RESPIRATORY

DISTRESS
SYNDROME
Definition

Neonatal respiratory distress

syndrome represented by any
breathing difficulties occurring
under the age of 28 days of
life
Ethiology
 Respiratory causes
1. Laryngeal and tracheal obstacles
2. BMH hyaline membrane disease
3. Meconium aspiration
4. Transient neonatal tachypnea
5. Congenital pneumonia
6. Congenital adenomatous malformations of lungs
7. Pulmonary limfangiectasia
8. Pulmonary agenesis/ hypoplasia
9. Pneumotorax
10. Pulmonary hemoragy
11. HTPP
Ethiology 2
 Cyanotic congenital heart malformations
 Neuromuscular diseases
1. Cerebral edema
2. Intracranian hemoragy
3. HIE hypoxy Ischaemic encephalopathy
4. Muscle diseases
5. Medullary affections
6. Phrenic nerve lesions
7. SNC Malformation
Ethyology 3
 Surgical
1. Diafragmatical hernia
2. Esophageal atresia
 Metabolic
1. Hypoglycemia
2. Hypocalcemia
3. Acidosis
4. Hyponatremia
5. Hypomagnesemia
Ethiology 4

 Hematological
1. Anaemia
2. Polyglobulia
3. Shock
 Drugs given to mom
1. Anesthetics
2. Opioids
HBD Hyaline membrane disease -
Definition

HMD It is an immature lung

disease and biochemical
surfactan deficiency, which
begins shortly after birth.
HMD – Incidence

 Inversely proportional to GA

20% nb with GA 32-34 wk.

40% nb with GA 30-32 wk.

0.5-1% nb at in-term borns

Fiziopathology

 The surfactant, a substance present in the

liquid from the surface of the alveoli, is
made in 90% of lipoproteins and
phospholipids which have a role in
decreasing tension.
 Its
synthesis easily degrade under
conditions of acidosis, hypoxia,
hypothermia and cardiovascular collapse.
Fiziopathology
 The lack of surfactant determine the alveoli collapse,
decreasing pulmonary compliance and increasing the effort
of filling the lungs; also due to increased tension will occur
transudation of fluid from the pulmonary capillaries into the
alveoli. The newborn ribs deforms easily, which aggravates
alveolar collapse. This will cause a decrease in gas exchange
surface, with many remaining unventilated alveoli, causing
hypoxemia, the hypercarbia and acidosis. The consequences
of these disturbances will increase pulmonary vascular
resistance and right-left circulatory expanded shunt (by
ductus arteriosus). Impaired pulmonary circulation will
decrease the synthesis of surfactant, resulting in a vicious
circle.
Surfactant functions

 Reduce tension and mainteins alveoli

relaxed during the respiratory cycle
(antiatelectatic action )
 Reduce the effort fan
 Increase pulmonary compliance
 Anti-edematous action,
 Anti-infection defense.
Anatomic pathology
 Macroscopic lungs are purple, with
firm consistency.

 Microscopic visualizes acidophiles

hyaline membranes that line the
alveoli, alveolar ducts and terminal
bronchioles, atelectatic areas
stretched up to hemorrhage
intraalveolar vascular congestion
and dilated lymphatic vessels.
PREMATURITATE ASFIXIE PERINATALA

Reduc sinteza, stocajul si eliberarea surfactantului

Scade cantitatea totala de surfactant

Creste tensiunea de suprafata la nivelul alveolelor pulmonare

ATELECTAZIE

Modificarea raportului hipoventilatie

ventilatie/perfuzie

Hipoxie retentie de CO2

ACIDOZA
Respiratorie/metabolica
Risks factors

 Primary surfactant deficiency:

- Prematurity
- Males
- Gemini II
- Caesarean before labor
- Maternal diabetes
- Abruption placentae
- Rhesus sensitization
Risks factors

 Secondary surfactant deficiency:

- Severe acute perinatal asphyxia
- Shock
- Pulmonary infection (eg. Pneumonia caused by
B-hemolytic streptococcus)
- Pulmonary hemorrhage
- Barotrauma / volumtrauma, O2 toxicity
- Diaphragm hernia, and pulmonary hypoplasia
HMD – clinical signs

 Occurs in 1-10 hours at birth with varying degrees of

respiratory distress

Evolution without treatment is characterized by

emphasizing the following symptoms in 24-72 hours
followed either spontaneous regression or
worsening to death or subsequent sequels
HMD – clinical

 respiratory disorders

- Tachypnea (60 breaths more than min.)

- Crises of apnea
- Expiratory grunt
- Retraction intercostal, subcostal, and general
- Nasal flaring
- Cyanosis to the normal air
HMD – lungs auscultation

Absent or diminished breath sounds

Bilateral crackles listened
HMD – signs of severity

 Hemodynamic Disorders
Hypotension
Capillary recovery time> 3 sec.
Oliguria
Heart Rhythm Disorders
Edema
 Disorders of thermoregulation – hypothermia
 Neurological Disorders - hypo / hypertonic
Respirator effort is determined by
Sillverman Score
Sillverman Score
Silverman Score – interpretation
and Clasiffication
 debut of RDS- 0- 3 points

 Medium to seriously RDS- 4-6 points

 Seriously RDS - 7-9 points

 Very badly RDS - 10 points

MHD - Laboratory exams
 Antenatal: determining the ratio in amniotic fluid
lecithin / sphingomyelin
Normal> 2
≤ 1.5 indicates an increased risk of
Haemolitic Membrane Desease

 postnatal:
I. noninvasive monitoring
-SaO2
-Transcutaneous blood gas
-Blood presure
MHD – Laboratory exams 2
 II. Acido-base balance monitoring can releave
- hypoxia
- hypercarbia
- Metabolic acidosis initially and then respiratory

 III. Radiological examination

In 10% of cases radiological examination may be normal
Were described four stages of damage and gravity
-Normal Image
-Buckling broadcast
-Drawing reticulo-granular
-Appearance of glass mat with air leakage bronhograma

 IV. ECG and Echocardiography necessary to determine cardiac

involvement
MHD – Laboratory exams 3

 V. Determinations Blood - Ht, Hb can be low

 VI. Blood ionogram , urea, creatinine, glucose - of

necessary to specify metabolic complications
 VII. Bacteriological culture for infective risk
assessment
MHD - Diagnostic

The history of risk factors

Clinical examination

Laboratory exams

Radiological examination

Evolution
MHD – Diagnostic 2

st.III
 It will be made between diferent pulmonary and extrapulmonar respiratory
disorders:
 Anemia, polycythemia, hypovolemia HMD – Differential



MCC
Aspiration Syndrome
Diagnostic
 Metabolic disorders: - hypoglycemia, hypocalcemia, hyponatremia,
hypomagnesemia, acidosis.
 Hypothermia
 Pneumomediastinum
 Pneumonia
 Pneumothorax
 Persistent ductus arteriosus
 Congenital abnormalities of the lungs
 DRS caused by neurological disorders: accompanied by tone disorder, seizures,
coma
MHD - Evolution

 It might be slowly progressive

 Before surfactant therapy, it could

load to death in 48-72 hours or to
spontaneous amelioration
HMD – Prevention

Intratracheal instillation of a
surfactant (Curosurf, Survanta)
immediately after birth to
premature infants at high risk of
developing RDS
HMD – Treatment

 Prophylactic
 Avoiding premature births and unjustified
caesarean section
 - Synthetic corticosteroid administration of 48-72
hours antepartum to all patients at high risk for
respiratory distress (except cases of diabetes,
toxemia caused by gravidity, kidney disease).
HMD – Treatment

 Ethyologic
Etyologic - administration of
exogenous surfactant natural or
synthetic. It can be used for
prophylactical purpose in the delivery
room; after 12h it can be repeated.
HMD – Treatment
Supporting meassures
 Maintaining thermal balance
 Monitoring vital signs
 Oxygenotherapy according to pulse oximetry and blood gases with:
- The mask
-CPAP
-Mechanical ventilation (SaHbO2 <88%, PaO 2 <45mmHG, PaCO2>
60 mm Hg, pH <7.25 FiO2 60%)
 Parenteral nutrition fluid restriction
 Antibiotic prophylaxy (ampicillin + gentamicin)
 Red blood cell transfusion if Ht keeps > 41%
HMD - Complications
 Precocious
Infections
Intaventricular hemorrhage
Ductus arteriosus
Pneumothorax
 Late
Bronchopulmonary dysplasia
Retinopathy of prematurity
Neurological sequelae
HMD – evolution and prognostic

Depends by:
1. Gestational age
2. Birth type
3. Complications
4. Level newborn department. (because of
technical conditions)

 Despite to all preventive measures and treatment -

mortality remains increased at a rate of 10-80%