NEONATAL RESPIRATORY DISEASES - PowerPoint PPT Presentation

Loading...

PPT – NEONATAL RESPIRATORY DISEASES PowerPoint presentation | free to download - id: 3d26cd-MTEzY



Loading


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation
Title:

NEONATAL RESPIRATORY DISEASES

Description:

NEONATAL RESPIRATORY DISEASES BY Dr.(Mrs) P. O. OBIAJUNWA Introduction Respiratory diseases usually present as respiratory distress in the neonate. – PowerPoint PPT presentation

Number of Views:229
Avg rating:3.0/5.0
Slides: 20
Provided by: effiweNet
Learn more at: http://www.effiwe.net
Category:

less

Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: NEONATAL RESPIRATORY DISEASES


1
NEONATAL RESPIRATORY DISEASES
  • BY
  • Dr.(Mrs) P. O. OBIAJUNWA

2
Introduction
  • Respiratory diseases usually present as
    respiratory distress in the neonate. It has four
    main clinical features.
  • Tachypnoea resp rate gt60c/min.
  • Recessions indrawing of the sternum and
    intercostals and subcostal regions.
  • Grunting.
  • Cyanosis.
  • All four symptoms may not be present in every
    case, but the presence of 2 or more symptoms
    qualifies for respiratory distress.

3
  • Causes of Neonatal Respiratory distress include
  • Respiratory distress syndrome (hyaline membrane
    disease),
  • Pneumonias, Pneumothorax, aspiration syndrome
    (meconium, milk, blood, Amniotic squames),
    Congenital diaphragmatic hernia, Transient
    tachypnoea of the newborn, Tracheo-eosophageal
    fistula, cardiac failure, Pulmonary hypoplasia,
    Persistent fetal circulation (Primary pulmonary
    hypertension), Broncho-pulmonary dysplasia,
    chronic pulmonary insufficiency of prematurity,
    (CPIP).

4
  • Respiratory distress syndrome (Hyaline membrane
    diseases)
  • This is due to lack of Surfactant, which is a
    phospholipids that lowers the surface tension
    within the terminal airway. Surfactant is
    secreted by the type 2 pneumocytes situated
    within the alveolar membrane. They are present by
    22 weeks of gestation but become functionally
    active by full term. Surfactant production can be
    switched on by stress, premature rupture of
    membrane, and exogenous steroid given to mother.
    Maternal diabetes suppresses development of
    surfactant so that their babies may have RDS even
    when term.

5
  • The birth process squeezes out fluid from the
    lungs by compression of the chest wall. The
    infants first breath expands the alveoli. In the
    presence of surfactant, the alveoli remain
    expanded, but if absent, the alveoli collapse
    down to their foetal state, and the babys next
    breath is another massive one to re-expand the
    terminal airways. Surfactant molecules form a
    monolayer on the inside of the alveolar membrane.
    They are poorly compressible and maintain the
    alveolus in an expanded state. In RDS, each
    breath is like the first breath in effort,
    respiratory distress results and baby gets tired.
  • About 1 of newborns infant have RDS. It is
    closely related to immaturity 60-70 of infants
    born atlt28 weeks and 20 of those born less than
    34weeks have it.
  • Risk factors for RDS are diadetes in mother, 2nd
    twin, ante partum haemorrhage, shock, maleness.

6
Pathology
  • Hyaline membranes are seen within the alveoli of
    dead babies dying of RDS, and are part of the
    inflammatory response to the condition. The
    infant shows signs of respiratory distress soon
    after birth, progressing over the first day,
    peaks at 48 hours. The infant may be oliguric
    initially,and may become oedematous, diuresis
    occurring as the infant starts to recover.

7
Diagnosis
  • Chest ray Ground glass appearance showing
    airless alveoli with an air bronchogram,
    air-filled eosophagus may be seen too.
  • Measuring directly or indirectly the amount of
    surfactant in the amniotic fluid or gastric
    aspirate. The lecithin sphingomyelin (LS) ratio
    reflects surfactant activity and a ratio of lt1.5
    predicts a high risk for RDS.

8
Management
  • It is self-limiting. The babys lungs recover
    with endogenous production of surfactant.
    Management is directed towards supporting the
    infant during respiratory distress.
  • In mild disease, give humidified oxygen
    supplements by headbox to maintain normal
    arterial blood oxygen tension.
  • In more severe cases continuous positive airway
    pressure (CPAP) is used to provide constant
    positive pressure during expiration which limits
    collapse of the alveoli.

9
Management (contd)
  • Mechanical ventilation is indicated when there is
    hypoxia, and there is hypercapnoae with a rising
    Pco2 gt8 kpa(60mmHg with falling pH( lt7.25) or
    there is apnoea.
  • General supportive treatment are chest
    physiotherapy, early infection treatment, blood
    pressure monitoring, optimal environmental
    temperature.
  • Exogenous surfactant replacement therapy can be
    given.

10
Complications of respiratory distress syndrome.
  • Pulmonary
  • Air leak including Pneumothorax,
  • Pulmonary interstitial emphysema,
  • Pneumonia, atelectasis, Lobar collapse, chronic
    lung disease.
  • Extrapulmonary ones are
  • Patent doctus arteriosus, Intraventricular
    haemorrhage, Retinopathy of prematurity,
    Subglottic stenosis.

11
Pneumonias
  • Neonatal pneumonia could be early, within 24
    hours of birth intrapartum that is through the
    birth canal, or later.
  • Early onset pneumonia is said to be mainly caused
    by Group B beta haemolytic Stretococcus acquired
    from mother (10 of women are carriers.) It
    causes pneumonia or meningitis. Presents as
    respiratory distress or apnoae. The child could
    have septicaemia and shock.

12
  • Chest X-ray may be similar to RDS.
  • Management includes respiratory support with
    oxygen supplement, mechanical ventilation,
    presumptive antibiotic management (ampicillin
    with gentamicin, 3rd generation cephalosporin).
    Change antibiotic according to sensitivity
    pattern.
  • Later onset pneumonias could be due to damaged
    lungs in ventilated babies, or acquired from
    those around the babies. Causative germs include
    Pseudomonas, Staph aureus. E-coli, Klebsiella,
    Mycoplasma, Chlamydia, unusually candida or
    viruses.
  • X-ray shows patchy opacities.

13
  • Treatment is with appropriates antibiotics,
    oxygen if needed.
  • Manage congestive cardiac failure if present.
  • Vigorous physiotherapy.
  • Air leak from the alveoli can occur. If the
    leakage is into lung interstium it is called
    pulmonary interstitial emphysema. Air can track
    along the perivascular spaces and rupture into
    the mediastinum causing Pneumomediastinum, into
    the pleural space resulting in Pneumothorax, and
    when air leaks into the pericardial space, it is
    pneumopericardium.

14
  • Pneumothorax may be spontaneous, but mostly
    following resuscitation especially with bag and
    mask.Risk afctors include RDS, meconium
    aspiration, and lung hypoplasiain conjuction with
    diaphragmatic hernia.
  • Diagnosis-suspect when there is a sudden
    deterioration in infants condition. There is a
    reduction of breath sounds over the affected
    lung. Left-sided tension pneumothorax may
    displace the heart to the right side with heart
    sounds.
  • Confirm by chest x-ray which shows a hyperlucency
    of the side affected with no air bronchogram.
    Treament involves placing a tube in the2nd
    intercostal space at the mid-clavicular line.
    Place the other end of the tube into a container
    of water below the infant.

15
  • Meconium aspiration syndrome. Intrapartum
    asphyxia may cause the foetus to pass meconium
    which baby can aspirate into the small bronchi
    when gasping. During resuscitation at birth, the
    meconium is further driven into terminal airway.
    Meconium is very irritant and causes an
    inflammatory reaction, Meconium plugs some
    airways causing a ball valve effect of the with
    some hyperinflation, and air leak. An intense
    inflammatory exudates develop and secondary
    bacterial infection occurs. Ventillation/
    perfusion inequality develops causing the infant
    to become more hypoxic and in severe cases
    pulmonary hypertension commonly develops.

16
  • Diagnosis is suggested when there is the presence
    of meconium in the liquor, in the airway with
    respiratory distress.
  • Chest X-ray shows hyperinflation with diffuse
    patchy opacities throughout the lung fields.
  • Management involves the use of Oxygen,
    antibiotics, and steroids.
  • Prevention careful evaluation of the child with
    meconium-stained liquor and sucking it out from
    mouth. If meconium is seen below the vocal
    cords, remove it and lavage the
  • Trachea with normal saline through an
    endotracheal tube.

17
  • Milk aspiration is common in infants with
    gastro-eosophageal reflux, those with apnoae and
    tetanus patients. Naso-duodenal feeding may be
    useful in these. Total parenteral nutrition may
    be considered.

18
Congenital diaphragmatic hernia.
  • Occurs I 1 in 2500 births. There is a defect in
    the postero-lateral part of the diaphragm in 80
    of cases. Severity depends on the defect size,
    amount of bowel in chest and timing of
    herniation. Bowel in the chest causes lung
    compression and hypolasia. Large bilateral
    defects is not compartible with life.
    development.
  • Their severe respiratory distress present from
    birth in severe cases.
  • Suggestive features are scaphoid abdomen, and
    apparent dextrocardia if defect is left-sided.
    Diagnosis is confirmed by chest x-ray showing
    loops of bowel in the thorax.

19
Management
  • Patient can be delayed a few days to stabilize
    before surgery. The bowel is returned to the
    abdomen and defect is repaired.
  • Medical treatment adequate ventilation, shock
    treatment, calories.
  • Prognosis depends on lung hypoplasia. Mortality
    of 60-70 in early presentation lt6 hours.
  • Transient tachypnoae of new born is diagnosed in
    retrospect and is due to delayed clearance of
    fluid from the lungs in term infants especially
    born by C/S soon after birth.
  • X-ray shows streakiness due to interstitial fluid
    and fluid in horizontal fissure.
About PowerShow.com