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B J Lavins and D L Hamilos obstructive airway physiology. Distal airway bronchomalacia resulting in severe http://chestjournal.chestpubs.org/content/97/2/489.
Distal airway bronchomalacia resulting in severe obstructive airway physiology. B J Lavins and D L Hamilos Chest 1990;97;489-491 DOI 10.1378/chest.97.2.489 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/97/2/489

Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1990by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692

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obtaining

information about for typing and help

Janigan

the accident andJoy with the manuscript.

Douglas

Karen

and

Table

l-Pilmonary

Test Resulte,

Function Prebronchodilator

Measurement

1980

September Pbstbronchodilator

REFERENCES L (% pred) L (% pred)

FEy,, 1 Guidotti

TL.

The

Environ

Res

1978;

15:443-72

2 Guidotti

TL.

Toxic

inhalation

and

oxides

changes.

functional

3 Jones

higher

CR,

exposure

EP,

Hall

AT,

to nitrous

4 Horvath

of nitrogen

fumes.

doPico

dioxide-induced

toxicology.

dioxide:

FVC,

JI.

Pulmonary

Thorax

GA,

1973;

pulmonary

effects

RA,

disease.

of acute

28:61-65

Dickie J Occup

Barbee

1.12 (35) 2.84 (80)

Nitrogen

HA. Med

1978;

chomalacia, not affecting the trachea or main-stem bronchi. She had been presumed to have severe steroid-dependent asthma and was referred to the National Jewish Center for Immunology and Respiratory Medicine (NJC).

20:

103-10 acid.

AJ,

JAMA

6 Crapo Hlth

Kropp

1955;

JD,

by

and

death

LY, Mercer

inhalation

from

fuming

nitric

RR. Alterations J Toxicol

in lung Environ

of oxidants.

13:301-21

7 Evans MJ. Cell death Witischi H, Nettesheim toxicology. Boca Raton, 8 Evans

Injury

BE, Chang

caused 1984;

S.

23:1022-24

Barry

structure

MJ.

cell renewal in small airways. In: P, eds. Mechanisms in respiratory Florida: CRC Press, 1982:192 gases. Environ Health Perspect 1984; 55:

Oxidant

and

85-95 9 Mustafa

MG,

in lung Dis

ozone

Ward

injury.

Rinaldo

DF. and

Biochemical

nitrogen

and

dioxide

metabolic

toxicity.

Am

changes Rev

Respir

118:1061-90

GO,

lung 11

Tierney

with

1978;

10 Till

PA.

Fed

JE.

Proc

Systemic

complement

1986;

Mediation

activation

and

acute

45:13-18

of ARDS

by leucocytes.

Chest

1986;

89:

590-93 12

Bone

RC,

Jacobs

syndrome.

In:

respiratory 96

failure.

Distal

Bone

Airway

Resulting Airway MAJ

ER,

Balk

RC,

New

George York:

BA.

Adult RB,

respiratory

Hudson

Churchill

LD,

distress eds.

Livingston,

Acute

1987:173-

Bronchomalacia

in Severe Obstructive

Physiology*

Bernardj

Lavins,

MC,

USA;t

B report

at

the

age

of

woman 18,

she

was in excellent began

to

health

experience

until

1980,

dyspnea,

when,

occasional

wheezing, and a productive cough. Results of pulmonary function tests (PFFs) in September 1980 are shown in liable 1. Her respiratory symptoms progressively worsened and from 1982 through 1985 required frequent bursts of steroid therapy. She was hospitalized in both 1984 and 1985 for exacerbations of her respiratory condition. Both ofthese exacerbations responded poorly to seven days of aggressive bronchodilator therapy and IV methylprednisolone. Table 2 shows results of PVFs from the 1985 admission.

By 1986, the patient was receiving continuous steroids. Between October 1986 and May 1987, prednisone in doses of3O to 100 mg/ day failed to relieve the dyspnea. In May 1987, the patient was referred to NJC for evaluation. At that time, she complained of occasional wheezing, dyspnea after walking 15 to 22.5 m, and a chronic cough, occasionally productive ofwhite sputum. The patient had no history of childhood asthma and had had chronic rhinitis with a negative skin test in 1982 and 1985. She had been employed as a hairdresser from 1978 through 1982 and had smoked one pack of cigarettes per day for three years but quit in 1981. Her family history disclosed no respiratory diseases. Her medications on admission were theophylline, 300 mg four times daily; prednisone, 30 mg daily; albuterol inhaler, two puffs four times daily, and 0.5 ml ofnebuhzed isoetharine every 4 h. The physical examination results were normal except for a respiratory rate of 20 breaths/min, a pulse rate of 120 beats/mm, a appearance,

and

significantly

decreased

breath

sounds,

with soft expiratory and

Daniel

L. HamiLos

M.D4

referred

steroid-d#{231}pendent

wheezes throughout both lung fields. A theophylline level was 17.5 g/ml and an a-antitrypsin level was 285 mg/dl (normal, 159 to 251 mg/dl). Results ofarterial blood gas analysis and pulmonary function tests are shown in ‘liable 3 and Figure 1; a pressure-volume curve is shown in Figure 2. A chest xray film exhibited evidence of air trapping and slightly increased

L ..

E of obstructive

R

adulthood

that

S

be confused with severe asthma. The following involves a 24-year-old woman with generalized

bron-

ronchomalacia pulmonary

may

woman,

A 24-year.old

cushingoid

for treatment of presumed asthma, was found to have generalized bronchomalacia. The diagnosis was based on an abnormal collapsibility of the bronchi on bronchoscopic examination and a lack of bronchial reversibility with aggressive bronchodilator therapy. (Chest 1990; 97:489-91)

A 24-year-old

severe

REPORT

CASE

5 McAdams

1.29(40)

3.24(91)

morphologic

Mol Pathol 1980; 33:90-103

Exp

Proudfoot

ofnitrogen-inhalation

is one of many causes disease in both infancy and

case

the National Jewish Center for Immunology and Respiratory Medicine, Denver. tFellow, Allergy-Immuno1og Fitzsimons Army Medical Center, Aurora, Co. jAssistant Professor of Medicine, University of Colorado School of Medicine; StaffPhysician, National Jewish Center for Immunology and Respiratory Medicine. The opinions or assertions contained herein are the private views ofthe authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of

PATIENT

PREDICTED 8

F1 L O Wc 0

5Fmm

Defense.

12

N D -8

-12

Ficua

1

VOLUME (LITERS)

.

Flow-volume

loop

obtained

at the

time

of admission

to

NJC.

CHEST

I 97

Downloaded from chestjournal.chestpubs.org by guest on July 10, 2011 © 1990 American College of Chest Physicians

I

2

I

FEBRUARY,

1990

489

Table

2-Pulmonary Admission

Measurement FEy,,

(%

L

*PFF5

Table

seven

days

ofIV

3-Pulmonary

1985)

Discharge

(1 1 Feb

1985)*

Prebronchodilator

Postbronchodilator

0.93

(31)

0.93

(31)

0.84

(26)

0.85

(26)

2.88

(72)

2.67

(67)

2.32

(53)

2.40

(62)

methylprednisolone,

IV aminophylline,

Test and Arterial

Function

Blood

Measurement

and inhaled

IV ampicillin,

Gas

Results

Analysis

Admission

TLC,

1985

Postbronchodilator

pred)

after

(6 Feb

February

Prebronchodilator

L (% pred)

FVC,

Test Results,

Function

3-agonists.

During

the Hospitalization

at NJC in May

PFTs

PFTs

Prebronchodilator

Postbronchodilator

1987

10 Days

Later*

Postbronchodilator

Lt

7.90

(158)

7.15

(143)

7.62

(152)

TGV, Lt

6.05

(224)

5.15

(191)

5.52

(204)

RV, Lt

4.33

(373)

3.40

(293)

4.03

(346)

2.64

(69)

2.93

(76)

3.11

(81)

0.66

(19)

0.66

(19)

0.76

(22)

FVC,

Lt

FEy,

Lt

%FEV/FVC

24

Rawt

12.11

SGawt

23 (853)

0.01

Dsbt Dsb/VAt

6.39

(105)

pH

7.41 mm

Hg

mm

Sa02,

Hg

in Denver,

34-38

mm

53 (normal

in Denver,

65-75

mm

function

nebulization PFTs

were

done 1,584

tValues

testing

(961)

0.01

(5)

Hg) Hg)

10 days

after

a pretreatment

in parentheses,

CT scan

chest

biopsy

study

pulmonary

but

(Fig

3) was

otherwise

methylprednisolone

triamcinolone 0.5

ml

(125 acetonide

albuterol

0.5%

complete

collapsibility

complete

collapsibility

No

study airways

mg

q 6 h),

(4 puffs by

qid),

of the of the

collapsibility

by

a panel

bronchi

were

passive

on

severe,

diffuse

expiration,

05%

(0.5

theophylline

Arterial

with

blood

fifth-generation

bronchi

and

bronchi.

There

gas

ml)

with

levels

values

20

mg

in the were

cromolyn

high

by

teens.

obtained

on

These room

air

third-generation

and

more

passive

expiration

techniques

and

not

a marked

a tapering Over

the

therapy

of

ensuing

except

improve

the

reduction

steroid

patient’s

in her

therapy

20 months

for

necessitated

symptoms,

bronchodilator

without

but therapy

a worsening

of

her

severely

brief by

disabled

the

patient

periodic upper

by her

bursts

has

been

(three

to

respiratory

pulmonary

off prednisone four

infections.

times

She

per

remains

condition.

was DISCUSSION

proximal

Collapse with

did

tolerate

symptoms.

year)

nearly

apparatus

did

and

this

including

fourth-generation

ofthe

of

of emphy-

present

revealed

she

bronchi.

Treatment

albuterol

and

nebulization.

breathing

An open

no evidence

results with

A thin-section

as normal

demonstrating

obliterans. the

normal. ofbronchiectasis.

interpreted

pathologists,

of

no abnormal

with

no evidence

Bronchoscopic

collapsibility

was

showed

or bronchiolitis

specimen.

qid),

% predicted.

markings

ofthe

of IV

(2 puffs

m).

peribronchial

sema

after

q 4 h, ipratropium

(altitude,

lung

13.60

(10)

90

*Pjlmony

four

36 (normal

%

(863)

0.02

(95)

Po2,

12.26

(5)

30.57

Pco,,

24

a resistor

passive

of the

bronchi

expiration,’3

should

and

its

normally

presence

not occur

in this

patient

during suggests

,;L P R

E C T

;

I 50

/

100

T L C

,. Patient

\c:A

\

baseline

g* I

0 -20

#{149}

0

#{149}

I

20

Predicted

range

2. Pressure

volume

curve

,

I

#{149}

40

I 60

at the

time

80

of admission

FIGURE

.



“C.

H20)

obtained

.C

‘‘,..

t

490

...

?o

,.,

50

(cm FIGURE

‘ ‘r”:ir’-’

b

PRESSURE

to NJC.

‘%._

b:1,

.:

E

D

;

‘*. ‘

3.

magnification

.

,

. ‘

‘I .

-

,, .

&C #{163}C’

‘-p

1.1

I

‘, ‘4

C-

‘1N

#{149}

..

..-\

md$

Open

(x

lung 170).

biopsy

specimen

Distal Airway

Downloaded from chestjournal.chestpubs.org by guest on July 10, 2011 © 1990 American College of Chest Physicians

obtained

Bronchomalacia

at NJC

(Lavins,

original

Hami!os)

the

diagnosis

diagnosed

of bronchomalacia.

by bronchoscopy, than 50 percent

by more forced such

as

is best

a narrowing

ofthe

lumen Partial

with coughing is pathologic. ofless than 50 percent, may occur during with other forms ofobstructive lung disease

collapse, expiration

bronchial

Bronchomalacia

where

emphysema,

but

does

not

occur

with

manuscript preparation.

and

1 Gandevia

B. The

collapse

in emphysema.

passive

2 Campbell

suggested

4 Nuutinen 63:380-87

J.

5 Campbell

AH,

Previous

by the

abnormal

bronchial

collapse

demonstrated

on bronchoscopy with passive expiration and the exclusion of other diseases such as asthma, emphysema, bmnchiectasis, and bronchiolitis obliterans. The patient also has a clinical history ofchronic bronchitis, but it is not uncommon for bronchomalacia to he associated with chronic bronchitis.6’7 Asthma

improve

is an unlikely

the

testing

on

sema

diagnosis

obstructive

multiple

with

lung biopsy, and the CT scan of the obliterans was ruled out as a potential lung

biopsy,

results

and

of the

bronchiectasis

chest

x-ray

Bronchomalacia

was

film

may

Congenital

be

an

isolated

matic

by age

years.6”

abthty

chest.

function Emphythe open

highly

unlikely of the

chest.

from

or

acquired.4.6.8

Acquired

bronchomalacia

hypothesizes bronchitis

case

of

acquired

except

an

that may

bronchomalacia

with

association

bronchomalacia

occur

when

usually

has

no

obvious

chronic bronchitis. Pohl associated with chronic

irritation

of many

1971;

years’

Keller

Med

bronchial

other

with

of obstructive

possible

causes

presumed

steroid-dependent cannot be demonstrated.

reversibility

lung

disease

asthma

its

Expiratory Bespir

R, Ailgower

M.

air-flow Dis

pattern

Special methods of the central

diseases

in trache-

92:781-91

1965;

of diagnosing

airways.

Chest

60:49-67

6 Johnson

Acquired

JH,

etiology

JJ,

RJ,

TH,

Wilson

collapse,

Feist

RJ.

diagnosis. JS.

Dis

1982;

of

a variant

1963; 57:174-80 Acquired tracheo-

JH.

109:577-80

differential Dunbar

J Respir

Br J Dis Chest

Wilson

1973;

Johnson

JD,

1963;

Tracheobronchial

disease.

Mikita

and

8 Baxter

IF.

Young

Radiology

7 Feist

Eur

bronchomalacia.

respiratory TH,

malacia.

Acquired

Chest

bronchomalacia:

1975;

Tracheomalacia.

68:340-45

Otol Rhinol

Ann

Laryn-

72:1013-23

SJ, Adler P. Scherer lacia) a non-allergic cause 1964; 22:20-25

9 Levin

RA.

Collapsible

trachea

of wheezing

(tracheoma-

in infancy.

Ann

Allergy

Andres

L.

This an

report acute

exposure.

Arteries After Acute to Carbon Monoxlde*

Marius-Nunez,

M.D.

describes

a 46-year-old

myocardial

infarction

The

showed

with Normal

Infarction

Coronary Exposure

man carbon

and

infarction.

The

in

where

monoxide

serum

coronary

one week after admission failed of coronaryobstructive lesions. The ofinterestbecause the clinical presentation

performed dence is myocardilal

who suffered

white after

electrocardiogram

myocardial

enzymes angiogram

to reveal

case

evi-

presented

of

suggestive

absent, the patient was found unconscious and his medical profile was negative for cornnary heart disease risk factors. It is assumed that COHb causes myocardial infarction by severe generalized tissue hypoxia and a direct toxic effect the myocardial snito-

was

infarction

on

chondria.

Contributing

myocardial

factors

oxygenation

are

and an increased

fusion

duration

with a congenital weakness ofconnective tissue or the elastic fiber system. One could speculate that this patient’s bronchomalacia was due to chronic bronchial irritation from her exposure to workplace chemicals as a hairdresser, but there are no real data to substantiate this contention. The prognosis of acquired bronchomalacia in the absence ofan obvious cause is not known. Since this patient presented with presumed steroiddependent asthma and was actually found to have acquired bronchomalacia, this case emphasizes the importance of seeking

in

expiratory tracheobronchial 32:23-31

that

might

an inadequate

thrnmbic

(Chest

C

arbon

monoxide

is considered

also

the

1990;

most

the

Edgewater

Hospital,

nearly

50

per-

percent

97:491-94)

common

intoxication with an average of 10,000 that need medical attention in the United series reported by Zanetti,’ of patients trial

year

decrease

myocardial

tendency.

combines

patients

assistance

1963;

Rev

obstructive

obstructive

gol

LW. Am

Myocardial

adults and can be caused by syphilis, relapsing polychondritis, tracheostomies, endotracheal tubes, and crushing chest trauma.”#{176}’ Chronic bronchitis has been associated with acquired bronchomalacia ofunclear etiology in patients older than age 50 with long smoking histories.” The treatment of bronchomalacia is aimed at preventing tracheobronchial collapse, through either surgery or physiotherapy. Physiotherapy includes pursed-lip breathing, expiration through a resistor apparatus, and possibly the use of continuous positive airway pressure. Surgery is reserved for localized bronchomalacia of the central airways but is not indicated for generalized bronchomalacia ofsmaller airways, which is best treated with physiotherapy. This

his

the

affects

etiology

H,

of gross

Q J

Faulks

treating

and

spirogram

collapse.

3 Herzog

by the open

CT scan

AH,

obronchial

Bronchiolitis

diagnosis

congenital

to

presents during infancy and is Most patients become asympto-

finding.

two

and

either

bronchomalacia

usually

the

defect by pulmonary from 1980 to 1987. the results of the Dsb,

occasions

is implausible

without

for

M.D.,

REFERENCES

reports of bronchomalacia associate this disorder with tracheomalacia; however, tracheomalacia was not observed in this case. The diagnosis of bronchomalacia in this patient was ir’46

Dolen,

WK.

indus-

cases States.’ treated

were found

per In at

uncon-

In KindwaIFs, and Zanetti’s,’ experience, the absolute COHb level did not show an association with the severity of intoxication. However, patients who were unconscious seemed to have a more ominous prognosis secondary to the high incidence of complications or death. Clinical and scious.

experimental 5Fmm

data

the Department

indicate

that

of Medicine,

myocardial Edgewater

isehemia

follow-

Medical

Center,

Chicago.

ACKNOWLEDGMENT:

J.

Waidren,

M.D.

The authors ,

and

G.R.

Cott,

thank M.D.,

E. Fernandez, for their review

M.D., of the

Reprint

iqtsests:

Dr.

Marlus-Nunez,

4523 North

Chicago

Artesian,

&J625 CHEST

I 97 I 2 I FEBRUAR’I

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1990

491

Distal airway bronchomalacia resulting in severe obstructive airway physiology. B J Lavins and D L Hamilos Chest 1990;97; 489-491 DOI 10.1378/chest.97.2.489 This information is current as of July 10, 2011 Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/97/2/489 Cited Bys This article has been cited by 1 HighWire-hosted articles: http://chestjournal.chestpubs.org/content/97/2/489#related-urls Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions.

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