Hyaline Membrane

Disease(HMD)
（ Respiration Distress Syndrome, RD
S）
NICU Affiliated Hangzhou First People’s

Hospital, Zhejiang University School of Medicine

 Outline
1. Definition: be known
2. Etiology: be known
3. Clinical findings: be mastered
4. Assistant examination: be mastered
5. Diagnosis: be mastered
6. Complication: be known
7. Treatment: be mastered
8. Prevention: be known
9. Prognosis: be known
This is a real case in China. The premature
baby in the video was only 790 grams at birth
and had difficulty breathing after birth.
A video of NRDS
 1. Definition

RDS is due to the lack of pulmonary

surfactant(PS), resulting in respiratory dis-

tress shortly after birth, and progressive

exacerbation of clinical syndromes, often in
premature infants.
 2. Etiology

HMD occurs primarily in premature infants.

 Infant less than 28wk of GA: 60-80%

 Infant between 28 and 32wk: 60%

 Infant between 32 and 36 wk of GA: 15-30%

 Infant beyond 37wk of GA: 5%

 But WHY?
Because of deficiency of pulmonary
surfactant (PS).
 The curve shows that PS is produced by the alveolar
type II cells and peaked at 35-36 weeks’ gestation.
So the premature infants with small gestational age
are more likely to have this disease.
 2. Etiology

The consequences of a lack of surfactant

are poor lung compliance and atelectasis.
The infant must expend a great deal of
effort to expand the lungs with each breath,
and respiratory failure ensues.
 3. Clinical Findings

(1)Symptoms
a) Onset near the time of birth or within 4-
6h after birth.
b) Rapid, shallow respiratory ≥60/min.
c) Intercostal and subcostal retractions and
progressive respiratory distress.
 3. Clinical Findings

d) Expiratory grunt.
e) Cyanosis and pallor.
f) Hypothermia.
g) Hypotension.
h) Pulmonary or intraventricular hemorrhage.
i) Course to death or improvement 3-5d.
 3. Clinical Findings

(2) Signs

On auscultation, air movement is

diminished despite vigorous
respiratory effort.
3. Clinical Findings
4. Assistant examination

(1) Laboratory examinations

foam test

lecithin/sphingomyelin(L/S)

blood gas analysis

4. Assistant examination Figure 1

(2) Imaging
 Mild: Chest x-ray
demonstrates diffuse
bilateral atelectasis,
causing a ground-glass
appearance in figure1.
4. Assistant examination Figure 2

 Moderate: Major
airways are
highlighted by the
atelectatic air sacs,
creating air
bronchograms in
figure2.
4. Assistant examination Figure 3

 Severe: NRDS is
characterized by
white lung in
figure3.
 5. Diagnosis

(1) Clinical manifestations

(2) Chest X ray

 6. Complication

(1) Pulmonary air leak.

(2) Patent ductus arteriosus.

(3) Intracranial Hemorrhage.

(4) Bronchopulmonary Dysplasia(BPD).

 7. Treatment
(1) Oxygen therapy.
(2) Early intubation and application of ventilator when
necessary.
(3) Placement of umbilical artery and vein lines.
(4) Exogenous surfactant replacement therapy.
(5) Antenatal administration of corticosteroids to the
mother.
 7. Treatment

Ventilation modes:
A ventilator that can deliver breaths synchronized
with the infant’s respiratory efforts(SIMV)
should be used if available.
High-frequency ventilators are also available for
rescue of infants doing poorly on conventional
ventilation or who have air leak problems.
Three exogenous surfactant
(Be given intratracheally)
 Why do newborns use PS?
1. Surfactant replacement therapy, used both in the
delivery room as prophylaxis and with established
HMD as rescue, decreases the mortality rate in
preterm infants and decreases air leak complications
of the disease.
2. During the acute course, ventilator settings and
oxygen requirements are significantly less in
surfactant-treated infants than in control subjects.
 Why do newborns use PS?

3. The availability of surfactant replacement therapy

has encouraged earlier intubation of infants with
HMD.
4. Surfactant replacement has also been used with
some success in term infants with secondary
surfactant deficiency resulting from pneumonia or
meconium aspiration.
 Why do newborns use PS?

5. A prophylactic strategy offers some advantage

in those infants born at 26 weeks’ gestation or
less.

6. For infants over 26 weeks’ gestation, early

rescue therapy is the strategy of choice.
 Method of use
 The first dose is administered as soon as possible
after birth, preferably before 2-4h of age.
 The second dose should be administered to infants
remains ventilated on over 30%-40% inspired
oxygen concentration.
 The usual dosing schedule is a total of two or three
doses given 6-12h apart. Rescue surfactant is given
as two to four doses 6-12h apart.
 8. Prevention

(1) Prevention of preterm labor.

(2) Promotion of fetal lung maturity.
(3) Prophylactic using PS.
 9. Prognosis

(1) Of infants with HMD, 80% to 90% survive,

and most of the survivors have normal lungs by
1 month of age.
(2) Those with a protracted chronic course have
a high incidence of respiratory illness with
wheezing in the first years of life.
 9. Prognosis

(3) Although most lung functions become normal,

they tend to have reduced expiratory flow rates and
in late childhood often have exercise or
methacholine-induced bronchospasm.
(4) Premature infants with neonatal respiratory
distress are more likely to have developmental
disbilities than prematurely born infants without
neonatal respiratory distress.
 Notice
There are two contents for the clinical
internship on October 10th, which I will teach.
The first content is about the characteristics of
normal full-term infants and premature
infants. The traditional teaching method will
be adopted, which is to watch the video in the
NICU classroom before going to the ward to
check the children.
 Notice
The second part adopts case-oriented
teaching mode. The specific case is as
follows. Please review relevant knowledge
according to today's lesson before the
probation class, then we will discuss on
clinical internship on October 10.
 A Case
The child, male, was admitted to hospital 10
minutes after birth due to shortness of air and
vomiting.
The child, G2P1, was
born at 31 weeks of
gestation by caesa-
rean section due to a
threatened of
premature labor.
 A Case

The birth weight was 1420g, without

prenatal hormone therapy, amniotic fluid
was clear at birth, no premature rupture of
membranes, Apgar score was 9 in 1 and 5
minutes after birth, and there were no
abnormalities in umbilical cord and placenta.
 A Case
After delivery, the child presented shortness
of breath and spitting, accompanied by groans,
no screams and convulsions, no milk has been
fed, no vomiting or abdominal distension,
defecation was resolved, and urination was not
resolved. The child was transferred to NICU
with T combined CPAP ventilation.
 A Case

Physical examination on admission

Body temperature 34.8℃

Pulse 103 beats/min

Respiration 60 beats/min

Blood pressure 62/19(31) mmHg

 A Case
Percutaneous oxygen saturation during T
combination use is about 80%, consciousness, well
reaction, scattered hemorrhagic spots can be seen
throughout the skin, breathing faster, auscultation
of low breath sounds in both lungs, no rales heard,
arrhythmias were maintained and no murmurs were
heard, liver and spleen were not swollen, umbilical
fresh, no bleeding, lower limb muscle tension,
attenuation of primary reflex.