Pericardiocentesis induced intrapericardial thrombus: Detection by two-dimensional echocardiography

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2. Cohen LS, Friedman WF, Braunwald E: Natural history of mild congenital aortic stenosis elucidated by serial hemodynamic studies. Am J Cardiol 30:1, 1972. 3. Bogart DB, Murphy BL, Wong BYS, Pugh DM, Dunn MI: Progression of aortic stenosis. Chest 76:391, 1979. 4. Cheitlin MD, Gertz EW, Brundage BH, Carlson CJ, Quash JA, Bode RS Jr: Rate of progression of severity of valvular aortic stenosis in the adult. AM HEART J 98:689, 1979.

Pericardiocentesis induced intrapericardial thrombus: Detection by two-dimensional echocardiography Allan H. Schuster, Rochester, N. Y.

M.D.,

and Navin

C. Nanda,

M.D.

Hemopericardium may complicate pericardiocentesis’ and may result in the failure of a patient with tamponade to respond with clinical and hemodynamic improvement after removal of pericardial fluid. We have recently used real-time two-dimensional echocardiography (BDE) to detect a large intrapericardial thrombus in a patient who failed to clinically improve after therapeutic pericardio-

From the Cardiology Unit, University of Rochester Medical Center. Supported by Research Training Grant HL 07220 from the National Heart, Lung and Blood Institute, National Institutes of Health and by a Grant-in-Aid from the American Heart Association, Genessee Valley Chapter. Received for publication Oct. 16, 1981; accepted Oct. 26, 1961. Reprint requests: Navin C. Nanda, M.D., Cardiology Unit-Box 679, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642.

August, 1992 Heart Journal

centesis. To the best of our knowledge this has not been reported previously. The patient was a 62-year-old former heavy smoker, 1 year after left lower lobectomy and radiotherapy (ECOG protocal 3578) for poorly differentiated adenocarcinoma with hilar metastases. He presented to the Emergency Department with a chief complaint of increasing dyspnea of 3 weeks’ duration. Physical examination revealed a tachycardia of 132 bpm, blood pressure of 110/80 mm Hg with 30 mm Hg pulsus paradoxicus. Jugular veins were distended, breath sounds were diminished at the lung bases, a pericardial friction rub was noted, and the extremities showed moderate edema. Initial real-time 2DE examination showed large anterior and posterior pericardial effusion spaces (35 mm in maximum width) which contained no echo densities (left panels of Figs. 1 and 2). Within the next 6 hours, because of declining blood pressure and presumptive clinical diagnosis of cardiac tamponade, emergency pericardiocentesis was performed and approximately 3’75 ml of serosanguinous fluid was removed. However, the patient’s blood pressure did not increase after pericardiocentesis and he remained dyspneic. Repeat echocardiographic examination, done about 12 hours after pericardiocentesis, revealed a new large crescent-shaped echo density measuring maximally 65 mm by 15 mm (middle and right panels of Fig. 1). In short axis, the mass measured 13 mm (middle and right panels of Fig. 2). This was contained within a persistent pericardial effusion space which measured maximally 25 mm (Figs. 3, 4, and 5). Subsequently, the patient underwent pericardiotomy and pericardial biopsy; 800 ml of serosanguinous fluid was removed and a spongy intrapericardial mass consistent with a thrombus was palpated by the surgeon. Cytological and pathological examinations were consistent

Fig. 1. Apical four chamber two-dimensional echocardiogram. Left, demonstration of a large pericardial effusion (PE) prior to pericardiocentesis. Middle, after pericardiocentesis, echocardiogram displays a large crescent-shaped intrapericardial thrombus (TH) present within the pericardial effusion. Right, schematic diagram of middle panel. RV = right ventricle; LV = left ventricle; RA = right atrium; LA = left atrium; R = right; L = left; S = superior; I = inferior.

0002-8703/82/080308+ 04$00.4O/Oa 1982 The C.V. Mosby Co.

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Fig. 2. Short axis two-dimensional echocardiogramat the aortic root level. Left, prior to pericardiocentesis,demonstration of a large pericardial effusion (PE) anteriorly. Middle, after pericardiocentesisa large echodensity, indicating thrombus (TH), is seenwithin the pericardial effusion. Right, schematicdiagram of middle panel. AV = aortic valve; RVO = right ventricular outflow tract; RA = right atrium; LA = left atrium; R = right; L = left; A = anterior; P = posterior.

Fig. 3. Magnified apical four-chamber two-dimensional echocardiogram showing thrombus (TH) as depicted by the diagram.

with fibrous and fibrinous pericarditis and revealed no evidence of intrapericardial malignancy. After treatment by continuous intrapericardial catheter drainage and intrapericardial instillation of the sclerosingagent, quinacrine, 2DE was repeated and revealed disappearanceof intrapericardial thrombus. The patient wassubsequently dischargedwith the diagnosisof radiation pericarditis. Echocardiography is currently the procedure of choice for diagnosisof pericardial effusion, having largely supplanted angiographic and roentgenographic diagnosis.2As first demonstrated by our laboratory, real-time 2DE

readily demonstrates the presence of fibrinous strands and adhesionswithin the intrapericardial space.3This has been subsequently confirmed by others who have also suggestedthat intrapericardial thrombus might be visualized by echocardiography. However, this has never been substantiated by surgical or pathological correlation. One limitation of echocardiography is the inability to differentiate between transudative pericardial effusions, exudative pericardial effusions, and hemopericardium without thrombus formation. In each of these three instances,an acoustically homogenousmedium results in

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August, 1982 Heart Journal

PE

Fig.

4. Magnified

Fig. 5. Parasternal pericardial effusion

short-axis

2DE view of the thrombus

(275) illustrated

by the diagram.

short-axis 2DE view of the left ventricle (LV) in cross section (PE) and thrombus (TH) as represented by the diagram.

the appearance of an echo-free space in the echocardiogram. Intrapericardial fibrin strands may be seen with both inflammatory and serosanguinous effusions, and therefore their presence does not help identify the nature of the pericardial effusion. However, the development of a large echo density after pericardiocentesis identifies the

demonstrating

presence of hemopericardium with thrombus formation. The rapid appearance of the echogenic mass after peticardiocentesis aids in distinguishing thrombus from tumor which may also be visualized in the intrapericardial space and which may present a similar appearance.5 In summary, we believe that serial echocardiographic examinations

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are useful in evaluating patients who are undergoing pericardiocentesis to identify patients at risk for tamponade related to iatrogenic hemopericardium with thrombus formation. REFERENCES

1. Darsee JR, Braunwald E: Diseases of the pericardium. In Braunwald E, editor: Heart disease: A textbook of cardiovascular medicine. Philadelphia, 1980, W. B. Saunders Co, chapter 41. 2. Feigenbaum H: Pericardial disease. In Echocardiography. 3rd ed. Philadelphia, 1981, Lea & Febiger, chapter 10. 3. Nanda NC, Gramiak R, Pocoski DP, Epps WE: Evaluation of pericardial and pleural effusions and adhesions by twodimensional echocardiography. Proceedings of the Twentythird annual meeting of the American Institute of Ultrasound in Medicine 1:68, 1978. 4. Martin RP, Bowden R, Filly K, Popp RL: Intrapericardial abnormalities in patients with pericardial effusion: Findings by two-dimensional echocardiography. Circulation 61:568, 1980. 5. Farooki ZQ, Hakimi M, Arciniegas E, Green EW: Echocardiographic features in a case of intrapericardial teratoma. J Clin Ultrasound 6:108, 1978.

Sudden death in aortic stenosis monitored by ear densitographic pulse and ECG George Nikolic, M.D., Bruce G. Haffty, M.S., Richard

L. Bishop,

M.D., Jang B. Singh,

M.D.,

Athanasios P. Flessas,M.D., and David H. Spodick, M.D. Worcester, Muss. A patient with valvular aortic stenosis(AS) died during continuous external pulse and ECG (Holter) monitoring, demonstrating terminal hypotension in the absence of significant arrhythmia. A previously described method from this institution (SHK system) for simultaneous external pulse and ECG monitoring was used.’ The patient was an 88-year-old woman with a long history of angina pectoris and exertional dyspnea secondary to AS and presumed coronary artery disease(CAD). Several syncopal episodeswere preceded by angina1pain with ischemic changeson ECG and followed by loss of palpable pulsesand grand ma1convulsions. The interval ECGs showed stable pattern of left ventricular (LV) hypertrophy with ST/T wave changesand prominent U waves; chest x-ray examination showedcardiomegalywith tortuous aorta and clear lung fields. A standard Holter monitor

study 2 days prior

to death showed

several brief

runs of ventricular (VT) and supraventricular tachycardia unassociatedwith chest pain or dizziness, occurring during sinus rhythm. At this stagequinidine sulfate, 300 mg four times daily, was added to her previous therapy of nitrates,

nifedipine,

From the Division ment Received Reprint Vincent

of Medicine,

OOOZ-8703/82/080311+

and

of Cardiology, St. Vincent University of Massachusetts

for publication requests: Hospital,

furosemide,

Jan.

‘7, 1982;

accepted

David H. Spodick, M.D., 25 Winthrop St., Worcester,

02$00.20/O

0 1982

phenytoin,

Hospital, Medical March

and

a

and the DepartSchool. 4, 1982.

Division of Cardiology, MA 01604.

The

Fig. 1. Sequential tracings showing important changes obtained from the continuous SHK recording of external pulse waves and ECG. See text for explanation.

C. V. Mosby

St.

repeat

Holter

monitor

with

ear densitographic

panel

5 to 7). She did

not

respond

to resuscitative

measuresover the following hour and died in asystole. Autopsy showed marked calcific stenosisof a tricuspid aortic valve. The heart weighed420 gm; the LV cavity was small with concentric wall hypertrophy of 2.5 cm and several old scars.The coronary arteries were patent. In direct observations of near syncope*and syncope or sudden death3*4 in AS, the primary

Co.

pulse

(SHK system’) was instituted. One hour later she was found pulselessand apneic, still in sinus rhythm (Fig. 1,

disturbance

appears to