Clin. Cardiol. 15,697-698 (1992)
Splenic Infarction: A Complication of Cardiac Catheterization MICHAL ROSE,M.D., DGANIT DINOUR, M.D., ROLAND CHISIN,M.D.* Department of Medicine, Hadassah University Hospital, Mount Scopus; *Department of Medical Biophysics and Nuclear Medicine, Hadassah University Hospital, Ein Karem, Jerusalem, Israel
Summary: Patients with extensive atherosclerosis are at increased risk of developing embolic complications during cardiac catheterization. We describe a 5 1-year-old man with unstable angina and bilateral leg claudication who developed fever and right upper abdominal pain shortly after cardiac catheterization. Liver-spleen scintigraphy demonstrated a wedge-shaped filling defect compatible with splenic infarction, and serial scans performed over a period of five months showed resolution of this finding. Splenic infarction tends to be under-diagnosed, and physicians should be aware of this potentially serious complication of cardiac catheterization. Key words: cardiac catheterization,complications, splenic infarction
Introduction Embolic complications, mainly strokes, occur in about 0.1% of patients undergoing cardiac catheterization. l s 2 They occur either as a result of thrombogenesis on the catheter or guide wire surfaces or by the dislodgment of a large particle from a mural thrombus or an atheromatous plaque on an arterial wall.' We report a patient who developed a symptomatic splenic infarction after cardiac catheterization, a complication of this procedure not described previously.
Address for reprints: Dr. Michal Rose Department of Medicine Hadassah University Hospital Mount Scopus P.O.Box 24035 Jerusalem 91240, Israel
Received: January 23, 1992 Accepted March 19, 1992
Case Report A 5 1-year-old man with unstable angina was referred to our catheterization laboratory for left heart catheterization. His risk factors for atherosclerosis included heavy smoking, hypertension, hypercholesterolemia,and obesity. He was suffering from bilateral leg claudication at 50 meters. He had suffered an inferior wall myocardial infarction seven years prior to catheterization and a non-Q wave anterior wall myocardial infarction 10 days prior to the pmcedure. For the latter infarction, he had been treated with 1,500,OOO IU of streptokinase intravenously and then intravenous heparin, 300 mg/day. Heparin treatment was discontinued two hours before catheterization. On physical examination he appeared well, was overweight, and a bruit was heard over his right carotid artery. Peripheral pulses were absent below the femoral arteries in both legs. Using the Judkins technique and a right femoral approach, cardiac and coronary catheterization were performed. The study showed good global left ventricle function with inferior and anterior hypokinesis and total occlusion of the left anterior descending and right coronary arteries. Immediately after the procedure the patient developed left upper abdominal pain, aggravated by breathing, and one h later his temperature rose to 39°C. His pulse rate was 120 beatshin. His abdomen was soft, with slight tenderness in the left upper quadrant. Examination of the heart and lungs was normal. Blood tests showed a leukocytosis of 16,500/ml with a shift to the left. Blood and urine cultures were sterile. A ventilation-perfusionscan of the lungs was normal. A tin-colloid-99mtechnetiumliver-spleen scan, performed six days after catheterization,showed a wedgeshaped filling defect compatible with splenic infarction. The patient was treated with analgesics and bedrest, and his fever and abdominal pain resolved within one week. Three serial liver-spleen scans performed over a period of five months showed resolution of the findings of the original scan.
Discussion Splenic infarction was diagnosed in our patient based on the clinical manifestationsof fever, left upper quadrant
698
Clin. Cardiol. Vol. 15, September 1992
abdominal pain and tenderness, and a liver-spleen scintigraphy showing a filling defect in the ~ p l e e n .Serial ~ . ~ scans, showing the resolution of this finding, further supported the diagno~is.~ Other imaging techniques used in diagnosing splenic infarction include computed tomography and ultras~nography.~ The most common cause of splenic infarction is thromboembolic disease, with emboli dislodging mainly from a diseased aorta, the left ventricle (in acute myocardial infarction and dilated cardiomyopathy), and vegetations on heart valve^.^^^ Busch et al. described a patient on an intraaortic balloon pump, who developed a splenic infarction, presumably caused by the disruption of an atheromatous plaque from the aortic Our patient had extensive atherosclerosis, with evidence of involvement of the abdominal aorta and the leg arteries, and was at increased risk of developing thromboembolic complications during arterial catheterization. Splenic infarction tends to be under-diagnosed. An autopsy series of 96 cases of the condition reported that it had been suspected clinically in only 10%of the patients, even though in 44% the infarction was found to have contributed substantially to morbidity and mortality? Three of the patients in this series had undergone angiography shortly before their death. Because splenic infarction is under-diagnosed, its true incidence after cardiac catheterization is difficult to determine. Physicians should bear in mind this potentially serious complication in patients developing abdominal pain after catheterization.
Acknowledgment The authors would like to thank Professor Drori BenIshay for his support and help in preparing this manuscript.
References 1. Grossman W: Complications of cardiac catheterization: Incidence, causes and prevention. In Cardiac Catheterization and Angiography. (Ed. Grossman W). Lea and Febiger, Philadelphia, (1986) 30-42 2. Johnson LW, Lozner EC, Johnson S, Krone R, Pichard AD, Vetrovec GW, Noto TJ: Coronary arteriography 1984-1987: A report of the Registry of the Society for Cardiac Angiography and Interventions. I. Results and complications. Cathet Cardiovase Diagn 17,5-10 (1989) 3. Jaroch MT, Broughan TA, Hermann RE: The natural history of splenic infarction. Surgery 100,743-749 (1986) 4. O’Keefe JH, Holmes DR, Schaff HV, Sheedy PF II, Edwards WD:Thromboembolic splenic infarction. Mayo Clin Proc 61, 967-972 (1986) 5. Caslowitz PL, Labs JD, Fishman EK, Siegelman SS: Nontraumatic focal lesions of the spleen: Assessment of imaging and clinical evaluation. Comput Med Imaging Graph 14, 133-141 (1990) 6. Busch HM, Cogbill TH, Gundersen AE: Splenic infarction: Complication of intra-aortic balloon counterpulsation. Am Heart J 109,383-385 (1985)
Splenic Infarction: A Complication of Cardiac Catheterization MICHAL ROSE,M.D., DGANIT DINOUR, M.D., ROLAND CHISIN,M.D.* Department of Medicine, Hadassah University Hospital, Mount Scopus; *Department of Medical Biophysics and Nuclear Medicine, Hadassah University Hospital, Ein Karem, Jerusalem, Israel
Summary: Patients with extensive atherosclerosis are at increased risk of developing embolic complications during cardiac catheterization. We describe a 5 1-year-old man with unstable angina and bilateral leg claudication who developed fever and right upper abdominal pain shortly after cardiac catheterization. Liver-spleen scintigraphy demonstrated a wedge-shaped filling defect compatible with splenic infarction, and serial scans performed over a period of five months showed resolution of this finding. Splenic infarction tends to be under-diagnosed, and physicians should be aware of this potentially serious complication of cardiac catheterization. Key words: cardiac catheterization,complications, splenic infarction
Introduction Embolic complications, mainly strokes, occur in about 0.1% of patients undergoing cardiac catheterization. l s 2 They occur either as a result of thrombogenesis on the catheter or guide wire surfaces or by the dislodgment of a large particle from a mural thrombus or an atheromatous plaque on an arterial wall.' We report a patient who developed a symptomatic splenic infarction after cardiac catheterization, a complication of this procedure not described previously.
Address for reprints: Dr. Michal Rose Department of Medicine Hadassah University Hospital Mount Scopus P.O.Box 24035 Jerusalem 91240, Israel
Received: January 23, 1992 Accepted March 19, 1992
Case Report A 5 1-year-old man with unstable angina was referred to our catheterization laboratory for left heart catheterization. His risk factors for atherosclerosis included heavy smoking, hypertension, hypercholesterolemia,and obesity. He was suffering from bilateral leg claudication at 50 meters. He had suffered an inferior wall myocardial infarction seven years prior to catheterization and a non-Q wave anterior wall myocardial infarction 10 days prior to the pmcedure. For the latter infarction, he had been treated with 1,500,OOO IU of streptokinase intravenously and then intravenous heparin, 300 mg/day. Heparin treatment was discontinued two hours before catheterization. On physical examination he appeared well, was overweight, and a bruit was heard over his right carotid artery. Peripheral pulses were absent below the femoral arteries in both legs. Using the Judkins technique and a right femoral approach, cardiac and coronary catheterization were performed. The study showed good global left ventricle function with inferior and anterior hypokinesis and total occlusion of the left anterior descending and right coronary arteries. Immediately after the procedure the patient developed left upper abdominal pain, aggravated by breathing, and one h later his temperature rose to 39°C. His pulse rate was 120 beatshin. His abdomen was soft, with slight tenderness in the left upper quadrant. Examination of the heart and lungs was normal. Blood tests showed a leukocytosis of 16,500/ml with a shift to the left. Blood and urine cultures were sterile. A ventilation-perfusionscan of the lungs was normal. A tin-colloid-99mtechnetiumliver-spleen scan, performed six days after catheterization,showed a wedgeshaped filling defect compatible with splenic infarction. The patient was treated with analgesics and bedrest, and his fever and abdominal pain resolved within one week. Three serial liver-spleen scans performed over a period of five months showed resolution of the findings of the original scan.
Discussion Splenic infarction was diagnosed in our patient based on the clinical manifestationsof fever, left upper quadrant
698
Clin. Cardiol. Vol. 15, September 1992
abdominal pain and tenderness, and a liver-spleen scintigraphy showing a filling defect in the ~ p l e e n .Serial ~ . ~ scans, showing the resolution of this finding, further supported the diagno~is.~ Other imaging techniques used in diagnosing splenic infarction include computed tomography and ultras~nography.~ The most common cause of splenic infarction is thromboembolic disease, with emboli dislodging mainly from a diseased aorta, the left ventricle (in acute myocardial infarction and dilated cardiomyopathy), and vegetations on heart valve^.^^^ Busch et al. described a patient on an intraaortic balloon pump, who developed a splenic infarction, presumably caused by the disruption of an atheromatous plaque from the aortic Our patient had extensive atherosclerosis, with evidence of involvement of the abdominal aorta and the leg arteries, and was at increased risk of developing thromboembolic complications during arterial catheterization. Splenic infarction tends to be under-diagnosed. An autopsy series of 96 cases of the condition reported that it had been suspected clinically in only 10%of the patients, even though in 44% the infarction was found to have contributed substantially to morbidity and mortality? Three of the patients in this series had undergone angiography shortly before their death. Because splenic infarction is under-diagnosed, its true incidence after cardiac catheterization is difficult to determine. Physicians should bear in mind this potentially serious complication in patients developing abdominal pain after catheterization.
Acknowledgment The authors would like to thank Professor Drori BenIshay for his support and help in preparing this manuscript.
References 1. Grossman W: Complications of cardiac catheterization: Incidence, causes and prevention. In Cardiac Catheterization and Angiography. (Ed. Grossman W). Lea and Febiger, Philadelphia, (1986) 30-42 2. Johnson LW, Lozner EC, Johnson S, Krone R, Pichard AD, Vetrovec GW, Noto TJ: Coronary arteriography 1984-1987: A report of the Registry of the Society for Cardiac Angiography and Interventions. I. Results and complications. Cathet Cardiovase Diagn 17,5-10 (1989) 3. Jaroch MT, Broughan TA, Hermann RE: The natural history of splenic infarction. Surgery 100,743-749 (1986) 4. O’Keefe JH, Holmes DR, Schaff HV, Sheedy PF II, Edwards WD:Thromboembolic splenic infarction. Mayo Clin Proc 61, 967-972 (1986) 5. Caslowitz PL, Labs JD, Fishman EK, Siegelman SS: Nontraumatic focal lesions of the spleen: Assessment of imaging and clinical evaluation. Comput Med Imaging Graph 14, 133-141 (1990) 6. Busch HM, Cogbill TH, Gundersen AE: Splenic infarction: Complication of intra-aortic balloon counterpulsation. Am Heart J 109,383-385 (1985)
