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patient for whom only a single-planeTEE wasused.Interestingly, the incidence of LAT’ in patients with atrial fibrillation by TEE appearsto be lessthan that noted during autopsy.l, 3,5Resumption of sinusrhythm and possibly the atria1 kick may have driven a thrombus out of the left atria1 appendagein the secondcase.Moreover, atria1 mechanical activity may lag behind its electrical stability. The recurrence of atria1 fibrillation may have alsobeen responsible for the formation of a new thrombus that embolized. The Framingham Study6 suggestsa clustering of thromboembolicevents shortly after recurrence of atria1 fibrillation, although other studies do not confirm that. There hasbeena lack of consensusregarding the need of anticoagulant therapy before cardioversion in patients with atria1 fibrillation. Recently, data from the retrospective study of Arnold et al.1°support the usualclinical practice of anticoagulation therapy before and after elective cardioversion of atria1 fibrillation. Embolic events were seenonly in patients with atrial fibrillation who were not receiving anticoagulant therapy. However, their study did not include TEE-documented absence of LAT/LASC. Both patients in this report were at low risk for thromboembolic events, did not have LAT/LASC, and had a contraindication for anticoagulant therapy. Our casessuggest that the decision to anticoagulate a patient with chronic atria1fibrillation shouldnot entirely dependon the absenceof LAT/LASC. These casessupport the conservative approach of anticoagulant therapy before and after cardioversion, regardlessof the absenceof LAT/LASC. A large-scalemulticenter trial is neededto resolvethe role of anticoagulant therapy for elective cardioversionin patients with nonrheumatic atria1 fibrillation. REFERENCES 1. Lee RJ, Bartzokis

2.

3.

4.

5.

6.

I. 8.

9.

10.

T, Yeoh TK, Grogin HR, Choi D, Schnittger I. Enhanced detection of intracardiac sources of cerebral emboli by transesophageal echocardiography. Stroke 1991;22: 734-9. Cujec B, Polasek P, Voll C, Shuaib A. Transesophageal echocardiography in the detection of potential cardiac source of embolism in stroke patients. Stroke 1991;22:727-33. Black IW, Hopkins AP, Lee LCL, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. J Am Co11 Cardiol 1991;18:398-404. Wolf PA, Dawber TR, Thomas HE, Kannel WB. Epidemiologic assessment of chronic atrial fibrillation and risk of stroke: the Framingham Study. Neurology 1978;28:973-7. Hinton RC, Kistler JP, Fallon JT, Friedlich AL, Fisher CM. Influence of etiology of atria1 fibrillation on incidence of systemic embolism. Am J Cardiol 1977;40:509-13. Wolf P, Abbott RD, Kannel WB. Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study. Arch Intern Med 1987;147:1561-4 Zincs DP. In Braunwald E. ed.: Heart disease. 1992:683. The Stroke Prevention in’ Atria1 Fibrillation investigators. Predictors of thromboembolism in atria1 fibrillation. I. Clinical features of oatients at risk. Ann Intern Med 1992;116:1-5. The Stroke Prevention in Atria1 Fibrillation investigators. Predictors of thromboembolism in atrial fibrillation. II. Echocardiographic features on patients at risk. Ann Intern Med 1992;116:6-12. Arnold AZ, Mick MJ, Mazurek RP, Loop FD, Frohman RG. Role of prophylactic anticoagulation for direct current car-

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dioversion in patients with atrial J Am Co11 Cardiol 1992;19:1851-6.

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or atria1

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Usefulness of traqsesophageal Doppler echocardiography in the surgical drainage bf a loeulated purulent pericardial effusion Robert J. Golub, MD, CandaceM. McNulty, MD, JosephR. McClellan, MD, Linda St. Laurent, RDCS, and Michael W. Prior, MD Providence, R.I.

Indications for transesophagealDoppler echocardiography (TEE) continue to evolve.l, 2 We would like to proposeyet another: surgicaldrainageof loculated purulent pericardial effusions guided by TEE. Current treatment of purulent pericarditis consistsof open surgical drainage and antibiotic agents.3a4 If drainageis inadequate, mortality increases.3Complete evacuation may be diicult becauseof multiple noncommunicating compartments of purulent material.3-5Thesesequesteredspacesmay not be appreciated at surgery, especially if there is hemodynamic improvement after the initial incision. A secondincision may be needed for complete drainage.The usefulnessof TEE becameapparent to us during surgicaldrainage of a loculated purulent pericardial effusion in a 63-year-old man. TEE detected continuing regional tamponade of the left ventricle and a secondloculated pericardial effusion following the initial evacuation, Drainage would have been inadequateif TEE had not been performed. A 63-year-old man developed progressivedyspnea and ankle edema;he had received chemotherapy for squamous cell carcinomaof the lung 2 weeksbefore these complaints. On admission,he was in mild respiratory distresswith a blood pressureof 110/70mm Hg, a heart rate of 100beats/ min, and a temperature of 38.9’ C. His jugular venous pressurewas increasedand pulsusparadoxus was 24 mm Hg; a pericardial rub wasnot heard. The white blood cell count was33,900with 85% polymorphonuclear leukocytes and 5% band forms. The electrocardiogram showedsinus tachycardia, poor R wave progression, and nonspecific ST-T wave changes.The chest x-ray film discloseda large cardiac silhouette and both a cavitating nodule and smalI pleural effusion on the left side.Transthoracic two-dimensional echocardiography (Fig. 1, A through C) revealed tamponade physiology and a large loculated anterior and posterior pericardial effusion.6-sNumerous linear echo strands extended between the parietal and visceral surfacesof the pericardium. Both the ventricular apex and the From The Division of Cardiology, Department of Internal Medicine, Memorial Hospital of Rhode Island, Brown University School of Medicine. Reprint requests: Candace M. McNulty, MD, Division of Cardiology, Memorial Hospital of Rhode Island, 111 Bpewster St., Pawtucket, RI 02860. Ah! HEART

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1. Still frames of transthoracic two-dimensional echocardiogramsfrom the subcostalwindow, showing a large anterior and posterior pericardial effusion (PE) in panels A and B. In panel A, there is collapse (arrows) of the free walls of the right ventricle (R V) and left ventricle (LV) during diastole. In panel B during systole, compressionof the LV and RV walls is no longer apparent (arrows). In patiel C, linear echo strands (LX) are shownwithin the pericardial effusion (PE), which suggestthe presenceof ,aloculated effusion. LA, Left atrium; RA, right atrium.

Fig.

atria were fixed to the pa&eta1 surface and divided the pericardial space into two separate noncommunicating compartments. The free walls of both ventricles collapsed during diastole. Right heart catheterization demonstrated elevation and equalization of the mean pulmonary capillary wedge, pulmonary artery diastolic, and mean right atria1 pressures.Surgical drainage was recommendedbecauseof the presenceof loculation. Before surgery, the patient’s blood pressurewas110/60mm Hg and pulsewas110 beats/min. TEE showedcompressionof the superior vena cava, right atrium, and right ventricle by the anterior effusion (Fig. 2, A and B) and of the left ventricle by the posterior effusion. The free walls of both ventricles collapsed during diastole. As the surgeonopened the pericardial sac with a subxiphoid incision, 300 cc of thick yellow pus poured out. When this occurred, the size of the superior vena cava, the right atrium, and the right ventricle (Fig. 2, C andD) increasedto normal; blood pressureroseto 130/80 mm Hg; heart rate dropped to 90 beats/min. All purulent material appearedto have been drained on visual inspection and manual exploration of the pericardial space.TEE imaging, however, showedcontinued diastolic collapseof the left ventricuhar free wall and compression of this chamberby an adjacent large posterior pericardial effusion (Fig. 3, A and B). A secondincision (left subcostalarea)was made and yielded an additional 400 cc of pus. Simultaneously, diastolic collapseof the left ventricular free wall resolved, waI1 motion became normal, and chamber size

increasedto normal (Fig. 3, C and D). The blood pressure rose to 150/90 mm Hg, the heart rate decreasedto 80 beats/min, and the pulsus paradoxus decreasedto 8 mm Hg. There were no complications related to TEE. Following placement of drainage tubes and closure, the patient was treated with intravenous penicillin and had an uneventful recovery. Culture of the purulent effusion grew Streptococcus

pneumoniae.

Purulent pericarditis is an uncommon diseasewith a mortality approaching 100% if undiagnosed.45,g When treated only with antibiotic agents,the mortality is 66% to 82%.g,l1 The addition of pericardiocentesisdecreasesmortality to 36%; however, pericardiocentesisis usually inadequate, asreaccumulation is common.12Complete surgical drainageis necessaryfor optimal care, and reducesmortality to less than 20%.3,4 If the space is not completely drained, the fibrinous exudative effusion continues to enlarge.5Eventually, extensive shaggyadhesionsdevelop between the pericardial surfacesand produce noncommunicating compartments containing purulent material5 This occurred in our patient. Both atria and the ventricular apex were firmly attached to the parietal pericardium. The inflammatory process effectively divided the pericardial spaceinto two separatenoncommunicatingcompartments. This was not initially appreciated with a subxiphoid approach.TEE demonstration of continuing tamponadeof the left ventricle and of a second effusion persuadedthe surgeonto make a second (subcostal) incision; only then

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Fig. 2. Still frames of transesophagealechocardiogramsfrom basalshort-axis (panels A and C) and fourchamber (panels B and D) views. Panels A and B showcompressionof the lumen of the superior vena cava (SVC) and of the right atrial (RA) and ventricular (RV) chambersby the pericardial effusion (PE). Panels C and D show an increasein the size of the SVC, RA, and RV simultaneously with the initial drainage of the pericardial effusion (PE). Ao, Aorta; LA, left atrium; LV, left ventricle.

Fig. 3. Still frames of transesophagealechocardiogramsfrom transgastric short-axis views. Panets A ad

B shopia pleural effusion (FZE) ‘and a large posterior perjcardial effusion (PE) adjacent to the free wall’ of the left ventricle (LV). Panel A ishowscompression(arrow) and flattening of the LV free wall during,diastole. Panel B showsthat the ro$nd c’ontour I(cj+row)of the LV,free wall: returns during systole. Panels C and D showan increasein LV chamber sizefollowing the secondincision atid drainageof the pericardial effusion. Panel D alsoshowsresolution of diastolic compression(arrows) of the LV free wall. RV, Right ventricle; LV, left ventricle.

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was there complete drainage o? the effusion and resolution of tamponade. In our patient, a complete pericardiectomy was considered but was not performed because of his poor medical condition and widespread malignant disease. The TEE was well tolerated by the patient. This case report illustrates that TEE is able to precisely determine both the location and the number of sequestered compartments of a loculated pericardial effusion. We feel that TEE is very useful during open surgical drainage of loculated Pericardial effusions because it accurately identifies location and loculation, ensuring adequate drainage. To our knowledge, this is the first reported case of TEE-guided surgical drainage of a loculated purulent pericardial effusion. Based on this case report, we suggest that surgical drainage of patients with loculated or purulent pericardial effusions be added to the list of indications for TEE. REFERENCES

1. FisherEA, Stahl JA, Budd JH, GoldmanME. Transesophagealechocardiography: procedures andclinicalapplication.J Am Co11 Cardiol1991;5:1333-48. 2. Aebischer N, Katz A, McNulty C,ParisiAF. Transesophageal echocardiography: its usein today’scardiology.RI Med J 1991;11:511-6.

Majid AA, OmarA. Diagnosis and management of purulent pericarditis.J ThoracCardiovascSurg 1591;2:413-7: CameronEWJ. Surgicalmanagement of stauhvlococcal Dericarditis.Thorax 19?$30:678-81. KlacsmannPG, Bulkley BH, Hutchins GM. The changed spectrumof purulentpericarditis.Am J Med 1977;63:666-73. EisenbergMJ, SchillerNB. Bayes’theoremandthe echocardiographicdiagnosisof cardiactamponade.Am J Cardiol _

I

199i;68:1242-4: I.

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ChandraratnaPAN. Echocardiography and Dopplerultrasoundin the evaluationof oericardialdisease.Circulation 1991;84(suppl I):I-303-10. HindsSW, ReisnerSA, AmicoAF, Meltzer RS. Diagnosis of pericardialabnormalities by ZD-echo:a pathology-echocardiographycorrelationin 85patients.AM HEART J 1992;123:14350.

Berk SL, RicePA, ReynoldsCA, Finland M. Pneumococcal pericarditis:a persistingproblemin contemporarydiagnosis. Am J Med 1981;70:247-51. 10. FeldmanWE. Bacterialetialogy and mortality of purulent pericarditis in pediatric patients. Am J Dis Child 1979;133:641-4. 11. JaiyesimiF, Abioye AA, Antia AU. Infective pericarditisin Nigerianchildren.Arch Dis Child 1979;54:384-90. 12. Weir EK, JoffeHS. Purulentpericarditisin children:ananalysisof 28cases.Thorax 1977;32:438-43. 9.

Purulent pericarditis caused by group streptococcus with pericardial tamponade

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M. Asad Karim, MD, Richard G. Bach, MD, Frederick Dressler, MD, Eugene Caracciolo, MD, Thomas J. Donohue, MD, and Morton J. Kern, MD St. Louis, Missouri From the Department of Internal Medicine, Division of Cardiology, St. Louis University Hospital. Reprint requests: Morton J. Kern, MD, J.G. Mudd Cardiac Catheterization Laboratory, St. Louis University Hospital, 3635 Vista Ave. at Grand Blvd., St. Louis, MO 63110.

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Purulent bacterial pericarditis is a rare complication in the postantibiotic era.l The vast majority of adult patients who have pyogenic pericarditis today have chronic underlying conditions or diseasessuch as prior thoracic surgery, chronic renal failure, carcinoma, diabetes mellitus, or a myeloproliferative disorder. Infection of the pericardium can occur via direct extensionfrom infectious endocarditis, pneumonia, a pleuritic process,or from a more distant source,such as otitis media, meningitis or skin infection.2 The most common bacterial pathogens of purulent pericarditis identified in a recent report2 were Staphylococcus aureus (22%), Streptococcus pneumoniae (22%), and Streptococcus pyogenes (17%). Enterobacteriaceae have alsobeenfound to causepurulent infection of the pericardium in the immunocompromisedhost. Pericardial infections causedby both group G and A streptococci were recently reported334 in a long-time alcoholic and in a previously healthy child. Streptococcus agalactiae is a group B streptococcus which is among the common flora of the pharynx, gastrointestinal tract, and vagina. Infections of the skin and puerperium and neonatal septicemiaare the most common clinical manifestations of S. agductiae infection. Thus far group B streptococcus has not been identified as a causeof primary purulent bacterial pericarditis. We report a case of a woman with cardiac tamponade caused by purulent pericarditis caused by group B streptococcus (S. ugaluctiae). A Bl-year-old Native American woman with diabetes mellitus and rheumatoid arthritis was seen in the emergency department for weakness,light-headedness, and dyspnea for 3 days. She denied any recent fever, chills, or flu-like symptoms.In the emergencyroom her blood pressure was88/62 mm Hg, pulse rate 90 beats/m& temperature 97.6” C, and respirations 22 per minute. A paradoxic pulse of approximately 10 mm Hg was present. She was alert and oriented and in no apparent distress. Jugular venous distention to 15 cm was observed. Heart sounds were distant and m&led. There was a 1 cm round circumscribed chronic-appearing skin ulcer on the medial malle01~s.Initial laboratory data revealed a white blood cell count of 15,000with 85% polymorphonuclear neutrophils. Electrolytes were within normal limits. Serum glucosewas elevated at 184 mg/dl. No serum or urinary ketones were found. A urine analysisrevealedthe presenceof white cells and bacteria. An electrocardiogram showednormal sinus rhythm, decreased voltage, and diffuse 1 to 1.5 mm ST-segment elevation in the precordial and inferior leads (Fig. 1). Chest roentgenogramrevealed a large cardiac silhouette with a blunted left costophrenic angle. A twodimensionalechocardiogramperformed in the emergency department revealed a largepericardial effusion with diastolic collapseof the:right ventricle consistent with pericardial tamponade. Left ventricular dimensionsand wall motion were normal. yhe patient wassubsequentlyadmitted to the intensive care unit with a diagnosisof pericardial effusion of uncertain causeand wastreated with fluid resus-

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