Echocardiographic Documentation of Splenic Anatomy in Complex Congenital Heart Disease Patrick W. O’Leary, MD, James B. Seward, MD, Donald J. Hagler, MD, and A. Jamil Tajik, MD plenic abnormalities are associatedwith complex, cyanotic congenital heart disease(CHD).*,* Patients with abnormal spleensmay also have an increasedsusceptibility to infection3F4or additional characteristic gastrointestinal anomalies2 For thesereasons, it is important to routinely define the splenic status of patients with complex CHD. In the past, determination of splenic status neededeither radiation exposure(computed tomography or radionuclide imaging)5~6or indirect evidence from blood smears (presence or absence of Howell-Jolly bodies).la7Ultrasonography can image the spleenconsistently and clearly.8 Routine ultrasonic imaging of the spleenas a part of a comprehensiveechocardiographic examination has not been reported. This study reports our recent experiencewith routine visualization of the spleenduring complete echocardiographic examinations of patients with complex CHD. We retrospectively reviewed the records of 57 patients who had a comprehensive echocardiographic evaluation for cyanotic CHD betweenMay 1989 and January 1990 (8 months). Data were recorded regarding the results of routine echocardiographic imaging of the spleen, cardiovascular anatomy and ultimate outcome. Results of the echocardiographic examination were compared with available hematologic, ra-

diographic and autopsy documentation of splenic status. To examine the spleen, the abdominal situs and position of the liver and stomach were determined from subcostal abdominal scans (Figure 1).9 The transducer was then transferred to theflank, posterior to the previously identified stomach. When a spleen was present it was invariably located posterior and lateral to the stomach, and superior to the kidney.l*lo~ll Scans from the flank demonstrated the spleen to be a distinct, homogeneous granular organ without the portal vascular pattern that is characteristic of the liver. Another feature that in our experience differentiated the spleenfrom the liver was that hepatic tissue was never imaged posterior and lateral to the stomach with this technique. The spleen was considered normal when it was single andfound in the previously described location (Figure 2). Polysplenia was diagnosed when there were multiple discrete areas of splenic or septated splenic tissue imaged in the appropriate location (Figure 3). The examination was consistent with asplenia when no areas with splenic characteristics could be identijed. Mortality rates in the 3 groups of patients were compared using chi-square analysis. Only p values SO.05 were considered signiJicant. From the Section of Pediatric Cardiology, Mayo Clinic and Mayo Echocardiography could be used to make a diagFoundation,200 First Street SW, Rochester,Minnesota 55905.Manuscript received May 21, 1991;revised manuscript received August 1, nosis of splenic status in each case. The spleen was

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1991,and acceptedAugust 3.

FIGURE 1. Normal subcostal (abdominal) sbrt-axis scan demenstrating gas-filled stemack that ebsuwes posterier shubres. WC = inferior vena cava; VB = vertebral body.

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FlGURE 2. Image from pmtehr naal spleen.

DECEMBER 1, 1991

lett flank dsmonstrating

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echocardiographically normal in 32 patients. Although normal, it was right-sided in 2 patients. The patients with normal spleens had a mean age of 6 years (range I day to 25 years). Polysplenia was diagnosed by echocardiography in 11 patients, and no splenic tissue could be identified in 14 (asplenia). Patients with polysplenia had a mean age of 6 years (range 6 months to 13 years). Asplenic patients had a mean age of 13 years (range 4 to 31). Patients with normal spleens had various cardiac malformations (Table I). All 11 patients with polysplenia had interruption of the inferior vena cava, with either azygous or hemiazygous continuation and independent hepatic vein drainage. Ten of these patients also had a complex form of single ventricle. The eleventh patient had complex double-outlet right ventricle. All 14 patients with asplenia had a form of complete atrioventricular canal defect with a functional single ventricle and pulmonary valve stenosis or atresia. Thirteen of these patients also had anomalous pulmonary venous connections. Fourteen of the 43 patients with echocardiographitally detectable splenic tissue had blood smears. Howell-Jolly bodies were absent in every case. Ten of the 14 asplenic patients had blood smears. All of these smears were positive for Howell-Jolly bodies. Fifteen patients underwent another diagnostic study that provided information on splenic anatomy (14 computed tomographic or magnetic resonance scans and 1 autopsy). Eleven other imaging studies were able to determine splenic status, and 4 studies were inconclusive. When these examinations were able to conclusively define splenic status, the findings always agreed with the echocardiographic description of the spleen. Fifty-four of the 57 patients in this study had a subsequent cardiovascular operation. Twenty-nine patients with normal spleens underwent surgery. There were 3 nonsurviving patients in this group (mortality 10.3%). All patients with polysplenia and asplenia underwent surgery. All 11 patients with polysplenia survived surgery. There was 1 nonsurviving patient in the group with asplenia (mortality 7.1%) who died secondary to sepsis. None of the other deaths were related to infection. There were 6 late deaths in the 50 initial surviving patients. Two patients had normal spleens, 1 had polysplenia and 3 were asplenic. Two of the 3 late deaths in the group with asplenia were secondary to sepsis. None of the other deaths were related to infection. The only statistically significant difference in outcome was in the group with asplenia. Even with antibiotic prophylaxis, these patients had a significantly higher rate of infection-related death (p = O.OI) than did those with normal spleens. The group with poly-

k

TABLE I Cardiovascular Malformations

in Patients with

Univentricular heart Complete transposition of the great arteries Pulmonary atresia with VSD Pulmonary atresia with intact ventricular septum Complete AV canal with tetralogy of Fallot Complex double-outlet right ventricle

11 6 5 2 2 2

*One patient had each of the following: tetralogy of Fallot; complete AV canal with hypoplasia of the left ventricle; tricuspid atresia; and truncus arteriosus. AV = atrioventricular; VSD = ventricularseptal defect.

splenia was too small to allow a valid statistical comparison.

Defining the splenic status of patients with complex CHD is clinically important for severalreasons.Patients with aspleniaare at higher risk of sepsisfrom encapsulated bacteria.3T4Even with prophylaxis, the rate of infection-related death in our patients with asplenia was greater than it wasin thosewith normal spleens.The fact that all of these patients had major surgery during the study period may, in part, explain the persistent risk of sepsis.Compliance may alsohave played a role. Regardlessof the explanation for this finding, when aspleniais diagnosed, daily antibiotic prophylaxis should be prescribedto decreasethe risk of sepsis.l 2Additionally, presenceof an abnormal spleenmay suggestthe coexistence of associatedanomaliesof the cardiovascularand gastrointestinal systems.1T2 The spleenand splenic anomaliescan be confidently identified during a comprehensiveechocardiographicexamination. In this series of 57 patients with complex CHD, the echocardiographicdiagnosisof splenic status was confirmed in every case in which complimentary studies were available.

FIGURE 3. Image from posterior lyspleni.

left Rank demonstrating

BRIEF REPORTS

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Echocardiographic screeningfor splenic anomaliesis convenient and accurate, and avoids radiation exposure. When results of echocardiographic screening are combined with thoseof a blood smear,the clinician obtains a complete anatomic and functional assessmentof splenic status. We recommendthat splenicimaging be included as a routine part of the completeechocardiographicevaluation of patients with complex CHD.

1. Van Mierop LHS, GessnerIH, Schiebler GL. Asplenia and polyspleniasyndromes.Birrh Defects 1972;8:36-44. 2. Ruttenberg HD. Corrected transposition of the groat arteries and splenic syndromes.In: Adams FH, EmmanouilidesCC, RiemenschneiderTA, eds.Moss’ Heart Diseasein Infants, Children, and Adolescents.4th ed. Baltimore: Williams & Wilkins, 1989;424-442. 3. Gopal V, Bisno AL. Fulminant pneumococcalinfections in ‘normal’ asplenic hosts.Arch Intern Med 1977;137:1526-1530.

4. Waldman JD, Rosenthal A, Smith AL, Shurin S, Nadas AS. Sepsisand congenital asplenia.J Pediatr 1977;90:555-559. 5. FreedomRM, TrevesS. Splenicscintigraphy and radionuclide venographyin the heterotaxy syndrome.Radiology 1973;107:381-386. 6. Myers MJ. Spleen imaging. Clin Lab Haematol 1983;12:395-420. 7. Fefer A. Enlargementof lymph nodesand spleen.In: PetersdorfRG, Adams RD, Braunwald E, IsselbacherKJ, Martin JB, Wilson JD, eds.Harrison’s Principles of Internal Medicine. 10th ed. New York: McGraw-Hill, 1983;298-304. 8. Niederau C, SonnenbergA, Muller JE, ErckenbrechtJF, SchohenT, Fritsch WP. Sonographicmeasurementsof the normal liver, spleen,pancreasand portal vein. Radiology 1983;149:537-540. 9. Seward JB, Tajik AJ, Edwards WD, Hagler DJ. Extracardiac anatomy. In: Two-Dimensional EchocardiographicAtlas. Vol 1: Congenital Heart Disease. New York: Springer-Verlag, 1987;66-68. 10. Stanger P, Rudolph AM, Edward JE. Cardiac malpositions:an overview basedon study of sixty-five necropsyspecimens.Circulation 1977;56:159-172. Il. PeoplesWM, Moller JH, Edwards JE. Polysplenia:a review of 146 cases. Pediatr Cardiol 1983;4:129-137. 12. Peter G, Lepow ML, McCracken GH, Phillips CF, eds. Immunization in special clinical circumstances.In: Report of the Committee on Infectious Diseases.22nd ed. Elk Grove Village, Illinois: American Academy of Pediatrics, 1991:52-53.

Frequency of Positive Blood Cultures During Transesophageal Echocardiography Heinz Vt)ller, MD, Christoph Spielberg, MD, Klaus Schrbder, MD, Dieter Gast, MD, and Rolf SchrOder, MD lthough recommendedfor a number of diagnostic and therapeutic proceduresin patients at increasedrisk for infective endocarditis, antibiotic prophylaxis is generally not considerednecessaryfor upper gastrointestinal endoscopy.1y2 Thus, the recent recommendation for antibiotic prophylaxis in transesophageal echocardiography is somewhatsurprising. With the increasing number of transesophagealexaminations,the matter clearly needsthe cardiologists’ attention. In this article, we report on the incidence and nature of positive blood cultures and smearsamplesfrom the echoprobe of patients undergoing transesophagealechocardiography in our department. In 144 consecutive patients undergoing transesophageal echocardiography becauseof central neurologic disorders, blood samples were drawn for blood cultures before (= 0 minutes), during (= 15 minutes) and after (= 30 minutes) the procedure. In 27 of these patients, smear samples of the echoprobe were additionally taken before and after the intervention. In a control group of 40patients without transesophageal echocardiography, blood was obtained for cultures at the same time intervals. After thorough skin disinfection with 70% isopropanol, an indwelling cannula with a 3-way stopcock was placed in the cephalic vein, The 3 blood samples From the Department of Cardiopulmonology, KIinikum Steglitz der Freien Universitlt Berlin, Hindenburgdamm 30, D 1000 Berlin 45, Federal Republic of Germany. Manuscript received May 10, 1991; revised manuscript received and accepted July 22, 199 1.

were each taken from a different disinfected outlet of the 3-way stopcock. Alcohol rather than iodine disinfection was chosen to make our results comparable to those of Gorge et al.3 Skin antisepsis is identical with both methods.” Our purpose in drawing blood samples with an indwelling cannula rather than a new phlebotomy each time was to reduce the possibility of local contamination through subsurface skin bacteria. The blood samples were cultured in aerobic (supplemented brain heart infusion) and anaerobic (thioglycollate medium) liquid media with further subculture on chocolate, MacConkey and malt agar. Smear samples were placed in sterile tubes with culture media. Processing of blood cultures and smear samplesfollowed standard microbiologic procedures. All patients were hospitalized at the time of the investigation. Exclusion criteria were acute or chronic infections, immunologic disorders, antibiotic or immunosuppressive medication or invasive procedures within the previous 3 weeks. A 2-week follow-up included daily physical examinations with rectal temperature readings and 3 blood counts. A furtherphysical examination was performed after 6 months. Of a total of 864 blood cultures from patients undergoing transesophageal echocardiography, 34 (3.9%) were positive with facultative pathogenic bacteria in 31 (Table I). Substracting the 6 cultures already found positive before the intervention leaves 28 positive cultures (3.2%) during or after the procedure. All smear samples were sterile before the intervention

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THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68

Echocardiographic documentation of splenic anatomy in complex congenital heart disease.

Echocardiographic Documentation of Splenic Anatomy in Complex Congenital Heart Disease Patrick W. O’Leary, MD, James B. Seward, MD, Donald J. Hagler,...
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