Radiologic

Appearance

of Viral Disease of the Lower in Infants and Children

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DENNIS

Respiratory

Tract

OSBORNE1

The radiologic findings in 123 hospitalized children with viral disease of the respiratory tract due to adenovirus, respiratory syncytial virus, parainfluenza, influenza, measles, or herpes virus were retrospectively reviewed. Bronchial wall thickening, peribronchial shadowing, and/or associated perihilar streaking were present in 107 cases. Patchy pulmonary shadowing thought to reflect disease at a sublobular or lobular level was present in 72 cases, while areas of coalescent more homogeneous pulmonary shadowing were present in only 20 cases. In general the pulmonary abnormalities were widespread; on the average, two to three lobes demonstrated abnormal pulmonary findings. Poorly defined small pulmonary nodules, while radiologically unimpressive, were noted in 49

tract irrespective of the virus, although there are individual variations at the cellular level which enable the pathologist to sometimes make a definitive etiologic diagnosis. In an effort to determine whether this common pathologic pattern had a recognizable radiologic counterpart, I retrospectively surveyed the hospital records and radiographs of 123 children with a presumed viral infection of the lower respiratory tract.

cases.

were

Air trapping

was observed

In 61 cases.

Subjects The

Hilar adenopa-

1978

respiratory for initial

After

review

children,

123

mentation

200

had

had titers

Cases

children

the laboratory adenovirus,

of the

hospital

cases

with

a virus

for

and

123

one,

(4)

separately

was the usual Radiologic of poorly

this

probably

or

subsecondary

with

quently

associated

was thought or lobar area

of focal

Mixed above,

29

[16],

pulmonary

Road,

Epsom,

but all films

abnormal about

the

basis

[16],

areas

3-6 of

at the

the

mm

of with

pathology,

secondary

although

lobular

it could

An

shadowing. measuring

discretely with

air

margins

bronchogram.

consolidation

although

area

at least

defined

an

pulmonary

representing

were

represent

collapse.

to represent

level

On

density

quite

cases examination

as follows:

measuring

level

pulmonary

sionally

presentation,

these

analysis,

Multiple

consolidation

areas of focal pulmonary of water

of

classified

margins.

lobular

shadowing

clinical

18,

measles;

examined.

density

defined

virus;

eight,

radiographic

were

represents

Coalescent

documentation.

race,

shadowing.

water

obvious between one virus

syncytial

radiographs

abnormalities

respiratory (1)

influenza;

admission

the

examination.

reasons:

respiratory

were

in

long interval sera, (3) only

of

sex,

docuin situation,

serum

for the radiologic

illness

pulmonary

shadowing rather

the

The

.

elevation

five,

of these

Included

radiologic

Age,

and

basis

a patient’s

Patchy

for resand influ-

clinical

following

had

simplex.

evaluated

during

the

inappropriately collection 65

illness,

analysis.

convalescent

parainfluenza;

herpes of

with

titers were sefor evaluation

radiologic

appropriate

inadequate

cases,

26,

duration

Hospital

of 5 years

radiographs and

fourfold

and for

and

further

and

acute

and

adenovirus;

age

routinely screens parainfluenza

clinical

in an

cultured

excluded

estimate,

records

who,

between

the

Auckland

the

fixation are sent

and

adequate

selected

children

were

Of

at

under

complement When sera

mixed infection, (2) an the primary illness and titer

Methods

laboratory

The children had all been admitted to Princess and the Paediatric Infectious Diseases Unit, AuckBoard.

were

viral

and

virus

virus analysis.

were

survey

Received February 28, 1977; accepted after revision August 3, 1977. ‘Department of Radiology. Princess Mary Hospital for Children, 189 St. Andrew’s

January

Over

enza viruses. Mary Hospital land Hospital

Viruses are the major cause of respiratory tract infections in children [1-4]. Chanock and Parrot’s 1965 study, along with others, established that respiratory syncytial virus is the single most important viral pathogen of the respiratory tract in early life. However, parainfluenza [5], adenovirus [6], and the influenzal virus [7] have also been shown to be important causes of acute disease of the lower respiratory tract in children. Although undoubtedly other viruses exist that cause respiratory tract infection, the above are responsible for the majority of lower respiratory tract viral infections in children requiring hospitalization. The respiratory viruses appear to produce an essentially surface infection of the respiratory mucous membranes with temporary multiplication of virus in the mucosa. Typically there is necrosis of the ciliated epithehal, goblet, and bronchial mucous gland cells. These cells subsequently slough to the level of the basement membranes. The bronchial and bronchiolar walls become edematous and infiltrated with mononuclear cells, often with involvement of the penibronchial tissue and interlobular lung septae. Occasionally there is extension of necrosis and edema into the terminal air passages and alveolae. While whole lobules may be involved, the focal inflammatory response can affect only the penbronchial portions of the lobule. Less commonly localized or generalized hemorrhagic pulmonary edema may occur, and capillary thromboses may be present. As the process resolves there is epithelial regeneration and proliferation [8-15]. These gross and microscopic findings are seen in viral disease of the lower respiratory

Ray Society

the

of respiratory viruses, pinatory syncytial virus,

Introduction

130:29-33, Roentgen

of

reviewed.

elevated lected

thy was seen in only four cases and was unimpressive. There was a striking absence of pleural eftusion, pneumothorax, pneumatocele, and lung abscess in the patients examined.

Am J Ro.ntgenol 0 1978 American

records

again

of abnormal

7-10

mm,

occa-

not

infre-

and This

shadowing

at the secondary

it could

have

lobular

represented

an

of both

of the

collapse.

shadowing. mixed

Auckland,

0361

A combination

sublobular

and

lobar

consolidation.

New Zealand.

-803X/78/01

00-0029

$02.00

30

OSBORNE TABLE

Radiologic

Findings

Finding

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No. patients Shadowing: Patchy

Coalescent Mixed involved

wall

Parainfluenza

18

26

39

10

14

10

4

3

4 3

4 3

2-3

thickening

Respiratory

65

...

Bronchial

of the Lower

Adenovirus

r:;?,S

No. lobes

1

in Viral Infections

Influenza

Measles

5

8

4

5 3

. .. ...

Herpes

Total

1

123 72

...

1

...

2

Simplex

2

20 9

2

2-3

1

107 49 61 4

penibronchial

,

60

18

21

Nodules

26

11

7

Airtrapping

41

8

12 3

shadowing,penihilanlineanity

Hilar

Tract

1

adenopathy

Pleural efffusion Abnormal heart size

. . .

1 1

. .. ...

3

4 5

... “

1 . . .

...

. . .

. . .

. . .

. . .

. . .

2

..

. . .

. . .

1

.

Bronchial wall thickening, peribronchial shadowing, and perihilar linearity. Parallel line water density shadows in the middle third of the lung fields, probably involving the bronchi distal to the

second

or third

changes

were

streaky

linear

order.

gross,

When

there

shadows

of

the

were

water

bronchi

often

and

penibronchial

associated

density

extending

penihilar toward

the

periphery.

Nodules. poorly

Small

defined

Air trapping. tion

of

six

posteroantenior an

increased

size,

Pulmonary anterior

overinflation

ribs

or

hilar

of lobes

more flattening

retrosternal

counted. and

shadows

projections,

The number

were

rounded

1-2

mm

in diameter

with

margins.

of

the the

by visualizadiaphragm

on

diaphragm,

and

space.

that

contained

In addition,

pleural

adenopathy

suggested above

were

pulmonary

effusion,

abnormalities

abnormal

heart

noted.

Results Respiratory

Syncytial

Virus Fig. 1.-Typical acute pulmonary overinflation bronchial wall thickening,

respiratory syncytial viral pneumonia. patchy but widespread bronchopneumonia, and peribronchial shadowing.

Note

The usual duration of respiratory syncytial viral infection from its inception was about 2_2h/2 weeks in the patients analyzed. The dominant radiologic findings were bronchial wall thickening, penibronchial shadowing, and penihilar linearity present in 60 cases (table 1; fig. 1). Patchy pulmonary shadowing, which was equated with sublobular or lobular consolidation, was seen in 39 cases, while coalescent rather more homogeneous pulmonary shadowing was present in only 10 cases. It was common to have multiple areas of lung involved in the disease process, and on the average two to three pulmonary lobes were affected to some degree. Poorly defined pulmonary nodules were present in 26 cases, but they were unimpressive and in fact were often better seen in the later stages and early convalescent phase of the illness. Pulmonary air trapping was especially prominent, occurring in 41 cases.

shadowing, and penihilar linearity which were present in all 18 cases to a moderate or marked degree (table 1; figs. 2 and 3). Patchy pulmonary shadowing of moderate severity was present in 10 cases and coalescent more homogeneous pulmonary shadowing was present in four cases. More extensive mixed pulmonary shadowing was present in four cases. The consolidation was generally more extensive than with respiratory syncytial virus, but as with respiratory syncytial virus, it was usual for two to three lobes to present pulmonary abnormalities. Small poorly defined pulmonary nodules were present in 11 cases but were not a striking feature. Radiologic evidence of air trapping was present in eight cases.

Adenovirus

Parainfluenza

The usual duration of adenoviral infection varied from 2 weeks to 3 months. One death occurred in a patient who had an associated myocarditis. The dominant findings again were bronchial wall thickening, penibronchial

The usual duration of parainfluenza complications frequently secondary monia, was 21/2 weeks to 3 months. bronchial wall thickening, penibronchial ,

,

infection or its bacterial pneuAgain, widespread shadowing, and

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PEDIATRIC

PULMONARY

perihilar linearity were the most frequent findings, occurring in 21 of 26 patients (fig. 4). Patchy pulmonary shadowing was present in 14 cases. As with adenovirus and respiratory syncytial virus, radiologic abnormalities were present on the average in two to three lobes. Hilar adenopathy was seen in three cases; it was not at all prominent in patients with the other respiratory viruses. Influenza,

Measles,

and

Herpes

Simplex

In influenza and measles (table 1), consolidation was prominent as well thickening, penibronchial shadowing, earity. In measles, small nodules (fig. five cases. The case of herpes was radiograph demonstrated extensive widespread bronchial wall thickening consolidation (fig. 6)

patchy pulmonary as bronchial wall and perihilar lin5) were seen in all fatal. The chest pneumonia with and penibronchial

VIRAL

DISEASE

31

enza, parainfluenza, measles, and herpes [8-10, 13-15] to be treated as one entity for the purposes of radiologic analysis [17]. The most striking radiologic findings in the cases studied were bronchial wall thickening, penibronchial shadowing, and penihilar linearity, although the latter was

less

common.

These

changes

were

frequently

gen-

eral.zed Patchy shadowing presumably reflecting disease at a lobular or sublobular level, was evident in 72 of the 123 cases. Coalescent more homogeneous shadowing, which I equated with lobular or lobar disease, occurred less frequently (only 20 cases). On the average, pulmonary changes were present in two or three lobes. Nodules were relatively common (49 cases) but were generally unimpressive. It is thought that they probably reflect small sublobular foci of inflammation. Air trapping was frequent (61 cases) and bronchial wall thickening, penibronchial shadowing, and penihilar linear streaking were observed in 107 cases. It was not possible to differentiate between individual viruses in any one case, but it is apparent from the .

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32

OSBORNE

so common. Their presence should suggest ity of an accompanying bacterial infection. differentiation between a viral, bacterial, monary infection depends on pathologic and culture of involved tissue, the findings here suggest that the radiologist should suspect the presence of a viral infection respiratory tract.

the possibilWhile

final

or other pulexamination described be able to of the lower

ACKNOWLEDGMENTS I thank

Drs.

infectious Mrs.

D. Becroft,

diseases

Sharron

pathologist,

specialist,

Chapman

for

and their

provided

W.

interest

valuable

R. Lang, and

pediatric assistance.

secretarial

assist-

ance.

REFERENCES 1.

Dingle

JH.

Feller

respiratory 2.

Chanock fancy for

AE:

tract. RM,

and prevention.

Noninfluenzal

N Engi

Parrot

childhood:

J Med

RH:

Acute

present

Pediatrics

viral 254:465-471, respiratory

understanding

36:21-39,

1965

infections

of

the

1956 disease and

in

prospects

in-

tiple right and

Fig. 4.-Parainfluenzal infection areas of patchy shadowing lower lobe, bronchial wall perihilar linearity.

of lower respiratory tract. Note mulwith coalescence in apical segment of thickening. peribronchial shadowing.

PULMONARY

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PEDIATRIC

3. Jacobs JW, Peacock DB, Corner BD, Caul EO, Clarke SKR: Respiratory syncytial and other viruses associated with respiratory disease in infants. Lancet 1:871-876, 1971 4. CouvreurJ: Viral infections in which respiratory manifestations predominate, in Clinical Virology, edited by Debr#{233}R, Celers J, Philadelphia, Saunders, 1970, pp 501-507, 554597

VIRAL

DISEASE

33-

5. Chanock AM, Parrott RH, Johnson KM, Kapikian AZ. Bell JA: Myxoviruses: parainfluenza. Am Rev Respir Dis 88, suppl. : 152-166, 1963 6. Van Der Veen J: The role of adenoviruses in respiratory disease. Am Rev Respir Dis 88, suppl.: 167-180, 1963 7. Banatvala JE, Anderson TB, Reiss BB: Viruses in acute respiratory infection in a general community. J Hyg (Camb) 63:155-167, 1965 8. Spencer H: Pathology of the Lung, 2d ed. Elmsford, N.Y. Pergamon Press, 1968 9. Becroft DM0: Histopathology of fatal adenovirus infection of the respiratory tract in young children. J Clin Pathol 20:561-569, 1967 10. Louria DB, Blumenfeld HL, Ellis, JJ, Kilbourne ED, Rogers DE: Studies on influenza in the pandemic of 1957-58. II. Pulmonary complications of influenza.J Clin Invest 38:213265, 1959 11 . Stuart-Harris CH: Viruses of diseases of the respiratory tract.BrMedJ 2:869-878, 1962 12. Stuart-Harris CH: Respiratory viruses, ciliated epithelium and bronchitis.Am RevRespirDis 93:150-155, 1966 13. Aherne W, Bird T, Court DS, Gardner PS, McQuillin J: Pathological changes in virus infection of the lower respiratory tract in children . J Clin Pathol 23 : 7-1 8, 1970 14. Hers JFP, Mulder J: Broad aspects of the pathology and pathogenesis of human influenza. Am Rev Respir Dis 83 : 8497, 1961 15. Knight V: Viral and Mycoplasmal Infections of the Respiratory Tract. Philadelphia, Lea & Febiger, 1973 16. Miller W: The Lung. Springfield, Ill., Thomas, 1937 17. Conte P, Heitzman E, Markarian B: Viral pneumonia: roentgen-pathological correlations. Radiology 95:267-272, 1970