Relationship of pneumothorax to occurrence of intraventricular hemorrhage in the premature newborn

Blood flow velocity was measured in the anterior cerebral after-ies by a transcutaneous Doppler technique in nine infants who developed pneumothorax in the first 3 days of life.. The ch

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1982;69;144

Pediatrics

Alan Hill, Jeffrey M Perlman and Joseph J Volpe

Premature Newborn Relationship of Pneumothorax to Occurrence of Intraventricular Hemorrhage in the

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Relationship of Pneumothorax to Occurrence

144 PEDIATRICS Vol 69 No 2 February 1982

Alan Hill, MD, PhD, Jeffrey M Penman, MB, and Joseph J Volpe, MD

From the Departments of Pediatrics, Neurology, and Biological Chemistry, Washington University School of Medicine, St Louis

ABSTRACT The relationship of pneumothorax to the

ob-jective of the study was to determine whether the

sys-temic hemodynamic changes that occur with

pneumotho-rax are reflected in the cerebral circulation and whether

these changes play a role in pathogenesis of IVH Blood

flow velocity was measured in the anterior cerebral

after-ies by a transcutaneous Doppler technique in nine infants

who developed pneumothorax in the first 3 days of life.

At the time of pneumothorax there was a marked increase

in flow velocity, especially during diastole, and, with

normal levels over the ensuing hours The changes in flow

velocity correlated closely with systemic hemodynamic

changes that occurred with pneumothorax, ie, an increase

in mean systemic blood pressure, especially diastolic

pres-sure IVH, documented by serial ultrasound scans, was

observed shortly after pneumothorax in the nine infants

The data thus demonstrate a marked increase in flow

velocity in the cerebral circulation at the time of

pneu-mothorax. This increase is of importance in the genesis of

IVH as is suggested further by the occurrence of IVH

soon after the cerebral hemodynamic changes. Pediatrics

69:144-149, 1982; pneumothorax, cerebral hemodynamic

changes, intraventricular hemorrhage.

Pneumothorax is a frequent complication of

me-chanical ventilation in the premature infant with

hyaline membrane disease.’ Recent studies2’3 have

reported an association between the occurrence of

pneumothorax and intraventricular hemorrhage

(IVH) in such infants However, a direct

Received for publication June 8, 1981; accepted Aug 28, 1981

Reprint requests to (J.J.V.) St Louis Children’s Hospital,

Wash-ington University School of Medicine, P0 Box 14871, St Louis,

MO 63178

American Academy of Pediatrics.

which occur as a result of the pneumothorax, and

which may lead to IVH, has not been demonstrated Because of the likelihood of disturbed cerebral

au-toregulation in the premature infant,4 such systemic

hemodynamic changes could be reflected directly

in the cerebral circulation with consequent rupture

IVH.5’6

The noninvasive measurement of cerebral blood flow velocity by a transcutaneous Doppler

tech-nique has been demonstrated in the newborn.7’8 In the present study, this technique was used to define

the changes in flow velocity in the anterior cerebral

arteries (ACAs) of newborn infants with

marked increases in flow velocity in the ACAS, followed by IVH.

METHODS Patient Population The study group comprised 80 newborn infants

admitted to the neonatal intensive care unit of St

Louis Children’s Hospital between September 1980 and July 1981 Birth weights ranged from 650 to

1,500 gm (mean 900 gm) Mean gestational age was

30 weeks.

Diagnosis of Intraventricular Hemorrhage

Intraventricular hemorrhage was diagnosed by real-time ultrasound scan with an ATL (Advanced Technology Laboratories) sector scanner with

5-MHz rotary scan head placed over the anterior

fontanel Coronal images were defined by a plane through the Sylvian fissures and the head of each

caudate nucleus. Parasagittal images were defined

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P1 : S-D

ARTICLES 145

by a plane through each lateral ventricle Scans

were performed on the first day of life and then

daily for patients requiring mechanical ventilation

Additionally, ultrasound scans were performed on

other occasions as indicated, eg, sudden

deteriora-tion in clinical condition or presence of RBCs in

CSF; specifically, following pneumothorax, the

ul-trasound scan was repeated as soon as possible

Measurement of Pulsatility Index

Blood flow velocity in the ACAS was measured

with a Doppler flowmeter (Medasonics Versatone

D-9) and two-channel recorder With the infant

quiet and in supine position, a 5-MHz transducer

(Medasonics P-94) was placed over the anterior

fontanel and directed toward each ACA

independ-ently Arterial pulsations were recorded and the

mean systolic and diastolic amplitudes of flow were

measured relative to a 1-kHz internal standard A

Bada et al7 from Pourcelot’s index of resistance.9

Excellent correlation has been shown between this

index and the extent of resistance to flow in the

carotid arteries, as demonstrated by cerebral

those with carotid occlusive disease.’#{176} The

deriva-tion of the index is shown in Fig 1 It can be seen

that P1 will vary inversely with blood flow velocity,

particularly diastolic flow velocity Thus, a high P1

is observed with low flow velocity, and a low P1 is

found with high flow velocity.

The P1 measurements in each ACA of individual

patients differed by <0.02 A sequence of at least

five peaks with highest amplitude were used for the

calculation of P1 P1 measurements were made daily

from the first day of life and more frequently if

there was change in the infant’s clinical state When

pneumothorax occurred, P1 was measured as soon

as possible and repeated frequently (not less than

three times daily) until the pneumothorax resolved.

Our normal value for P1 in the first month of life is

0

Fig 1. Tracing of pulsations in anterior cerebral arteries

(ACA) showing internal calibration of 1 kHz, mean

sys-tolic (5), and mean diastolic (D) amplitudes of flow and

formula for calculation of pulsatility index (P1).

gestational age from 30 to 40 weeks, without obvious evidence of cardiac, respiratory, or intracranial dis-ease

Diagnosis and Management of Pneumothorax The diagnosis of pneumothorax was made on the basis of clinical findings, ie, deterioration in clinical

condition, pallor, increased respiratory distress,

de-creased breath sounds on the affected side, and deterioration in blood gases, and was confirmed by

radiologic findings ofextra-alveolar air with or

with-out shift of mecliastinum Treatment was by chest tube connected to underwater drainage Subse-quent chest radiographs were obtained to assess

resolution of the pneumothorax, and to check chest

tube placement.

Measurement of BlOOd Pressure Seven patients had an umbilical artery catheter

in place; thus, both systolic and diastolic blood pressures were recorded The catheter was con-nected by a Sorensen Intraflo System to a trans-ducer (Bell and Howell) and a continuous record of blood pressure was provided by an Abbott’s arterial

pressure monitor In the remaining two patients, systolic blood pressure was recorded by a transcu-taneous Doppler technique.

RESULTS Relationship of IVH to Pneumothorax Nine infants with tension pneumothorax, which

occurred between birth and 3 days of age, were

observed The age of occurrence of pneumothorax was <12 hours in four infants and between 12 and

36 hours in five infants In each case, IVH, docu-mented by ultrasound scan, was observed soon after

pneumothorax

The temporal relationships of IVH to the occur-rence of pneumothorax are presented in Table 1 In

six infants (patients 1 through 6), serial ultrasound scans demonstrated absence of IVH prior to the

pneumothorax The interval of time between

nor-mal ultrasound scan and occurrence of

pneumotho-rax was two hours in two patients, and 12 hours in four patients In these six infants, IVH was diag-nosed 0.5 hour after pneumothorax in one patient, two hours in one patient, six hours in one patient,

patient In three infants (patients 7 through 9),

ultrasound examination was not performed prior to occurrence of pneumothorax In patient 7, pneu-mothorax was observed at the age of 1 hour, and a small IVH was detected on the first ultrasound scan

at the age of 11 hours The size of the IVH

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TABLE 1 Temporal

and Intraventricular He

Relationships of Pneumothorax

morrhage (IVH)

Diagnosis of

Pneumotho-rax (hr)

Interval from Normal

Ultrasound Scan to

Diag-nosis of Pneu-mothorax (hr)

Interval from Diagnosis of

Pneumothorax

to Diagnosis

of IVH (hr)

36

-t 2t

11 0.5

* See text for details

t Pneumothorax occurred prior to ultrasound scan

strictly normal) prior to diagnosis of pneumothorax

Fol-lowing pneumothorax, however, ultrasound scan showed

massive extension of IVH

mined by serial ultrasound scans) remained

con-stant until recurrence of extraalveolar air at age 36

exten-sion of IVH In patient 8, pneumothorax was

ob-served at the age of 10 hours, and IVH was seen on

the first ultrasound scan at the age of 16 hours In

patient 9, whose condition was stable clinically until

the pneumothorax occurred at the age of 6 hours,

IVH was diagnosed within 0.5 hour

Changes in Pulsatility Index with Pneumothorax

The changes in P1 that accompanied

pneumotho-rax are listed in Table 2 Prior to pneumothorax,

the P1 values in patients 1 through 7 ranged from

0.54 to 0.69 (mean ± SE 0.63 ± 0.04) With the

occurrence of pneumothorax, the range of P1 values

decreased to 0.35 to 0.52 (mean ± SE 0.41 ± 0.06).

In patients 8 and 9, P1 and ultrasound studies were

not obtained prior to development of

pneumotho-rax However, at the time of pneumothorax, the P1

values were low in each case (0.42 and 0.36)

Follow-ing drainage of the pneumothorax, the P1 values

increased to normal in the eight infants on whom

measurements were made (range 0.64 to 0.74, mean

± SE 0.70 ± 0.03). This normalization of blood flow

velocity occurred during a period of 30 hours (Fig

2) The decrease in P1 at the time of pneumothorax

and the return to normal values following resolution

are statistically significant (P < 001) (During the

course of this study we observed one infant who

exhibited similar changes in P1 with pneumothorax,

but who did not develop IVH.)

In Fig 3 are shown the changes in the cranial

Doppler tracings, before, at the time of, and after

resolution of pneumothorax, in a typical case The

decrease in P1 is principally due to a marked in-crease in the diastolic component of flow velocity

in the ACM, and to a lesser extent, to an increase

in systolic flow velocity (Fig 3) These changes appear to reflect the changes in diastolic and sys-tolic blood pressure (see next section), which may

be transmitted to the cerebral vessels in a pressure-passive manner because of impaired autoregula-tion.4

TABLE 2 Relationship of Pulsatiity Index (P1) to

Pneumothorax

Pa-tient

Pulsat iity Index (Mean ± SE)

Pneumothorax

4 0.69 ± 0.03 0.47 ± 0.02 0.68 ± 0.04

* Data shown refer to second pneumothorax (see Table 1); no measurements were made prior to or at time of first

pneumothorax, which occurred at another hospital.

t Pneumothorax occurred prior to P1 measurements.

TIME (HOURS)

Fig 2. Time course of changes in pulsatiity index (P1)

with occurrence and resolution of pneumothorax Note marked decrease in P1 at time of pneumothorax and

subsequent return to normal values within 30 hours

Fig 3. Typical Doppler tracing in an infant before (A),

at the time of (B), and following resolution (C) of pneu-mothorax Note increase in diastolic flow velocity and

thus decrease in pulsatility index at time of pneumotho-rax

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ARTICLES 147

TABLE 3. Pressure (BP) to Pulsatility Index (P1) Before and at Time of Diagnosis of Pneumothorax

7*

Changes in Blood Pressure with Pneumothorax

pneumothorax are shown in Table 3 In each of the

these infants there was a consequent narrowing of

pulse pressure The mean blood pressure increased

in all cases These changes in diastolic pressure (P

pressure (P < 01) are statistically significant.

Changes in pH and Pco2 Values in Infants with

Pneumothorax

The pH and Pco2 values were determined in each

pH occurred in each infant at the time of

pneumo-thorax and an increase occurred following

resolu-tion Mean values ± SD prior to, at the time of, and

following resolution of pneumothorax were,

There was an increase in Pco2 in each infant at the

resolution Values prior to, at the time of, and

following resolution of pneumothorax were,

respec-tively, 42 ± 5, 54 ± 4, and 45 ± 4 The individual

changes in pH (P < 0001) and Pco2 (P < 01) for

each patient were statistically significant

CASE REPORT

The following case history illustrates the major

rela-tionships between pneumothorax, IVH, and blood flow

velocity in the ACAs

The patient was born at 27 weeks’ gestation to a

20-year-old gravida 2, para 0 following a pregnancy that was

uncomplicated until the time of premature labor Birth

weight was 1,000 gm and Apgar scores were 4 and 7 at

in-tubated immediately following delivery Chest radiograph

Pressure Respirator At age 4 hours, an ultrasound scan

of the head was normal (Fig 4, top) and the P1 was 0.63

At age 6 hours, there was a sudden clinical deterioration,

characterized by pallor and marked deterioration in blood gases Transillumination of the chest indicated

pneumo-thorax, which was confirmed by chest radiograph The P1

underwater drainage Thirty minutes following insertion

of the chest tube, ultrasound scan of the head showed

massive IVH (Fig 4, bottom) Subsequent chest radio-graphs showed resolution of the pneumothorax, but two

Fig 4. Ultrasound scans (coronal section) of patient 1

prior to (top) and 30 minutes following (bottom) pneu-mothorax Top, No defmite hemorrhage in subependymal

intraventricular hemorrhage, greater on right than on left

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IDECREASEDVENOUS RETURN]

OUTPUT

PRESSURE

INCREASE PRES

) VENOUS

URE

IN GERMINAL MATRIX CAPILLARIES

the infant died.

DISCUSSION

The present data report marked changes in blood

flow velocity in the ACAS with the occurrence and

resolution of pneumothorax in premature newborns

direct relationship between pneumothorax and IVH

has also been described The changes in flow

veloc-ity suggest a mechanism by which pneumothorax

may lead to IVH in the premature newborn.

A close association between pneumothorax and

the occurrence or exacerbation of IVH has been

reported previously.2’3 Thus, Lipscomb et al3 have

reported that of 14 ventilated premature infants

who developed pneumothorax, 12 (86%) developed

IVH In an extensive study of IVH, reported by

Dykes et al,2 the presence of extraalveolar air was

shown to be a significant risk factor for the

devel-opment of IVH These studies raised the question

IVH are separate consequences of some common

event(s) The data presented in this report suggest

that the relationship between pneumothorax and

IVH is an etiologic one and that the pathogenetic

mechanism includes an abrupt increase in cerebral

blood flow at the time of pneumothorax.

A proposed scheme of the sequence of systemic

and cerebrovascular hemodynamic events by which

pneumothorax may lead to IVH is shown in Fig 5

It has been shown in animal studies that

pneumo-thorax causes an increase in intrathoracic pressure

which, in turn, causes a decrease in venous return

to the heart.’ The decrease in venous return may

be accentuated by the increase in pulmonary

vas-cular resistance that follows lung collapse.’ The

important result is a decrease in cardiac output.

Thus, Simmons et al,” in a study of acute

circula-tory effects of pneumothorax in dogs, have

demon-strated a decrease in cardiac output followed by a

compensatory increase in peripheral vascular

re-sistance and an increase in mean systemic blood

pressure In related experiments in human adult

patients, increased intrathoracic pressure (eg, as

occurs with the Valsalva maneuver) has been shown

to cause a decrease in both cardiac output and in

pulse pressure.’2 The narrow pulse pressure, by

and aortic arch receptors, causes reflex

vasocon-striction of the systemic circulation.’2 Animal

stud-ies have also confirmed that a narrow pulse pressure

produces an increase in systemic blood pressure

secondary to an increase in peripheral

vasoconstric-tion.’3 Our observations agree with these findings;

NCREASED PERIPHERAL RESIS ‘ANCE

BLOOD PRESSURE

(PRINCIPALLY DIASTOLIC)

ftpH,tpCO

VELOCITY IN ACA

Fig 5. Proposed scheme of sequence of systemic and

pneumo-thorax may lead to intraventricular hemorrhage (see text

for details) ACA, anterior cerebral arteries; P1, pulsatility index.

thus, a consistent increase in diastolic and mean systemic blood pressure, together with a narrow

pulse pressure, was documented with

pneumotho-rax The decrease in P1 in the ACAS at the time of

principally diastolic flow velocity These changes in cerebral blood flow velocity reflect the systemic

the presence of impaired cerebral vascular autoreg-ulation in the premature infant with

pneumotho-rax,4 the increase in mean systemic blood pressure,

particularly diastolic blood pressure, may be

trans-mitted directly to the cerebral vessels in a

pressure-passive fashion and a disproportionate amount of the systemic arterial circulation may be directed

toward the cerebral vessels during diastole The

increase in Pco2 (and acidemia) that may

accom-pany pneumothorax could act further to increase blood flow to the brain by dilating cerebral vessels.’4 Finally, in addition to the effects on the arterial side of the circulation, impeded venous return to

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ARTICLES 149

the heart may result in generalized venous

conges-tion and, more importantly, an increase in cerebral

venous pressure (Fig 5)#{149}15 The latter might be

ex-pected to cause a decrease in arterial flow velocity

rather than the increase that we have reported The

fact that an increase does occur suggests that the

cerebral capillary bed is subjected to simultaneous

pressure-flow stresses from the arterial and the

venous sides of the circulation Those capillaries

most vulnerable to such stresses, eg, those of the

germinal matrix, would be likely to rupture and

result in IVH. This final result, ie, P/H, was

docu-mented shortly after pneumothorax and the

asso-ciated alterations in cerebral blood flow velocity.

Note Added in Proof. Since the submission of this

manuscript, we have observed six additional premature

infants in whom IVH was documented within ten minutes

to six hours after the occurrence of pneumothorax in the

first two days of life In each case, the changes in blood

flow velocity described in this report were documented.

REFERENCES

1 Monin P, Vert P: Pneumothorax Clin Perinatol 5:335, 1978

2 Dykes FD, Lazzarra A, Ahmann P, et al: Intraventricular

hemorrhage: A prospective evaluation of etiopathogenesis.

Pediatrics 66:42, 1980

3 Lipscomb AP, Thornburn RJ, Reynolds EOR, et a!:

Pneu-mothorax and cerebral hemorrhage in preterm infants

Lan-cet 1:414, 1981

4. Lou HC, Lassen NA, Friis-Hensen B: Impaired

autoregula-tion of cerebral blood distressed newborn J

Pediatr94:118, 1979

5 Pape KE, Wigglesworth JS: Hemorrhage, Ischemia and the Perinalal Brain. London, Spastics International Medical Publications, 1979

6 Volpe JJ: Neurology of the Newborn. Philadelphia, WB Saunders Co, 1981

7 Bada HS, Hajjar W, Chua C, et a!: Noninvasive diagnosis of

neonatal asphyxia and intraventricular hemorrhage by

Dop-pler ultrasound J Pediatr 95:775, 1979

8 Hill A, Volpe JJ: Decrease in pulsatile flow in the anterior cerebral arteries in infantile hydrocephalus Pediatrics 69:4, 1982

9 Pourcelot L: Diagnostic ultrasound for cerebral vascular disease, in Donald I, Levi S (eds): Present and Future in Diagnostic Ultrasound. Rotterdam, Kooker Scientific Pub-lications, 1976, p 141

10 Grossman BL, Wood EH: Doppler ultrasonic evaluation of

extracranial cerebrovascular disease, in Tarases JM,

Fisch-gold H, Dilenge D (eds): Recent Advances in the Study of Cerebral Circulation. Springfield, IL, Charles C Thomas,

1970,p 175

11. Simmons DH, Hemingway A, Ricchiuti N: Acute circulatory effects ofpneumothorax in dogs JAppiPhysiol 12:255, 1958

12 Sharpey-Schafer EP: Effect of respiratory acts on the

cir-culation, in Dow P (exec ed): Handbook of Physiology.

Section 2: Circulation, vol 3; WF Hamilton (section ed) Washington DC, American Physiological Society, 1965, pp 1875-1886

13 Ead HW, Green JH, Neil E: A comparison of the effects of pulsatile and nonpulsatile blood flow through the carotid

sinus on the reflexogenic activity of the sinus baroreceptors

in the cat JPhysiol 118:509, 1952

14. Lessen NA: Control of cerebral circulation in health and disease.Circ Res 34:749, 1974

15 deLemos RA, Tomosovic JJ: Effects of positive pressure ventilation on cerebral blood flow in the newborn infant

Clin Perinatol 5:395, 1978

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1982;69;144

Pediatrics

Alan Hill, Jeffrey M Perlman and Joseph J Volpe

Premature Newborn Relationship of Pneumothorax to Occurrence of Intraventricular Hemorrhage in the

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