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Pneumothorax in Preterm Infants: Ventilator Therapy Complication, Slides of Pathology

The occurrence and clinical implications of pneumothorax in preterm infants with hyaline membrane disease (HMD), particularly those receiving continuous distending pressure (CDP) or intermittent positive pressure ventilation (IPPV. The document emphasizes the importance of prompt diagnosis and treatment to prevent persistence or recurrence of pneumothorax and improve outcomes.

What you will learn

  • How does the use of CDP or IPPV affect the risk of pneumothorax in infants with hyaline membrane disease?
  • What are the clinical signs and symptoms of pneumothorax in infants with hyaline membrane disease?
  • What is the incidence of pneumothorax in infants with hyaline membrane disease?

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Archives
of
Disease
in
Childhood,
1975,
50,
449.
Pneumothorax
in
the
newborn
Changing
pattern
V.
Y.
H.
YU,
S.
W.
LIEW,
and
N.
R.
C.
ROBERTON*
From
the
Department
of
Paediatrics,
University
of
Oxford,
John
Radcliffe
Hospital
Yu,
V.
Y.
H.,
Liew,
S.
W.,
and
Roberton,
N.
R.
C.
(1975).
Archives
of
Disease
in
Childhood,
50,
449.
Pneumothorax
in
the
newborn:
changing
pattern.
The
clinical
course
of
pneumothorax
and
its
allied
conditions
was
studied
in
34
newborn
infants
who
presented
over
a
2a-year
period.
We
found
an
overall
incidence
of
3/1000
live
births.
11
term
infants
without
obvious
pulmonary
pathology
presented
early
(9
within
minutes
of
birth);
6
of
these
had
aspirated
meconium
or
blood.
The
remaining
23
were
preterm
infants
with
hyaline
membrane
disease
(HMD)
and
accounted
for
68
%
of
the
infants
in
this
series.
In
contrast,
they
presented
late
(mean
45
hours)
and
16
were
on
continuous
distending
pressure
(CDP)
or
intermittent
positive
pressure
ventilation
(IPPV)
at
the
onset
of
pneumothorax.
15
%
of
all
infants
with
HMD
who
required
CDP/
IPPV
developed
pneumothorax;
this
increased
incidence
was
most
evident
in
infants
who
received
CDP
only.
All
except
2
of
the
11
term
infants
in
the
first
group
were
managed
conservatively
and
all
survived.
When
pneumothorax
occurred
as
a
complication
of
HMD
in
preterm
infants,
14
of
the
16
infants
required
intrapleural
drainage.
Persistence
or
recurrence
of
pneumothorax
occurred
in
9
infants,
7
of
whom
were
receiving
CDP/IPPV
at
the
time.
Lung
expansion
was
affected
only
after
replacement
with
a
patent
chest
drain
through
the
same
incision
or
insertion
of
a
second
drain
on
the
same
side
of
the
chest.
All
5
deaths
occurred
in
the
group
of
preterm
infants
with
HMD.
3
resulted
direct-
ly
from
respiratory
failure
due
to
severe
HMD
complicated
by
pneumothorax.
We
emphasize
the
increasing
importance
of
pneumothorax
as
a
complication
of
HMD
in
preterm
infants,
particularly
in
those
receiving
CDP.
Successful
management
depends
on
prompt
diagnosis
and
treatment
of
pneumothorax,
which
may
occur
as
unexplained
sudden
deterioration
at
any
time
during
the
course
of
illness
in
this
group
of
high
risk
infants.
Pneumothorax
may
be
associated
with
severe
respiratory
distress,
and
particularly
in
the
presence
of
hyaline
membrane
disease
(HMD)
it
is
a
frequent
cause
of
sudden
deterioration
or
collapse.
Never-
theless,
it
is
one
of
the
few
pulmonary
diseases
in
the
newborn
period
in
which
prompt
treatment
can
be
life
saving.
Detection
in
newborn
infants
depends
as
much
on
a
high
degree
of
awareness
of
its
possibility
as
on
the
knowledge
of
its
predispos-
ing
factors
and
cincial
features.
We
present
our
experience
of
this
condition
over
the
last
2A
years
and
emphasize
the
increasing
importance
of
its
Received
11
November
1974.
*Present
address:
Department
of
Paediatrics,
Addenbrooke's
Hospital,
Cambridge.
occurrence
in
low
birthweight
infants
with
HMD
during
intermittent
positive
pressure
ventilation
(IPPV)
and
continuous
distending
pressure
(CDP).
Pneumomediastinum
and
pneumopericardium
are
included
in
the
analysis
as
they
are
probably
a
variant
of
the
same
underlying
pathology.
Clinical
observations
The
clinical
course
of
pneumothorax
and
pneumo-
mediastinum
was
studied
in
34
newborn
infants.
These
patients
represent
all
recognized
cases
of
pneumothoraces
and
allied
conditions
occurring
in
the
special
care
nursery
during
a
2A
year
period,
January
1972
to
July
1974,
with
the
exception
of
2
for
which
case
notes
were
incomplete.
3
infants
were
referred
from
other
hospitals
on
the
first
day
of
life.
449
pf3
pf4
pf5

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Archives of Disease in Childhood, 1975, 50, 449.

Pneumothorax in the newborn

Changing pattern

V. Y. H. YU, S. W. LIEW, and N. R. C. ROBERTON*

From the Department of Paediatrics, University of Oxford, John Radcliffe Hospital

Yu, V. Y. H., Liew, S. W., and Roberton, N. R. C. (1975). Archives of Disease in

Childhood, 50, 449. Pneumothorax in the newborn: changing pattern. The

clinical course of pneumothorax and its allied conditions was studied in 34 newborn

infants who presented over a 2a-year period. We found an overall incidence of 3/

live births. 11 term infants without obvious pulmonary pathology presented early (

within minutes of birth); 6 of these had aspirated meconium or blood. The remaining 23

were preterm infants with hyaline membrane disease (HMD) and accounted for 68 % of

the infants in this series. In contrast, they presented late (mean 45 hours) and 16 were

on continuous distending pressure (CDP) or intermittent positive pressure ventilation

(IPPV) at the onset of pneumothorax. 15 % of all infants with HMD who required CDP/

IPPV developed pneumothorax; this increased incidence was most evident in infants

who received CDP only.

All except 2 of the 11 term infants in the first group were managed conservatively and

all survived. When pneumothorax occurred as a complication of HMD in preterm

infants, 14 of the 16 infants required intrapleural drainage. Persistence or recurrence of

pneumothorax occurred in 9 infants, 7 of whom were receiving CDP/IPPV at the time.

Lung expansion was affected only after replacement with a patent chest drain through

the same incision or insertion of a second drain on the same side of the chest.

All 5 deaths occurred in the group of preterm infants with HMD. 3 resulted direct-

ly from respiratory failure due to severe HMD complicated by pneumothorax. We

emphasize the increasing importance of pneumothorax as a complication of HMD in

preterm infants, particularly in those receiving CDP. Successful management depends

on prompt diagnosis and treatment of pneumothorax, which may occur as unexplained

sudden deterioration at any time during the course of illness in this group of high risk

infants.

Pneumothorax may be associated with severe

respiratory distress, and^ particularly in^ the^ presence

of hyaline membrane disease (HMD) it is a frequent

cause of sudden deterioration or collapse. Never-

theless, it is one of the few pulmonary diseases in

the newborn period in which prompt treatment can be life saving. Detection in newborn infants depends as much on a high degree of awareness of

its possibility as on the knowledge of its predispos-

ing factors^ and^ cincial^ features.^ We present our

experience of this condition over the last 2A years and emphasize the increasing importance of its

Received 11 November 1974. *Present address: Department of Paediatrics, Addenbrooke's Hospital, Cambridge.

occurrence in low birthweight infants with HMD

during intermittent positive pressure ventilation

(IPPV) and continuous distending pressure (CDP). Pneumomediastinum and^ pneumopericardium are included in the (^) analysis as (^) they are (^) probably a variant of the same underlying pathology.

Clinical observations

The clinical course of pneumothorax and^ pneumo-

mediastinum was^ studied^ in^34 newborn infants.^ These

patients represent all^ recognized cases^ of^ pneumothoraces

and allied conditions (^) occurring in the (^) special care

nursery during a 2A year period, January 1972 to July

1974, with the exception of^2 for^ which^ case^ notes were

incomplete. 3 infants^ were^ referred^ from^ other^ hospitals

on the first day of life.

Yu, Liew, and Roberton

The overall incidence of pneumothoraces and (^) allied conditions was 3/1000 live births. This study includes 26 infants with pneumothoraces all of whom were symptomatic and in whom deterioration in respiratory symptoms had led to chest x-ray. 6 out of the 26 had coexisting pneumomediastinum (23%) and one had coexisting pneumopericardium. 6 other infants had isolated pneumomediastinum and 2 had severe pul- monary interstitial emphysema with lung cysts; these 8 were asymptomatic and were diagnosed on routine x-rays. Males were more than twice as common as females (24: 10). Pneumothoraces were found nearly twice as frequently on the right as on the left (R:L = 14:8) and 4 patients (15%) had bilateral pneumothoraces. The (^) infants studied can be separated into two distinct groups depending on whether there (^) was associated idiopathic respiratory distress syndrome-presumably HMD (Table I). The first group, that (^) of infants

TABLE I

Clinical data of infants with pneumothoraces and

allied conditions

Infants' without HMD Infants with HMD

No. 11 23 Gestation (w) 40 (38-41) 34 (27-38) Birthweight (g) 3453 (2710-4130) 2307 (990-3510) Age of onset (h) Birih 45 (12-140) (2 at 14 h) Apgar score at birth 4 or less 4 7 Endotracheal intubation and IPPV at birth 4 8 Aspiration of meconium or blood 6 0 CDP or IPPV at onset of (^) pneumothorax - (^16)

HMD, hyaline membrane disease; CDP, continuous (^) distending pressure; IPPV, intermittent positive pressure ventilation.

without obvious pulmonary disease, used to be the most

common: (^) they were (^) usually diagnosed in the first (^) hour of life, being mainly term or post-term infants presenting

with respiratory difficulty at delivery. There was often

a history of fetal distress, difficult delivery, or over-

zealous resuscitation, and evidence of aspiration of meconium, blood, or^ mucus. This group of 11 infants accounted for only 32% of pneumothoraces in Oxford. Their mean gestational age was 40 weeks (range 38 to (^41) w) and mean birthweight 3453 g (range 2710-4130 g). In 9 infants the signs were evident at delivery, while (^) in the remaining 2 pneumothorax was not obvious until 14 and 15 hours of age, respectively. There was a strong possibility of aspiration of meconium or blood as a predisposing event^ in^6 out of the 11 infants and the possible aspiration ofmucus could not be ruled out in (^) any infant. 4 ofthe pneumothoraces occurred in resuscitated infants, but it is not possible to ascertain to what extent overzealous resuscitative efforts or the underlying cause

of apnoea is responsible for the pneumothoraces.

3 infants in this group had coexisting pneumomediasti- num. In the second group, pneumothorax and pneumo- mediastinum occurred as a complication of HMD in 23 infants, and these accounted for 68% of the infants in this series. The types of air leak developing in the 23

cases are shown in Table II. Their mean gestational

TABLE II

Types of pneumothoraces and allied conditions

Infants without Infants with HMD (11) HMD (23)

Pneumothorax alone 7 12 Pneumothorax with pneumomediastinum 3 3 Pneumothorax with pneumopericardium 0 1 Pneumomediastinum alone 1 5 Severe pulmonary interstital emphysema 0 2 with lung cysts

age was 34 weeks (range 27-38 w) and mean birthweight was 2307 g (range 990-3510 g). All suffered from respi- ratory distress syndrome presumably due^ to^ HMD. Initial x-rays were (^) compatible with HMD and did not show (^) pneumothoraces. Onset of (^) pneumothorax was later than in the first group and occurred at a mean of 45 hours (^) postnatally (range 12 to (^140) h). The (^) diagnosis was strongly suspected in all 16 infants with (^) pneumo- thorax in this group before x-ray confirmation. 4 infants presented with acute collapse and 12 with un- explained but more gradual clinical deterioration during the course of the respiratory distress syndrome so that repeat chest x-rays were taken to detect possible pneu- mothorax. The remaining 7 infants, 5 of whom had pneumomediastinum without pneumothorax and 2 with severe pulmonary interstitial emphysema and lung cysts were^ detected^ by routine^ chest^ x-ray without antecedent clincial (^) suspicion. 12 of the 16 infants with pneumothorax were on either CDP (8 cases, mean duration 30 h, range 2-70 h) or IPPV (4 (^) cases, mean duration 23 h, range 2-120 h) at the time of onset of pneumothorax. All infants received a maximum CDP of 10 cm H20 except one early case in whom 15 cm H was (^) applied for a (^) period of 9 hours. The 4 infants (^) who developed pneumothorax (^) during IPPV were (^) being ventilated at a pressure of 40 cm H20. Only one infant was subjected to IPPV in association with positive end-expiratory pressure and this was discontinued 20 hours before the onset of (^) pneumothorax. The overall incidence of pneumothorax and allied conditions occurring in infants with HMD was 11% (23 out of 216). 15% of infants with HMD on CDP or IPPV developed these (^) complications (16 out of 106). This increased incidence was most evident in infants who had (^) received CDP alone and was lqwer in infants on IPPV (Table III).

Yu, Liew, and Roberton

have shown pneumothorax in 1 to 2% of all new-

born infants (Davis and Stevens, 1930; Solis-

Cohen and Bruck, 1934; Steele et al., 1971) and

the incidence of symptomatic cases was reported

to be 0 05-0 (^) 07% (Harris and Steinberg, 1954;

Howie and Weed, 1957; Chernick and Avery,

1963; Malan and de V. Heese, 1966). In some of

these earlier reports on 'spontaneous' pneumo-

thorax in the newborn, infants who had received

oxygen under positive pressure (Chernick and

Avery, 1963; Malan and de V. Heese, 1966) or who

had underlying HMD (Malan and de V. Heese,

1966) were excluded. Reports of pneumomediasti-

num and pulmonary interstitial emphysema, when

unaccompanied by pneumothorax were also not

included in these case summaries (Harris and

Steinberg, 1954; Howie and Weed, 1957), though

they are^ probably related (Ovenfors, 1964; Cald- well, Powell, and^ Mullooly, 1970; Thibeault et al., 1973). In this series, a (^0 3) % incidence of pneumo-

thorax and its allied conditions is reported. Low

birthweight infants with HMD accounted for 68%

of our cases. Previous studies have suggested that

the term infant is most at risk (Peterson and

Pendleton, 1955; Emery, 1956; Chernick and Avery,

1963), and it has even been suggested that in

preterm infants HMD is not a common predis-

posing factor (Kirschner and Strauss, 1964;

Grosfeld, Clatworthy, and Frye, 1970). More

recently it^ has^ been^ recognized that HMD^ signifi-

cantly increases the incidence of pulmonary inter-

stitial emphysema and pneumothorax (Thibeault

et al., 1973). With the increasing use of CDP

or IPPV in infants with HMD, pneumothorax has

become even more frequent (Lancet, 1973; Baum

and Roberton, 1974). Signs of air leak develop in

as many as 30% of infants on positive pressure

ventilation plus positive end-expiratory pressure

(Blake et al., 1973). In this series, 15% of infants

with HMD requiring CDP and/or IPPV developed

this complication and 24% of those treated with

CDP alone. The detection of pneumothorax in

this group of infants depended on a high degree of

awareness that the diagnosis must always be

considered when such infants have sudden or

unexpected deterioration at any time during CDP

or IPPV. Radiological confirmation may be

difficult as an anteroposterior x-ray may not be

sufficient. A horizontal beam, lateral ('cross- table') view of the chest with the patient in the supine position should always be done (Roberton,

1975). Pneumomediastinum as well as intra-

pleural air collecting at the top of the thoracic

cavity can be seen better in such a view.

Pneumothorax as a result of overzealous positive

pressure resuscitation of the apnoeic newborn

(Chernick and Reed, 1970; Chernick and Avery,

1963) is^ a^ less^ frequent occurrence, and in 7 of^ our

11 early pneumothoraces no IPPV had been given.

Neonatal resuscitation is safer today than in the

past. It is known that the water manometer

system in resuscitation apparatus can be unreliable

when used with excessively applied oxygen flow

(Mathias, 1966) and modification of such systems

by the addition of a deadweight relief valve (Hey

and Lenney, 1973) had been carried out in our

delivery rooms.

Breathing 100% oxygen accelerates the resorption

of a pneumothorax (Chernick and Avery, 1963;

Northfield, 1971). This form of^ therapy has

generally been successful in our group of infants

without HMD who had only moderately severe

respiratory difficulty from pneumothorax or who

had a pneumomediastinum alone. In contrast,

most of the infants in this series with underlying

HMD who developed pneumothorax did require

insertion of a chest drain. A continued air leak

into the pleural space, particularly in conjunction

with CDP or IPPV required application of suction

to prevent reaccumulation of air. But, in spite of

this, over half in this group had persistence or

recurrence of pneumothorax: 5 of these 7 were on

CDP or IPPV at the time. Such complications

often occurred in situations where the chest drain

became blocked or was clamped too soon. We

found it useful to replace a new drain through the

same incision or to insert a second one on the same

side of the chest under such circumstances. We

have maintained a policy of leaving the chest drain

in situ during the period in which the infant was

still receiving CDP or IPPV.

Overall mortality rate for pneumothorax in this series was 0 04 % (5 in 11 169 live births). The

prognosis for pneumothorax occurring in infants

without HMD was uniformly good and all the

deaths occurred in the preterm infants with HMD.

Mortality rate^ in^ the infants with HMD developing

pneumothorax was 31% (5 of 16), compared with a

mortality rate of 14% in cases of HMD without

pneumothorax (27 of 200). This difference is not

statistically significant (^) (X2 =^ 3X15, P > 0 05) and

clearly pneumothorax is likely to be more common

in infants with severe HMD since pulmonary

interstitial emphysema is more likely to occur and

higher inflation pressures with IPPV are necessary.

Thus the deaths in cases complicated by pneumo-

thorax, when promptly and (^) adequately treated, may

be more indicative of the severity of the HMD than

of the consequence of this complication.

452

Pneumothorax in^ the newborn^453

We thank Professor^ J. P. M. Tizard^ for advice^ and

help in the preparation of the manuscript.

REFERENCES Baum, J. D., and Roberton, N. R. C. (1974). Distending pressure in infants with^ respiratory^ distress^ syndrome.^ Archives^ of Disease in Childhood, 49, 771. Blake, A. N., Collins, L. M., Durbin, G. M., Hunter, N. J., MacNab, A. J., Reynolds, E. 0. R., and Sellens, G. (1973). Simplified mechanical ventilation for hyaline-membrane disease. Lancet, 2, 1176. Caldwell, E. J., Powell, R. D., and Mullooly, J. P. (1970). Inter- stitial emphysema: a study of physiological factors involved in experimental induction of the lesion. American Reviews of Respiratory Disease, 102, 516. Chernick, V., and Avery, M. E. (1963). Spontaneous alveolar rupture at birth. Pediatrics, 32, 816. Chernick, V., and Reed, M. H. (1970). Pneumothorax and chylo- thorax in the neonatal period. J7ournal of Pediatrics, 76, 624. Davis, C. H., and Stevens, G. W. (1930). Value of routine radio- graphic examinations of the^ newborn.^ American^ Journal of Obstetrics and Gynaecology, 20, 73. Emery, J. L. (1956). Interstitial emphysema, pneumothorax, and air-block in the newborn. Lancet, 1, 405. Grosfeld, J. L., Clatworthy, H. W., Jr., and Frye, T. R. (1970). Surgical therapy in neonatal air-block syndrome. Journal of Thoracic and Cardiovascular Surgery, 60, 392. Harris, L. E., and Steinberg, A. G. (1954). Abnormalities observed during the first six days of life in 8716 live-born infants. Pedi- atrics, 14, 314. Hey, E., and Lenney, W. (1973). Safe resuscitation at birth. Lancet, 2, 103. Howie, V. M., and Weed, A. S. (1957). Spontaneous pneumo- thorax in the first 10 days of life. Journal of Pediatrics, 50, 6.

Kirschner, P.^ A., and Strauss, L. (1964).^ Pulmonary^ interstitial emphysema in the newborn infant, precursors and sequelae. A clinical and pathologic study. Diseases of the Chest, 46, 417. Lancet (1973). Increasing the transpulmonary pressure in respira- tory-distress syndrome, 2, 244. Malan, A. F., and de V. Heese, H. (1966). Spontaneous pneumo- thorax in the newborn. Acta Paediatrica Scandinavica, 55,224. Mathias, (^) J. (1966). Resuscitation of the newborn. Lancet, 1, 262. Northfield, T. C. (1971). Oxygen therapy for spontaneous pneumo- thorax. British Medical J7ournal, 4, 86. Ovenfors, C. 0. (1964). Pulmonary interstitial emphysema: an experimental roentgen-diagnostic study. Acta Radiologica, 244, 1. Peterson, H. G., and Pendleton, M. E.^ (1955). Contrasting^ ro- entgenographic pulmonary patterns of the^ hyaline^ membrane and fetal aspiration syndrome. American^ journal of^ Roentgen- ology, 74, 800. Roberton, N. R. C. (1975). Recent Advances in Respiratory Diseases. Ed. by T. H. Stretton. Churchill, London. (In the press.) Solis-Cohen, L., and^ Bruck,^ S.^ (1934).^ A^ roentgen^ examination of the chest of 500 newborn infants for pathology other than enlarged thymus. Radiology, 23, 173. Steele, R. W., Metz, J. R., Bass, J. W., and Du Bois, J. J. (1971). Pneumothorax and pneumomediastinum in the newborn. Radiology, 98, 629. Thiebeault, D. W., Lachman, R. S., Laul, V. R., and Kwong, M. S. (1973). Pulmonary interstitial emphysema, pneumo- mediastinum, and pneumothorax. American journal of Diseases of Children, 126, 611.

Correspondence to Dr. V. Y. H. Yu, Department of

Paediatrics, John Radcliffe Hospital, Headington,

Oxford OX3 9DU.