RESPIRATORY DISORDERS

IN THE NEWBORN

OA MOKUOLU & OO
ADESIYUN
Neonatal Intensive Care Unit
University of Ilorin Teaching Hospital,
Ilorin
ANATOMY
Development of the Lung

 Alveolar development

 Vascular development
Development of the Lung

 Alveolar development

◦ The tracheo-bronchial airway system

begins as an embryonic bud, which then
divides and branches

◦ This process consists of FIVE phases

Development of the Lung
 Alveolar Development
◦ Embryonic phase (through week 5)
 Development of the proximal airway. Anomalies can
lead to agenesis or TOF

◦ Pseudoglandular Phase (week 5-16)

 Development of lower conducting airway Closure of
diaphragm occurs.

◦ Canalicular Phase (week 17-24)

 Formation of Gas exchange acini (respiratory
bronchioles) with apposition of the capillaries
Development of the Lung
◦ Terminal Sac Phase (Week 24-37)
 Further Development of acini. Capillary invasion
becomes more extensive

◦ Alveolar Phase (Week 37 – 3years)

 Continued alveolar proliferation and development

 Vascular Development
◦ Increase in length and diameter of pulmonary arteries
◦ Muscularization of fetal pulmonary arteries
 Normal Physiology I
 O2 is carried in the blood in chemical combination
with haemoglobin and to some extent in physical
solution

 The binding of O2 to Hb is usually expressed as a

percentage saturation SaO2.
Normal Physiology II
 O2 delivery to the tissues is determined by a
combination of
 Cardiac Output
 Total haemoglobin concentration
 Arterial PO2

 Haemoglobin affinity for O2.

 Normal Physiology III
 Before birth, the lung is a fluid-filled organ
receiving 10-15% of the total cardiac out-put

 Within the first minutes of life, a large portion of

the fluid is absorbed and the lungs fill with air,
with  blood flow 8-10 fold.
Normal Physiology iv
 Fluid re-absorption occurs;
◦ during passage through the vaginal canal  squeezing
out of fluid

◦ During labour   production of β-agonist  ultra-

filtration of fluid into pulmonary system

◦  Surfactant Synthesis and release  Helps to maintain

surface tension thereby preventing leakage of fluid back
into alveoli.
 Normal Physiology V
 For normal respiration, there should be
◦ Stable (Non compliant) ribcage
◦ Compliant lungs – gas exchange surface
◦ Patent air passages – for conduction of the gases
◦ Mature and well co-ordinated high centre control
 monitoring and variation in strategy of respiration
◦ Peripheral mechanical and chemical sensors
◦ Adequate pulmonary circulation.

 Respiratory distress can occur once there is

interference with any of these mechanisms
RESPIRATORY DISEASES
IN THE NEWBORN
 OVERVIEW
 Respiratory difficulties, to a large extent reflects a
change in normal respiration occasioned by
◦ inadequate supply of O2 to tissues,
◦ disorders of acid-base balance or
◦ local/central effects on normal respiratory mechanisms due to
◦ a variety of local/systemic problems.

 The end result is usually that of

◦ hypoxaemia,
◦ acidosis with or without hypercapnea
◦ leading to postpartum asphyxia.
 Overview-contd

 Critically, the life of the baby is at stake because of

inadequate tissue oxygenation or abnormal
biochemical environment.
 The goals of therapy are
◦ Ensure adequate oxygenation
◦ Correct acid base imbalances
◦ Identify the cause,
◦ Administer calorie
◦ Monitor patient.
 MANIFESTATIONS OF RESP
DISORDER
 CYANOSIS
◦ Bluish discoloration of the mucus membrane /extremities
 GRUNTING
◦ Expiratory sound
 RETRACTION
◦ Chest wall in-drawing
 TACHYPNEA
◦ Fast breathing
 APNEA
◦ Cessation of breathing
 SHOCK
◦ Severe hypotension or decrease tissue perfusion
 CAUSES

 PULMONARY

◦ Lungs
 Difficult Transition
 Transient Tachpnoea of the Newborn
 Aspiration Syndromes
 MECONIUM, AMNIOTIC FLUID, TOF, FEEDING,
 Respiratory Distress Syndrome
 Pneumonia
 Pnuemothorax
 Pulmonary Hypoplasia /Diaphragmatic hernia
 Pulmonary haemorrhage
 CAUSES II
◦ Upper Airway Obstruction
 Choanal atresia
 Laryngo/Tracheomalacia
 Laryngeal web

◦ Rib Cage
 Rib cage deformity
 Fractured rib
◦ Diaphragm
 Paralysis in association of upper brachial plexus
 Eventration
 CAUSES III
 EXTRA PULMONARY
◦ Vascular
 Persistent Fetal Circulation
 CHDs
 Polycythemia
 Anemia
◦ Metabolic
 Acidosis
 Hypothermia
◦ Neuromuscular
 Cerebral oedema
 Phrenic nerve damage
 Drugs e.g. Theophylline toxicity
 Difficult Transition
 This is probably the commonest reason for
respiratory distress in the newborn
◦ Presents at birth
◦ frothy secretions from the mouth and sneezing incessantly
◦ They may require oxygen
◦ They are invariably normal by four hours of age

 Contributory factors include

◦ Poor suctioning of the mouth and nostrils,
◦ precipitous delivery and
◦ hypothermia
 Transient Tachypnoea
 Predisposing factors
◦ Fetal distress
◦ Maternal sedation
◦ Maternal DM
◦ ±C/S Delivery without labour
 Presentation
◦ Presence of one or more risk factors
◦ Tachypnoea with RR ranging between 60-120bpm
◦ There may be grunting
◦ Resolves with 48-72 hours (Usually 24 hours)
◦ Hypoxemia at room air (corrected by an FiO2 0.40)
◦ Never requires ventilatory support
 TTN-2
 Chest X-RAY
◦ Hyperinflation of the lungs
◦ Vascular markings prominent on x-ray

 Management
◦ Self limiting
◦ Oxygen rarely more than FiO2 of 0.4
◦ All infants recover completely without residual pulmonary
disability
 Persistent Pulmonary Hypertension (PPHN)
 Definition
◦ Persistent elevation of the Pulmonary Vascular Resistance
leading to R to L (DA or FO) shunt and Hypoxaemia
 Risk Factors
◦ Post term delivery
◦ Placental insufficiency
◦ Meconium staining
◦ Perinatal asphyxia
◦ Bacterial pneumonia/sepsis
◦ Hypoglycemia
◦ Hypothermia
◦ Polycythemia
 PPHN-2
 Pathophysiology
◦ Maladaptation:
 Pulmonary vascular bed is structurally normal but PVR
remains high.
 So PPHN is due to active vasoconstriction
◦ Maldevelopment
 Pulmonary vessels are abnormal impinging on the lumen and
increasing PVR
 Presentation
◦ Labile hypoxaemia out of proportion with lung
parenchymal disease
◦ Affected infants are mostly TERM
◦ History of risk factor
◦ Loud Single S2
 PPHN-3
 Management
◦ Self limiting and treatment is generally supportive

◦ Decrease O2 demand by nursing in Neutral Thermal

environment

◦ Correct underlying problems

◦ Aim at increasing PBF and decrease R to L

 Give oxygen and correct Acidosis

 Sildenafil
 PNEUMONIA
 Infection of the Lungs in the NB may be acquired
◦ Transplacentally
◦ During the birth process or
◦ Postnatally

 Aetiology
◦ Gram negative enteric bacilli (E. coli, Klebsiella)
◦ Group B Streptococcus
◦ Listeria Monocytogenes
◦ Staphylococcus
 PNEUMONIA-2
 Presentation
◦ Depends on onset
◦ Characteristically there is respiratory distress
 Tachypneoa and chest wall in-drawing
◦ Fever
◦ Early onset types may be difficult to distinguish from RDS

 X-Ray
◦ Patchy opacity bilaterally

 Management
◦ Supportive care and
◦ Antibiotics
 Amniotic Fluid Aspiration
 Aspiration of amniotic fluid peripartum

 There is dilution of surfactant

 Respiratory distress noticed immediately after

birth

 Gets worse over the next few hours

 Stays at a peak for 24-48 hours and thereafter

makes steady improvement
 MECONIUM ASPIRATION
SYNDROME
 Aspiration of meconium by the fetus, leading to
chemical pneumonitis and mechanical obstruction of
bronchi after delivery.

 Meconium stained amniotic fluid (MSAF) occurs in

about 9-20% of deliveries.
 Meconium is a viscous greenish Fluid that fills the
fetal GIT.
 It contains gastro-intestinal secretions, cellular
debris, bile and pancreatic juice, mucus, lanugo and
vernix
 MAS-2
 In utero meconium passage may occur
◦ In response to hypoxia with a transient period of hyperperistalsis and
relaxation of anal sphincter

◦ or as normal physical event during gut maturation.



Aspiration of meconium may occur
◦ in utero as the compromised fetus begins to gasp

◦ But more frequently occurs with the initial breaths after delivery

 MAS is often most severe in post-term infants who have

reduced amniotic fluid volume, because the less dilute,
thicker meconium is more likely to cause airway
obstruction.
 MAS-3
 Pathogenesis
◦ Acute airway obstruction

 A ball valve mechanical obstruction contributes to air trapping

leading to increase AP diameter of the chest, increased
functional residual capacity

 Complete obstruction of small airways may result in regional

atelectasis

◦ Decreased lung tissue compliance with PPHN

◦ Lung parenchymal damage

 FETAL COMPROMIS E

PERINATAL AS PHYXIA

PAS S AGE OF MECONIUM

AS PIRATION OF MECONIUM

MECHANICAL OBSTRUCTION CHEMICAL PNUEMONITIS

AIR INCREAS ED AIR WAY RES IS TANCE ALVEOLAR OEDEMA

And
S URFACTANT DYS FUNCTION

AIR TRAPPING INTRAPULM S HUNT(R L)

UNEVEN VENTILATION

AIR LEAKS HYPOXIA PFC

ACIDOS IS
 MAS-4
 Clinical Presentation
◦ Meconium found below the vocal cords on direct
laryngoscopy defines MAS

◦ Respiratory distress presenting at birth

◦ Progressively gets worse over the first 48 hours

◦ There after reaches a peak for the next 3-4 days before
making a very slow progress over the next 5-10 days

◦ There may be mediasternal shift as a result of air leaks

 RESPIRATORY DISTRESS
SYNDROME
 A syndrome caused by deficient surfactant manifested
clinically by respiratory distress in the preterm infant.

 Previously called HMD

 Risk factors include:

◦ Prematurity (Incidence increases with decreasing GA)
◦ Male Sex
◦ Maternal diabetes
◦ Non-black races
 RDS II

 Surfactant (surface acting material)- an

Apolipoprotein produced by the type II
alveolar epithelial cells

 It is composed of phospholipid (81%) with

small amounts of neutral fat (5%), cholesterol
(4%) and protein (10%)

 The primary active molecule is saturated

dipalmitoyl phosphatidylcholine (DPPC)
 RDS III
 Surfactant acts by:
 Lowering the surface tension at the alveolar air-
fluid interface.

This reduces the pressures required to expand the

alveoli. According to Laplace's law.
P = 2T/R where T = Tension, R = Radius
by lowering T; P is reduced
Therefore there is an increase in compliance.
Compliance = V /P.
 RDS IV
 T varies with the size of the alveoli:

◦ This equilibrates the pressure in adjacent

alveoli, otherwise the small alveoli will empty
into the big ones.

◦ Assuming T is constant for all alveoli. Then an

alveoli with

◦ R = r, has a PS = 2T/r and one with

◦ R = 2r, has PL = 2T/2r.

 RDS V
◦ Therefore the PS > PL and this pressure gradient
causes air flow from the small alveolus to the large
ones, resulting in over distended alveoli alternating
with atelectatic ones. Overdistended alveoli may
rupture and produce air leaks.
◦ With a dynamic change in T with alveolar size,
 PS = 1/2 (2T)/r = T/r
 PL = 2T/2r = T/r
 And PS = PL.
 Hence there is equilibration of the pressures and no
airflow in between adjacent alveoli.
 RDS VI
 Consequences of surfactant Deficiency
◦ The alveolar collapse

◦ Increasing interstitial edema independently worsen lung

compliance, and impair surfactant production and function,
thus perpetuating the process.

◦ There is overdistended alveoli interspersed with collapsed

alveoli. The overdistended alveoli may predispose to air
leaks.

◦ Overall respiratory effort is inefficient and ineffective

 RDS VI
 Clinical Presentation
◦ Typical history is that of preterm baby with respiratory
distress at birth

◦ The infants are tachypnoiec, with retractions and grunting

respiration.

◦ Cyanosis at room air and breath sounds are diminished

 RDS VII
◦ The RD presents shortly after delivery OR within 1 hour
and

◦ progressively gets worse, reaching a peak at 72 hours,

maintaining the plateau for another 48 hours and
◦
◦ gradual resolution in 5 days.

◦ Total course lasts about 10 days, if there are no

complications.

◦ Improvement heralded by diuresis

 RDS VIII
 X-ray
◦ Diminished lung volume
◦ Diffuse reticular, granular, ground glass appearance with
air bronchogram
◦ When severe there is complete white out.
 Prevention
◦ Avoid preterm delivery if possible
◦ Administration of corticosteroids before delivery if
preterm delivery is inevitable
◦ 12mg betamethazone IM 12 hourly for at least 24 hours
 RDS IX

 Treatment
◦ Surfactant replacement therapy through ET
◦ Two types of surfactant therapy
 Prophylactic therapy: surfactant instilled in the trachea soon
after birth before diagnosis of RDS can be established.
Indicated especially if GA <30 wks
 Rescue therapy: for treatment of established RDS
 APPROACH TO MANAGEMENT OF
RESPIRATORY DISTRESS
 Careful assessment and resuscitation
◦ History of onset, progression, effect on activity, relationship to
feeds etc
 Ensure adequate ventilation and oxygenation
 Maintain Acid-Base Homeostasis
 Monitor blood gases PO2, PCO2, pH, SpO2
 Fluid and electrolyte balance + calorie
 Infection surveillance and control
 Nurse in neutral thermal environment
 Specific therapy as appropriate