Download Hypoplasia of Right Ventricle and Tricuspid Valve

HYPOPLASIA OF RIGHT VENTRICLE AND TRICUSPID VALVE IN SIBLINGS
in case of functional impairment of the lung due to
excessive pleural thickening or to confirm the diagnosis
of asl~estosisby open biopsy in difficult cases. T h e outlook for workers exposed to asbestos has improved greatly since the advent of better dust control systems; greater
awareness of the condition; early removal of the affected
worker from the job; better health care facilities for the
workers; and the use of antibiotics and ancillary measures for improved tracheobronchial toilet. Patients now
often live long enough to demonstrate the possil~lecarcinogenic or cocarcinogenic effect of asbestos fibers.
273
20 \Vagner JC: Eu~wrimc*ntnlprotluction of mt.sothc.lia1 trlmors of the pleura I)y implant;~tionof t111stsin lal,aratan;
animals. S a h ~ r e1%: 180, 196.3
21 Smith WE, Sliller L, Elsasser RE, et al: Tests for carcinogenicity of aslwstos. Ann S Y Acad Sci 132:4.56, 196.5
22 Thornson \lL, Pelzer A, Smithcr \\'J: Thcs discriminitnt
value of p~~lmonary
function tests in asl)t.stosis. Ann S Y
Acacl Sci 132 :42l, 1965
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Reprint requests: Dr. Smyth, 106 In.ing Strcvt, S\V. \\';lhlrington, D.C. 20010
Hypoplasia of Right Ventricle and
1 Hueper WC: Occupational and nonnccupational exposures to asbestos. Ann S T Acad Sci 1 3 2 184, 1965
2 Wagner JC, Slaggs CA, Marchand P: Diffuse pleural
mesothelioma and asbestos. Brit J Indust %fed 17:%0,
1960
3 Enticknap JB, Smither WJ: Peritoneal tumors in aqhestosis. Brit J Indust Sled 21 :20, 1964
4 Selikoff IJ, Churg J, Hanlnlond EC: Asbestos exposure
and neoplasia. JA\!A 188:22. 1964
5 Selikoff IJ, Hamrnond EC, Cli~lrgJ : Ashestos exposure,
smoking and neoplasia. JASfA, 240: 106, 1968
6 Selikoff IJ: The occurrence of pleural calcification among
asbestos insulation workers. Ann S Y Acad Sci 132:351,
1965
7 Eisenstadt HB: Asbestosis pleurisy. Dis Chest 46:48.
1964
8 Hinshaw HC. Garland LH: Diseases of the Chest, second
edition, Philadelphia, W. B. Saunders, 1963, p 742
9 Slurray HS1: Report of the departmental committee on
compensation for industrial dkease. London, HSfSO 1907
10 Gilson JC: Problems in perspectives: the changing hazards of exposure to asbestosis. Ann NY Acad Sci 132:696,
1965
11 Dreessen WC, Dalla Valle JS1, Edwards TI, et al: A
study of asbestosis in the asbestos textile industry. US
Treasury Dept Pub Health Service. Public Health Bulletin, No. 241, Waqhington, DC, 1938, p 68
12 Case 4, 1967, case records of Sfassachusetts General
Hospital. New Eng J Sled 276:230, 1967
13 Selikoff IJ, Churg J, Hammond EC: The occurrence of
asbestosis among asbestos insulation workers in US. Ann
NY Acad Sci 132:139, 1965
14 Stewart h1J: Asbestos bodies in the lungs of guinea pigs
after three months of exposure in an asbestos factory. J
Path Bact 33:848, 1930
15 Stewart SIJ, Haddow AC: Demonstration of peculiar
bodies of pulmonary asbestosis ( asbestos bndies ) in material obtained by lung puncture and in the sputum. J Path
Bact 32: 172, 1929
16 Sluis-Cremer GK: Asbestosis in South Africa-certain
geographical and environmental considerations. Ann NY
Acad Sci 132:215, 1965
17 Kiviluoto R: Pleural calcification as a roentgenologic sign
of non-occupational endemic anthophyllite-asbestosis.
Acta Radiolog Suppl 194, 1-67, 1960
18 Hammond EC, Selikoff IJ, Churg J : Neoplasia among
insulation workers in the United States with special reference to intra-abdominal neoplasia. Ann NY Acad Sci
132:519, 196.5
19 Selikoff IJ, Churg J, Hammond EC: Relation between
exposure to asbestos and mesothelioma. Sew Eng J hied
272:560, 1965
Tricuspid Valve in Three siblings*
Anton E. Becker, J1.D.; .\lies I. Rcckcr. .\l.D.;
l a n ~ e sH . .\faller, .\l.D.; ant1 Jcsse E . Etl~~.urtls,
.\l.l)
A case of hypoplasia of the right ventricle and tricuspid
valve is reported in the third affected sibling of a family.
The condition, which has a strong familial tendency,
usually is responsible for death in infancy. Exceptional
patients live to adult life. The functional problem is that
of inflow obstruction into the right ventricle. A transatrial
right-to-left shunt is characteristic and results in cyanosis.
Diminished right ventricular forces in the electrocardiogram represent an important point in differential diagnosis among patients with cyanotic congenital heart
disease.
strong familial tendency1,? is noted in congenital
isnlrted hypoplasia of the right ventricle and tricuspid valve.
This report describes the case of the third sibling in a
family to be afflicted with this entit).. T h e cases of the
first and second siblings of the family concerned were
reported earlier by Raghib and associates:' and by Davachi and m- worker^,^ respectively. A brief summary of
*Iven
t h e cases of the hvo sihlings reported will b e k'
before a more detailed description of the present and
third case.
A
CASE1 ( Reported by Raghib and associates:' )
A male infant, first born of the family, was first examined
at the age of two days because of cyanosis. There were no
cardiac murmurs and no signs of congestive hrart failure.
The electrocardiogralii sho\ved a QRS electrical skis of 100
degrees with a precordial pattern indicating either left ventricular hypertrophy or hypoplasia of the right ventricle.
A thoracic roentgenogram revealed that the heart was
slightly enlarged and the pulmonary vascr~lar markings appeared to be decreased. A venous angiocartliogram revealed
+
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*From the Department of Pathology, The Charles T. \filler
Hospital, St. Paul, Slinnesota and the Departments of
Pathology and Pediatrics, University of \linnesota, \finneapolis, hfinnesota.
This study was supported by Public Health Service Research
grant 5 R01 HE05694 and Research Training grant 5 TO1
HE05570 from the National Heart Institute and h p the
Srtherlands Organization for the Ativancemvnt of Purt.
Research ( Z.W.O. ) .
CHEST, VOL. 60, NO. 3, SEPTEMBER 1971
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BECKER, ET AL
catheterization, the catheter could not be advanced into the
right ventricle. Venous angiocardiography revealed a massive
right-to-left shunt at the atrial level; no opacification of a
right ventricle was apparent. The pnlmonary arteries became
opi~cifieclby way of the dttctt~sarteriosus. A selective left
ventriculogram showed a 1lyp)plastic right ventricle hut the
ronte by which the contrast niaterial entered the chamber
was not evident. Cardiac arrest occurred on tlle third day of
life and the child tliecl.
The necropsy findings in this case were essentially similar
to those described in case 1. The main abnormalities were
11yp)pIasia of the right ventricle and tricuspid valve, while
the pulmonary valve was h;nically normal. The foramen
ovale and tlnctns arteriosus were patent. The ventricular
sephnn was intact. Chromosomal sh~dies,using samples of
skin taken at the time of necropsy, revealed no abnorn~alities.
CASE3 (Present Case)
FICXJHE1. Thoracic roentgenogram. Normal-sized heart.
Ditninisl~etlj>r~ltnon;~ry
vascular markings.
a n~i~ssive
right-to-lrft shrlnt at the atrial level with opacification of t l ~ right
r
ventricle, thereby excl~tclingtricuspid atresia.
111 the neonatal peri(n1, a cliagnosis of pulmonary valvular
atresia was then n ~ a d ebut, at operation, no al)norniality of
the j~rtltnonaryvalve was fo~tndand no cvrrective procedure
was clone. In the interval between the time of the operation
;u~dcleat11 at tht. age of three tnonths, the infant manifested
progressivc4y increasing cyanosis and clyspnea.
At necrojxy, I)oth the right ventricle and tricuspid valve
were hyp~pl;~stic,
while the pulmonary valve was normal. A
p;~tentforatnr.n ovale was present.
A f ~ t n i ~ infant
le
and the second sibling of the family was
horn kthout 1% years after the first sibling (case 1 ). In the
ei~rlypostnatal state, cyanosis ant1 tachypnea were noted. At
the ;tge of two days, a grade II/IV, systolic murnirlr was present along thr left sternal border with radiation over the precordir~n~
and back and a continnous munlntr was heard in the
Icft seconcl intercostal space. The liver was enlarged. The
c~li*ctrocartliogramshowed a QRS electrical axis of +45
tlt.grc.es ant1 was essentially si~nilarto the findings in case 1.
The thoracic romtgenogratn revealed cardiac enlargement
; ~ n dtli~ninisl~t.tl
p~lltnouaryvascular markings. During cardiac
This male infant, k i n g the third consecr~tivesibling in the
family, was born approximately three years after the second
child (case 2 ). No abnormalities during pregnancy had been
noted. Cyanosis was noted shortly after birth and this increased in degree within 24 hor~rs.When admitted at the age
s , physical examination showed a vigorous,
of 36 h o ~ ~ r the
cyanotic, ~iialeinfant. The lungs were clear. The heart was
not enlarged. The first cardiac sound nppeared normal and
the second sound was single. A grade II/VI, systolic, ejectiontype nnlrmltr was present along the upper left sternal border.
The liver was palpable 2 cm lwlow the right costal margin.
Thoracic roentgenograms revealed a nornlal-sized heart
with diminished pulmonary vascr~larmarkings ( Fig 1). The
electrcxardiogranl, being similar to that of cases 1 ancl 2,
showed a QRS axis of +60 degrees with a precordial lead
pattern of absence of right ventricular forces ( Fig 2 ).
Angiocardiography showed a hypoplastic right ventricle
with a normal pulmonary valve ( Fig 3 ) . A right-to-left shunt
was present at the atrial level and a left-to-right shunt
through a patent d~lctusarteriosns.
When the infant was two days old, a surgical anastomosis
between the right polmonary artery and the ascending aorta
(Waterston's procedure) was performed. This resulted in
diminution of the cyanosis hut chronic cardiac failnre persisted in spite of digitalization.
The patient was readmitted at the age of three months with
cyanosis, tachypnea and tachycardia ancl snbcostal and inter-
2. Electrocardiogram when
FICUHE
patient was one day old.
CHEST, VOL. 60, NO. 3, SEPTEMBER 1971
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FICUHE
3. Early stage of selective right atrial angiocardiogran~at one day of age showing simultaneor~sfrontal ( a ) and lateral ( 11) views. The right atrium ( RA ) is enlarged. The right ventricle
( R\'), outlined by arrows, is small and leads to the pulmonary arterial system ( P A ) which is of
nonnal caliber. A large right-to-left shunt at the atrial level accor~nbfor pronounced opacification
of the left atrium ( LA ) and ventricle ( L\'). Aorta ( Ao ) also opacified.
costal retraction. Examination showed the lungs to he clear
1)11tthe cardiac size \\,as enlargetl. A soft, continr~or~s
nlrlrnlur
was present o\,er the 1)ack. A gallop rhythun was present.
Treahnent consisted of increasing the dosage of digitalis and
administration of diuretics ant1 osygen.
Cardiac catheterization and angiocarcliography were rewated. These studies showed the right ventricnlar pressure
to be 32/0-13 (Inn1 H g ) . The right atrial mean pressure was
9 n1n1 Hg with a and v waves being 19 and 8 mm Hg,
respectively. Press~~res
in the left atrium were as follows:
mean 13, a 16, v 20.
The angiocardiograms again revealed hypnplasia of the
right ventricle and a right-to-left shunt at the atrial level. The
aorticopl~l~noni~ry
anastomosis appeared to he functioning
poorly. A balloon atrial septostomy (Hashkind's procedure)
was perfonnetl b r ~ tthe general condition of the child did not
improve. One week later, a Blalock-Taussig anastomosis wxs
carrietl out, following which the child experienced extreme
respiratory difficulties and died 36 hor~rs after the latter
operation at the age of 14 weeks.
The main pathologic findings were restricted to the heart.
The left vtmtricr~larchaml)er was large, in contrast to the
presence of a small right ventricle (Fig 4 ) . The great vessels
were nor~nnllyrelated. Signs were evident of the previously
perforn~cdWaterston's procedure and the recently done leftsided Bl;~lock-Taussig procedr~re.The diameters of the pulInonary trunk and of each main p ~ ~ l ~ n o n artery
a r y were 8 and
5 mm, rr-sln~ctively.
XI;~rkcdtlcgrees of hypnplasia of the right ventricle and
the tric~~spitlvalve were apparent. The tricr~spid orifice,
12 111111 in diameter, was guarded by a
which ~nt~;tsr~red
hypoplastic tricuspid valve. The tricuspid leaflets and their
basal attachn~r-ntswere otherwise norn~al( Fig 41) and c ).
The right ventric~~lar
sinus (inflow) portion wits hypnplastic (Fig 4c). The distance behveen the tricuspid val\wlar
ring and the apex of the right ventricle was 15 mln. The
distance between the right ventricular apex and the pr~ln~onary valve was 20 nun. The crista supraventricnlaris was
normally positioned. The infr~ndibular portion of the right
ventricle, lying cranial to the aforementioned crista supraventricolaris, was normal in :~.pect ( Fig 4 d ) . The tlistance
between the crista and the pulmonary semilunar cusps was 8
mm.
In addition to the papillary muscle of the conus ant1 a
pnsttbrior and an anterior papillary muscle, an anon~illous
papillary muscle was located between the latter hvvo. The
ano~nalousmuscle had chordal connections to the septa1 half
of the posterior tricuspid leaflet.
The right ventricular entlocardium was slightly thickened
by gray, fihror~stissue. Each of the three pulmonary c ~ ~ s p s
was nor~nallyfonned and delicate. The orifice of the valve
measuretl 8 mm in diameter.
The right atrium was nonnally formed, though its wall was
markedly hypertrophic. The chamber was dilated. The Hoor
of the fossa ovalis. which was 1 mm thick. showed a tear 8
lnln in length representing the previously performed atrinl
septosto~ny.
The c;~rtliacchaml)crs on the left side of the heart wr-re
dilated ;tntl hypertn~phiedI)ut otherwise normal. There arrre
no valvuli~rano~naliesin the left side of thr 11c.art.
Crossly, the lungs showed no al~nor~nalities.Histologic
study of the pulmonary vessels showed medial hypertrophy
with a slight degree of arterialization of pl~ln~onary
veins.
The muscular pulmonary arteries were slightly thin-w;~llt-d.
T h e congenital anomaly herein reported, that of Ilypoplasia of the right ventricle and tricuspid valve, is
CHEST, VOL. 60, NO. 3, SEPTEMBER 1971
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LOCALIZED UNl LATERAL PULMONARY EDEMA
all affected sil~ling.
Of al)r)ut 14 ciises of the mndition reported in the
E ~ ~ g l i sliterature,
h
it is common that death occurs in
infiincy. E x c e p t i o ~ ~ ciises
al
have however, 11ee11reported.
Popper a n d associates!' reported an isolated case of
I~ypoplnsia of the right v e ~ ~ t r i c laen d tricuspid viil\,e
occurring in a 39-yeiir-old miin. Sackner and associates2
reported the c o ~ ~ d i t i oton occur in three s i l ) l i ~ ~ \\it11
g s the
respective ages of 13, 22 and 39 years. 111an isolated anti
rlnreported case referred to us Ijy 1)~s.Ann 13. Catts and
Coolidge S. Wakai, the patient was 39 years old at the
time o f death.
In hypoplasia of the tricuspid valve and right ventricle, the pri~lciplesof treatment are similar to those o f
other congenital collditions causing obstruction to flow
into the right ventricle, such as tricuspid atresia or
pulmonary atresia with hypoplasia of the right ventricle
and intact ventricular septum.
REFERESCES
I Sltultl \VE, Ser~feldH S , \Veidnian \VH, et al: Isolatetl
2
3
1
.5
6
hyp~pl;isiaof the right ventricle ancl tricnspitl v;ilvr- in
sildings. Brit Heurt J 23:2.5, 1961
S a c k ~ i ~SIA,
r Rol~inson 51J, Jamison Wl,, et al: Isolatt.tl
right ventricr~larhypoplasia with atrial srpt;il tlrfcct or
patent foriumen ovale. Circr~lotion24: 1388, 1961
Haghi11 G . Amplatz K, Sloller JH, tat al: Hypopl;tsia of
right vrntriclr and of tricr~spidvalve. Anirr Heart J 70:
806, 1965
Di~\.ucltiF, \lcI,riu~ RH, Sloller JH, et al: Hypoplasia of
thr right vrntriclr ant1 tricr~spidvalve in sil~lings.J 1'rtli;it
7 1 :8li9, 1967
Fay JE, Lynn RH: Isolated right ventricrllar Iiypopli~sia
\\,it11 iitri;il septiil tlt.fect. Canad SlAJ 88:812, 11.963
C;;isrtl BSI, \Veinl,erg 51 Jr, Laun LL, et al: Sltperior vt.lia
correction for piitic-nts with El~stcin's nnonioly ant1 for
congtbnital hypoplastic right ventricle. JASIA 171: 1797,
19.51)
7 Okin JT, Vogc.l JIIK, Pryor R, et al: Isolatr.tl right vciitricular 1iyp)pl;isia. A111t.rJ Cardiol 24: 133, 1961)
8 Khortry <;Il, <;ill>ertEP, Cliang CH, et al: Tlic~hypoplustic
right 1ic;irt comples. Clinical, Iletiiodynaniic. ~itliologic
;uitl sltrgical considerations. Amrr J Cardiol 23:702, 1969
9 P o p ~ r rH, Kashnrr. DS, <;as111H: Adult fil,roelasttais \\.it11
congewitill tric~~spitl
stc.nosis. Circr~lation 14:420, 19.56
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-
. --
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rare as is generally believed. The exact underlying mechanism is not clear but various hypotheses put forward to
explain the unilateral distribution include the effect of
gravity and posture, variations in the pulmonary venous
pressure and some disturbance of the neurogenic control
bf capillary size and permeability. We believe that a
wider recognition of the unilateral presentation of acute
pulmonary edema is important to avoid unnecessary delay
in diagnosis and proper management.
nilaterill pulmonary edema presents an interesting
U a 1 1 d c o n f u s i ~ ~diagnostic
g
pro1)lem. Lack of awareness of the fact that pi~lrnoniiryedema can I)e i ~ r ~ i l a t e r a l
may lead to mistakes in diagnosis and important delay in
treatment of the calldition. T h e usual a n d more \r,idely
recognized form of roentge~~ologic
presentation of pulmonary edema is one of 1)ilaterally s>mmetrical opacity
occupying t h e central zones of the lungs with a 1)il)asilar
predomi~iance.Although a few case reports of rll~ilateral
o r segmental pulmo~laryedema have appeared in t h e
literature,'-:{ the existence of such a n entity is not commonly appreciated.
In this report w e describe a patient with an unusual
presentation of left heiirt failr~re,in that unilateral pulmonary edema, d u e to mitral insufficiency, was seen
radiographically to b e lociilized largely to the right
upper l o l ~ e .
A 62-year-old white man was atl~tiitted to Harnrs Hospital on January 12, 11961.). Zle was well utitil Dcct*ml~er1.
1968, when he clevt-lo1x.d pain in the ugpcar ;~htlot~ic~n
and Ivft
lower cliest. Tlie pain rtsrtolly fo1lowt.d a rne;~lant1 was D;irtially relieved 11y antacids. An elrctroc.artliogr;i~n~ 1 1 o ~ST
t~d
seg~nenta l ~ n o r n ~ a sr~ggestive
li~
of antrrolatc.ri~l myocarclial
injury. Examin;ition 11y his private ~hysiciatisllowetl ~narkrd
tachycardia and an upical p;uisystolic nirtrtnur which had not
Iwen 11e;ird I~c.forr.Thr chest roentgrnogr;u~~
revralrcl an in-
-
Reprint rc.rlr~t.sts: Dr. Jesse E. Etl\v;ircls, Charles T. \liller
Hospital, 12.5 \l-tlst Collegr Avenrle. St. 1':11tl 5.5102
Localized Unilateral Pulmonary
Edema: An Unusual Presentation of
Left Heart ~ailure*
A patient with mitral insufficiency caused by infarction
of the anterior papillary muscle, presenting with localized
unilateral pulmonary edema, i s reported. On the basis of
previous reports it appears that unilateral presentation
of acute pulmonary edema, although unusual, is not so
--'Frotii the Dc.partnient of Slt.tlicint., Cardiovascular Division
ant1 Tlie Slallinckrotlt Institute t ) f Radiology, \\'ashinaton
Imiversitv School of SIt*tlicine.St. Lollis, Slissonri.
This work was supporttd \,y USI'HS (;rant No. HE-11034.
~
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F I C U I ~1.E Frontal chest rot~ntg'nogram on atlmission sliowing riglit-sitlt.tl alvrolar proctAssinvolving pritilarily the right
upper lobe. Some platc-like ( tliseoitl ) atc.li.cta~sis is prcscbnt
;~l>ovethe Irft Iie~mitliaphragn~.
CHEST, VOL. 60, NO. 3, SEPTEMBER 1971
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LOCALIZED UNl LATERAL PULMONARY EDEMA
all affected sil~ling.
Of al)r)ut 14 ciises of the mndition reported in the
E ~ ~ g l i sliterature,
h
it is common that death occurs in
infiincy. E x c e p t i o ~ ~ ciises
al
have however, 11ee11reported.
Popper a n d associates!' reported an isolated case of
I~ypoplnsia of the right v e ~ ~ t r i c laen d tricuspid viil\,e
occurring in a 39-yeiir-old miin. Sackner and associates2
reported the c o ~ ~ d i t i oton occur in three s i l ) l i ~ ~ \\it11
g s the
respective ages of 13, 22 and 39 years. 111an isolated anti
rlnreported case referred to us Ijy 1)~s.Ann 13. Catts and
Coolidge S. Wakai, the patient was 39 years old at the
time o f death.
In hypoplasia of the tricuspid valve and right ventricle, the pri~lciplesof treatment are similar to those o f
other congenital collditions causing obstruction to flow
into the right ventricle, such as tricuspid atresia or
pulmonary atresia with hypoplasia of the right ventricle
and intact ventricular septum.
REFERESCES
I Sltultl \VE, Ser~feldH S , \Veidnian \VH, et al: Isolatetl
2
3
1
.5
6
hyp~pl;isiaof the right ventricle ancl tricnspitl v;ilvr- in
sildings. Brit Heurt J 23:2.5, 1961
S a c k ~ i ~SIA,
r Rol~inson 51J, Jamison Wl,, et al: Isolatt.tl
right ventricr~larhypoplasia with atrial srpt;il tlrfcct or
patent foriumen ovale. Circr~lotion24: 1388, 1961
Haghi11 G . Amplatz K, Sloller JH, tat al: Hypopl;tsia of
right vrntriclr and of tricr~spidvalve. Anirr Heart J 70:
806, 1965
Di~\.ucltiF, \lcI,riu~ RH, Sloller JH, et al: Hypoplasia of
thr right vrntriclr ant1 tricr~spidvalve in sil~lings.J 1'rtli;it
7 1 :8li9, 1967
Fay JE, Lynn RH: Isolated right ventricrllar Iiypopli~sia
\\,it11 iitri;il septiil tlt.fect. Canad SlAJ 88:812, 11.963
C;;isrtl BSI, \Veinl,erg 51 Jr, Laun LL, et al: Sltperior vt.lia
correction for piitic-nts with El~stcin's nnonioly ant1 for
congtbnital hypoplastic right ventricle. JASIA 171: 1797,
19.51)
7 Okin JT, Vogc.l JIIK, Pryor R, et al: Isolatr.tl right vciitricular 1iyp)pl;isia. A111t.rJ Cardiol 24: 133, 1961)
8 Khortry <;Il, <;ill>ertEP, Cliang CH, et al: Tlic~hypoplustic
right 1ic;irt comples. Clinical, Iletiiodynaniic. ~itliologic
;uitl sltrgical considerations. Amrr J Cardiol 23:702, 1969
9 P o p ~ r rH, Kashnrr. DS, <;as111H: Adult fil,roelasttais \\.it11
congewitill tric~~spitl
stc.nosis. Circr~lation 14:420, 19.56
- -
-
-
-
. -
-
. --
-
-
-
- -
rare as is generally believed. The exact underlying mechanism is not clear but various hypotheses put forward to
explain the unilateral distribution include the effect of
gravity and posture, variations in the pulmonary venous
pressure and some disturbance of the neurogenic control
bf capillary size and permeability. We believe that a
wider recognition of the unilateral presentation of acute
pulmonary edema is important to avoid unnecessary delay
in diagnosis and proper management.
nilaterill pulmonary edema presents an interesting
U a 1 1 d c o n f u s i ~ ~diagnostic
g
pro1)lem. Lack of awareness of the fact that pi~lrnoniiryedema can I)e i ~ r ~ i l a t e r a l
may lead to mistakes in diagnosis and important delay in
treatment of the calldition. T h e usual a n d more \r,idely
recognized form of roentge~~ologic
presentation of pulmonary edema is one of 1)ilaterally s>mmetrical opacity
occupying t h e central zones of the lungs with a 1)il)asilar
predomi~iance.Although a few case reports of rll~ilateral
o r segmental pulmo~laryedema have appeared in t h e
literature,'-:{ the existence of such a n entity is not commonly appreciated.
In this report w e describe a patient with an unusual
presentation of left heiirt failr~re,in that unilateral pulmonary edema, d u e to mitral insufficiency, was seen
radiographically to b e lociilized largely to the right
upper l o l ~ e .
A 62-year-old white man was atl~tiitted to Harnrs Hospital on January 12, 11961.). Zle was well utitil Dcct*ml~er1.
1968, when he clevt-lo1x.d pain in the ugpcar ;~htlot~ic~n
and Ivft
lower cliest. Tlie pain rtsrtolly fo1lowt.d a rne;~lant1 was D;irtially relieved 11y antacids. An elrctroc.artliogr;i~n~ 1 1 o ~ST
t~d
seg~nenta l ~ n o r n ~ a sr~ggestive
li~
of antrrolatc.ri~l myocarclial
injury. Examin;ition 11y his private ~hysiciatisllowetl ~narkrd
tachycardia and an upical p;uisystolic nirtrtnur which had not
Iwen 11e;ird I~c.forr.Thr chest roentgrnogr;u~~
revralrcl an in-
-
Reprint rc.rlr~t.sts: Dr. Jesse E. Etl\v;ircls, Charles T. \liller
Hospital, 12.5 \l-tlst Collegr Avenrle. St. 1':11tl 5.5102
Localized Unilateral Pulmonary
Edema: An Unusual Presentation of
Left Heart ~ailure*
A patient with mitral insufficiency caused by infarction
of the anterior papillary muscle, presenting with localized
unilateral pulmonary edema, i s reported. On the basis of
previous reports it appears that unilateral presentation
of acute pulmonary edema, although unusual, is not so
--'Frotii the Dc.partnient of Slt.tlicint., Cardiovascular Division
ant1 Tlie Slallinckrotlt Institute t ) f Radiology, \\'ashinaton
Imiversitv School of SIt*tlicine.St. Lollis, Slissonri.
This work was supporttd \,y USI'HS (;rant No. HE-11034.
~
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F I C U I ~1.E Frontal chest rot~ntg'nogram on atlmission sliowing riglit-sitlt.tl alvrolar proctAssinvolving pritilarily the right
upper lobe. Some platc-like ( tliseoitl ) atc.li.cta~sis is prcscbnt
;~l>ovethe Irft Iie~mitliaphragn~.
CHEST, VOL. 60, NO. 3, SEPTEMBER 1971
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