Reversible Tricuspid Stenosis

Reversible Tricuspid Stenosis* Demonstration with Two-dimensional Echocardiography and ContinuousWave Doppler Mitclw/1 A. Ranwhiu ..\1 ./J.: Su.wm H. ,,.,·frt. M./J .; mu/ Man>iu R,.,-gn: .\1./J .. FC.C.P

We report a case of pseudotricuspid stenosis as a result of extrinsic compression of the tricuspid valve by a large right-sided pericardia) effusion. Two-dimensional echocardiography and continuous-wave Doppler enabled accurate noninvasive diagnosis and hemodynamic assessment.

(Chest 1991; 100:852-!).'J)

T

ricuspid st(•twsis du!' to t•xtrinsic t·ompn'ssion of tht• tricuspid valve is a rare dinical !'ntity. Previously reportt'd cast•s have n•quired right heart cathett'fization and cint•angiography to t•stahlish the <-~>rred diagnosis.' ' We descril)(' a patient in whom an a<.-curatt• diagnosis was madt• noninvasively. Two-dinwnsional echocardiography reVt'aled a large . loculatt•d pericardia) effusion t·ompn•ssing rightsided cardiac strul'tures. Continnous-waw Doppler ultrasound dt•monstratt•d a signilkant pn•ssun• gradient across tlw tricuspid valve.

A 42-yt•ar-old human inmnm<>vt"r, and dyspnt>a on t•x.-rtion . lit• had bt•t•n admitlt·d to the hospital li>r similar t'>mplaints I month c·arlit·r and was limnd to ha\'1' a largt• Ilt'rkardial effusion by two-dinwnsional t•t·hc><·•mliography. Perkardit><·t•nlt'sis rt·n·al..d a nonht·morrlmgie. granulomatous t•xndatt'. Skin tt>sling dt•mtmstratt-d am·rgy. and allt·nltnn·s and stains Wt're nt>gativt'. lit> was slmyl'in for presnmpti\'1' tub.. n·nlosis. At the tinu· of hospital disl'hargt•. lw *From tlw Division of Cardiolo,.,•y. Dt•partmt•nt of Medicint•, Beth lsnll'l Mt•dieal Ct'nlt•r. Nt•w "•rk. NY. and tlu· Departmt>nt of Medicint•. the Mount Sinai Sehoul of Mt•dieine of tilt' Citv · llniwrsitv of Nt'w York . IU·IIrilll rt'~JIW.,Is: Dr: Ranwhiu. Ot 'JNIItiiU'III of Cardiology, Bl'lh hml'i 1/o.•l>ilal. Wth Stn·l'l at First

Atlf'rlllt' .

N<•w )(>rk

J(}(J().J

was asymptomatic. and a rt'pt>ated two-dimt>nsionalt't·lul(·ardiogram showt'ffnsion. Physical examination at hospital admission demonstrated a blood prt•ssnn· of I 10no mm I Ig without pulsus pan>t'rahrrt• of3R.R°C. lit• had jugular venous distt>nsion to the anglt> of the mandihle at 90°. Kussmaul's sign was abst>nt. and lung fit>lds wt•re dear. A gradt· 114 diastolic murmur was heard on inspiration at the lower left stt•rnal horder. llepatome~aly was present. There was 4 + pitting edema of the lower t•xtrt>mities to the thighs. Cht>st rot•ntgenognun displayt•d a massivt'ly enlargt.J cardiac silhmlt'lte. Lnw voltagt• was present tm l'lt'l'trt><·ardiogram. Two-dimensional t'l'hocardiography demonstrated a large. ltl(·nlated right-sided I>t ~ ricardial effusion with l'unpression of the right wntricle, right atrium. and tricuspid valvt> (Fig I. left). Thetricuspid and mitral leallt>ts were normal in appt>arance. Continuous-wave Doppler revealed in~·reased velocity acmss the tricuspid valw that varied with respimtion (Fig l, right). Vdcl(·ities rangt>d fmm a expiration to 2.2 m/s during inspiration. minimum of 1 m/s durin~ of approximately 19 This t'lrresponded to a I>t'ak diastnlic ~mdient nun Jig. A mmputed tomogram oftht> chestt1>nflrmed the prt>sen<.-e and location of the effusion (Fig 2). Following the echocardio~ram, acute hemodynamic det·ompt>nRi~ht sation developed and the patient required t>mergent sur~ery. heart catheterization was not believed to he necessary hecanse At sufficient informatinn had heen nhtained hy eehtl(·ardio~raphy. surgery. a loculated ri~ht-sided pt>ricardial effusion was limnd l'lmpressin~ the right cardiac structures. Anterior pt>ricardiedomy was pt>rfnrmed, and 2 L of straw-<.,,)ored fluid was remnved. Patholo~ic study demonstrated a thick pt>ricardial sac with focal hl'morrhage and fihrin deposition. Again. all Ruid and tissue cultures and stains were negative. A follow-up two-dinlt'nsional eehocardiogram J>t'rfnrrned I month later showed a minimal JK>Sterinr effusion and normal tricuspid velocity hy l1mtinuous-wave Dnppler. The patit>nt's leg swelling had impmve murmurs. OtSCUSSION

Pseudotricuspid stenosis resulting from extrinsic <.·ompression of the tricuspid valve is usually caused by a loculated pt'ricardial effusion. These effusions may be hemorrhagic, serous, or infectious and have been observed in <.'
------A--Fu:t'HE I. Left: Mndified apical fmrr-chamher view showing marked mmpression of the ri~ht cardiac chaml>t•rs and tricuspid valve {armw). LV= left ventricle; PE =pericardia! effusion; RV = ri~ht ventricle. Hight: Cnntinuous-wavt• Dnpplt>r showing increased velocity acmss the tricuspid valve. Note further incrt>ase associated with inspiration.

852

R811ersible Tricuspid Stenosis (Baruchin, Hecht, Barger)

Check-valve Mechanism as a Cause of Bilateral Spontaneous Pneumothorax Complicating Cell Bronchioloalveolar Carcinoma* Hinmolm Miuami , M.IJ.; Shu::o Sakai, M.D .. FC.C.I'; Atsushi \Vatmudw. M.D.; mul K11on. Shirrwkata, M.n .. J·: C .C: . I'

Fl<:liRE 2. Computed tomo~ram the ri~ht (PE) mrnpromisin~

a large pericardia! effusion showin~ cardiac chambers (arrows).

An intrapericardial hematoma se<.·ondary to chest trauma no definitive . 1 Althou~h also resulted in similar findin~s was made in our patient, he was treated for dia~-,rnosis of tuberculosis based on his immune status and the findin~ pericardial effusion. a ~ranulomatous of In our patient, extrinsic compn·ssion caused narmwin~ the tricuspid valve orifice, resulting in a hemodynamic picture similar to that of intrinsic valvular stenosis. As shown, there was an increased forward-How velocity across the tricuspid valve at rest and a pronounced rise in velocity are typical of tricuspid on inspiration. Both these findin~s stenosis.'·' Pulsus paradoxus is usually an important physical findin~ in cardiac tamponade. Howewr, as demonstrated in this pericase, it is often absent in predominantly ri~ht-sided cardia) effusions. 6 Therefore, physical examination alone may not accurately determine a patient's hemodynamic condition. In this situation where immediate decision may he required, continuous-waw Doppler and two-dimensional proceechocardiography can obviate invasive dia~nostic dures. Serial studies are easily performed to evaluate the efficacy of the rapeutic intervention. REFEHENCES

Cintron GB. Snow JA , Fletdlt'r RD. Saini N . Pericarditis tricuspid valvular disease. Chest 1977; 71:770-72

rnimiekin~

2 )imn~

SG, Greortos G. Swain JA , Joyo Cl. Delayed postoperative

cardiac tamponade

rnirnickin~

sevt•re tricuspid stenosis. Chest

191i4; &5:824-26 3 \Vray TM. Proehaska J, Fisher RD. Shaker lj. Traumatic pericar· dial he matoma simnlatin~

tricuspid valve obstruction. Johns

Hopkins Med J 1975; 1:37:147-50 4 Parris TM, Panidis II~ Hoss J, !\Iintz GS. Doppler e choeardio~in rheumatic tricuspid ste nosis. Am J Cardioll987; raphy findin~s 60:1414-16 5 Halle L. An~les

e n

B. Dia~nosis

and assessment of various heart

lesions. In: Halle L. ed. Doppler ultrasound in cardioloJ.:y physk·al principles and clinical applications. 2nd ed. Philadelphia: Lea &

Febi~er

;

19&5:151-53

6 Reddy PS. Curtiss El , OT<>ole JD, Shaver JA. Cardiat· tamponade: hemodynamic observations in man. Circulation 1978; 58:26572

We present a rare case of simultaneous bilateral pneumothorax complicating bronchioloalveolar cell carcinoma. Autopsy revealed that numerous subpleural alveolar spaces were distended and most of the small airways were narrowed by cancer cells. We conclude that a check-valve mechanism may be responsible for pneumothorax in patients with bronchioloalveolar cell carcinoma. (Chest 1991; 100:853-.55)

S

all histolo~ic pontant•ous pneumothorax complkatin~ cann·r has been reported.' " hut few typt•s of lun~ in patit•nts with hronchiodescriptions of this <.~nnplication loalvt•olar cell carcinoma exist. 1· 1 Sen·ral pathophysiolo~ic explanations li1r pneumothorax in lun~ cancer have lwt•n propost•d, hut the exact mechanism in bronchioloalveolar cdl carcinoma is not known. \\'t• report a rart· case of hronchiosimultaneous bilateral pneumothorax complicatin~ loalveolar cell carcinoma, in which the check-valve nwchanism appeared to he the cause of tlw pnt•umothorax . CASE HEI'OI\T

A 47-year-old man was admiltt•d to tilt' hospital with a !-month Tht• du··st dyspnea and prodnctiw con~h. history of pro~ressivt' at the tinw of hospital admission rt'\'Palt·d dilfnst• · nof..'ram rot•nl~t and arlt'rial hoth hm~s. nodular and infiltrativt' shadows involvin~ examination of St'Vt•ral showed hypoxt·mia. Baclt'riolo~ie blood ~ases haett•ria, acid-fast haeilli , sputum samples failed to n•n·al patlu1~enie A Inn~ hiopsy spt•<:imen ohtaiolt'd hy fiht·rhrondu>Sl"PY or fnn~i. showed bronehioloaln•olar eelleardnoma of tilt' Inn~ . of )() mw'sIhorat~s intervention was madt• at that time. Six days latt-r. tht• lt•ft mort• st•vt•re. ami tilt' dyspnea l~ei.'re. a chest tnhe l'>nnt•t·lt·d to a llt•imlieh valve was inst·rted relief of the into the left pleural spat·t·, whid1 resulted in a sli~ht tilt' pulmonary infiltrations ht•dyspnea. llowever, radiolo~ieally. eamt• worse, and the palit•nt's t1mdition dt'teriorated pro~rt•ssivt·ly. lit• died of respiratory failnn· 31 days aftt·r the start of chemotlu•rapy, chest tuhe insertion. durin~ Autopsy revealed small pnennwthoran•s hilatt•rally. Macrost,lpi· was replat't.'d hy eally, almost all the parendoyma of hoth lnn~s nodular tnmors that had t•mleseed. and there were numerous small There was '"' mali~nant hoth lnn~s. cavities scattered thron~hont of the hronchi. The site of ori~in invasion of the pleura or lar~er two pneumothoraces t•mld not l~t• idt•ntified in the visceral pleura. *From the Departmt•nl of holt•rnal 1\lt•dicint•, tlw Japanese Hed First llospital. (Drs. Minami and Sakai). and tht• Cross Na~oya Uniwrsity SchtH>I First Department oflnternall\ledieint•, Na~oya Japan. of Medicine (Drs. Watanabt• and Shimokata), Na~oya, Slwwa-ku, .'IJagoiJll Rt•1Jrint n•quests: Dr. Shimokuta , T .,~~nlllllli-cho, -166. )aJHm CHEST I 100 I 3 I SEPTEMBER. 1991

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