressive atelectasis symptoms are progressing
tachypnea greater than 60 breaths per minute usually first sign
audible expiratory grunt
nasal flaring
cyanosis increased

Diagnosis of RDS

Signs and symptoms as previously described
hypoxemia defined as arterial PaO2 level less than 50 millimeters of mercury on room air
chest x-ray reveals low lung volumes hazy lung fields and find a direct nuclear granular pattern of density with air bronco

Differential diagnosis with respiratory distress syndrome

Pneumonia-similar signs and symptoms and radiographic features can be found in neonates with pneumonia
transient tachypnea of the newborn can be present with the same signs and symptoms, but these infants usually require less than 40% oxygen, improve quic

Pulmonary complications of RDS

Air leaks pulmonary edema and BPD

Cardiovascular complications with RDS

PDA
systemic hypotension

Renal complications with respiratory distress

Olaguria
immature renal function with decrease glomerular filtration in very low birth weight infants
natural diuresis will occur approximately 48 to 72 hours as the infant's condition improves

Metabolic complications with RDS

Acidosis
hyponatremia hypernatremia
hypocalcemia
hypoglycemia

Neurologic complications with RDS

Seizures may result from hypoglycemia or IVH
ventilator manipulations, rapid fluid infusions, shock, and acidosis are all factors causing changes in cerebral blood flow and may precipitate IVH

Management of RDS

RDS is a disease that is self-limited and transient. Adequate surfactant can be produced by premature infant within 48 to 72 hours
goal of treatment is supportive until disease resolves and to prevent further lung injury

Surfactant replacement therapy

Benefits include reduce morbidity and mortality
improve compliance and decrease resistance in the lungs
improve ventilation in low lung volumes
Prophylactic treatment soon after birth infants born less than 27 to 30 weeks
rescue treatment of infants with

Prevention of RDS

Maternal glucocorticoid steroidsUse of L/S ratio, fetal lung maturity, PG to turn to determine timing of labor

Perinatal management to avoid RDS

Maternal hypotension
over sedation
maternal hypoxia
feel distress without prompt delivery
Neonatal
delayed resuscitation
uncorrected hypoxia or acidosis
hypothermia, hypoglycemia, hypovolemia

Pneumonia

Intrauterine infection: passage of infecting agent by infection of fetal membranes, trends placental transmission, aspiration of meconium or infected amniotic fluid during delivery
Neonatal infection: acquired during nursery stay, pathogens are generally

Etiology of pneumonia

Risk of infection gratis in premature infants
immature ciliary system and the tracheal bronchial tree, leading to sub optimal removal of inflammatory debris, mucus, and pathogens

Pathophysiology of congenital pneumonia

If it may be born critically ill or still born to a mother with history of chorioamnionitis
prolonged rupture of membranes greater than 24 hours; asending organisms may infect amniotic fluid
infective organisms may cross the placenta and the enter fetal c

Neonatal pneumonia

Infection occurs days to weeks after birth pathogenic organisms is required from hospital personnel parents or other infected infants
poor handwashing, contaminated blood products, infected human milk, and open skin lesions are common ways of transmitting

Clinical presentation of pneumonia

Labor greater than 24 hours: prolonged rupture of membranes, maternal fever, foul-smelling purulent amniotic fluid, fetal tachycardia, decreased fetal heart rate variability
Signs and symptoms are often indistinguishable from those of other forms of RDS a

Management of pneumonia

Antibiotics
maintain temperature
monitor glucose levels
monitor blood pressure entreat for hypertension
use oxygen with or without ventilation
monitor for evidence DIC
provide family support

Transient tachypnea of the newborn

Delayed clearance of fetal lung fluid
term in near-term infants
tachypnea, grunting and retractions in the first few hours
minimal cyanosis may require fractional inspired oxygen of less than 40%
duration may be 1 to 5 days transfer text

Pathophysiology of TTN

Fetal lung fluid has a higher fluoride concentrations in plasma, interstitial fluid, or amniotic.
During labor, and active transport chloride stops fluids reabsorbed via a protein gradient and removed by the lymph system
two thirds of the lung fluid are r

Infants at highest risk for TTN

Birth at her near-term
C-section without labor
breech delivery
second twin
IUGR
precipitous delivery
delayed cord clamping- results in a transfusion of blood which may transiently elevate central venous pressure
macrosomia
males
maternal sedation

Diagnosis of TTN

Early signs and symptoms may be difficult to distinguish from other respiratory problems; they're usually milder.
Chest x-ray reveals diffuse haziness streaking is both lung fields.
Diagnosis is frequently one of exclusion

Management the TT N

Oxygen
care regulation
adequate fluid intake
maintain ABG's within normal
maintain blood sugar at normal
if respiratory rate is greater than 60 delay feedings to avoid aspiration
if history indicates risk of infection, broad-spectrum antibiotics have been

Persistent pulmonary hypertension of the newborn

Caused by right to left shunting through the fetal shots at the atrial and ductal levels
secondary to persistent elevation of pulmonary vascular resistance and pulmonary artery pressure

Pathophysiology of PPHN

After delivery adequate oxygenation depends on lung inflation, closure of shots, decrease PVR, an increase pulmonary blood flow
over the first 12 to 24 hours of life, PVR falls by 80%
when PVR remains high, adaptation from fetal to neonatal circulation is

Etiology of pulmonary hypertension of the newborn

Maladaptation: the pulmonary vascular bed structurally normal but PVR remains high Maldives in general results from vasoconstriction which may be transient or persistent
Hypoxia/asphyxia. This is the most calming precipitating factor in PPHN
pulmonary dis

Clinical presentation of PPHN

History of hypoxia auris pixie at birth
respiratory abnormalities - Conine staying fluid, nuchal cord, abruption, any acute blood loss
cardiovascular abnormalities - blood pressure is usually lower than normal systolic murmur is frequently heard usually f

Management of persistent pulmonary hypertension

The main goal to just correct hypoxia and acidosis and promote pulmonary vascular dilation
management will depend on the calls
goal is to keep PO to greater than 90 mmHg
hyperventilate keep CO2 values in a low normal range
nitric oxide-selective pulmonary

Using vasopressors to treat pulmonary hypertension

The goal is to keep systemic pressure above pulmonary pressure to decrease shunting
Dopamine is the drug of choice. Has a short half-life.
Dobutamine is a synthetic catecholamine with primary beta one affects to support blood pressure in patients with sho

Meconium aspiration syndrome

Meconium is a mixture of epithelial cells and bile salts found in the fetal intestinal tract
With intrauterine stress at risk pixie of, peristalsis is stimulated and relaxation of the anal sphincter occurs, releasing meconium into the amniotic fluid.
Aspi

Pathophysiology of meconium aspiration syndrome

Complete or partial airway obstruction can occur
atelectasis or ball valve air trapping leads to hyperinflation
a chemical Pneumotosis
meconium decreases levels of surfactant

Clinical presentation meconium aspiration syndrome

Disease of term or post term infants. Rarely seen in infants born less than 36 weeks
asphyxia and results of chronic hypoxia may predispose these infants to pulmonary hypertension
vigorous resuscitation is frequently needed in the delivery room
respirator

Complications of meconium aspiration syndrome

Pulmonary air leaks; pneumothorax
pneumonia
pulmonary hypertension
BPD
Anabolic acidosis
hypoglycemia
hypocalcemia
Neurologic complications will depend on the degree of asphyxia

Delivery room management and prevention of meconium aspiration

Suction nasopharynx oropharynx and hypopharynx with delivery of bed to remove meconium before first breath is taken
If the infant is the press with no respiratory effort, muscle tone and heart rate is less than 100, direct suctioning of the trachea soon a

Bronchopulmonary dysplasia

36 week infant with 02 requirement, abnormal chest x-ray, abnormal physical examination findings
An infant less than 32 weeks gestation who has reached 36 weeks was treated with oxygen greater than 28 days and requires oxygen and 36 weeks are positive pre

BPD and oxygen toxicity

High inspired oxygen concentration causing production of reactive oxygen species and the release of chemotactic factors that attract neutrophils to the lung, initiating the inflammatory cycle.
Inflammatory mediators and proteolytic enzymes are released.
O

Three pathways of injury for BPD

Structural injury to the airway and alveoli in conjunction with inhibition of the maturation of processes.
Stimulation of elastic tissue production and the accelerated fibrosis.
Activation of an intense inflammatory response which contributes to ongoing a

Ventilation and its contribution to BPD

Intubation interrupts normal pulmonary function.
Correlation exists between severity of initial pulmonary process and BPD.
Their trauma is related to intensity and mount time exposed to the elements of positive pressure ventilation. Repeated distention of

Other causes of BPD

Increase left right shunting via the PDA.
Excessive fluid intake in the first four days of life.
Gestational age and weight - 31 weeks and less than 1500 g

Clinical presentation of BPD

Increase in ventilatory requirements or inability to be weaned from the vent
hypoxia, hyper car be a, respiratory acidosis
retractions
increase secretions
bronco spasms
x-ray showing hyperinflation, infiltrates, blips, cardio Magaly

Complications of BPD

Intermittent bronchospasm
inability to be ween from vent or oxygen
recurrent infections
congestive heart failure from core pulmonary
BPD spells - infant becomes irritable, agitated, and dusky; has increased respiratory effort, hypoxia
reflux
developmental

Prevention of BPD

Administration of antenatal steroids reduces the incidence of RDS and need for mechanical ventilation
surfactant rescue therapy
routine use of steroids is not recommended
gentle ventilation, permissive hypercarba,
SI MV
aggressive nutrition is needed to p

Management of BPD

Continue assisted ventilation; weaning should be slow
diuretics are used to control fluid retention; Lasix is most often used.
Chloro thiazide has been use with results similar to those seen with Lasix
bronchodilators - long-term outcome data on prolonged

RSV: BPD

Infants are at high risk for outbreaks and account for many it readmissions
RSV prophylaxis decreases severity of infection decreases hospitalization and reduces incidence of recurrent otitis media
Prophylactics should be given to infants are less than tw

Chronic lung disease in premature infants

Changes in pulmonary structure and function occurring without underlying disease
majority of cases are seen in infants weighing less than 1500 g
abnormal distribution of air due to characteristics of the premature lung
chest x-ray reveals poorly defined,

Pulmonary hypoplasia

Defective or inhibiting growth of the lungs, either unilateral or bilateral. Developmental disorder that results in decreased numbers of alveoli, bronchioles, arterioles
Conditions that compress the lungs or limit lung growth including diaphragmatic herni

Pulmonary hemorrhage

Localized areas of bleeding into the alveoli; also known his hemorrhage pulmonary edema
can be massive generalized bleeding event
Usually occurs is complication of other disorders
may be due to trauma from improper suctioning technique
usually due to larg

Suctioning the airway

Suctioning of the mouth and nose and tubes should be performed on an as needed basis
criteria for suctioning include evidence of secretions; changes in vital signs Emmy: agitation and restlessness; and changes in oxygenation for ventilation
do not advance