Spontaneous cardiac tamponade due to sternotomy wire suture James W. Mimbs, M.D. Alan N. Weiss, M.D.
st. Louis, Mo.
Spontaneous pericardial tamponade is m o s t frequently due to neoplastic invasion, idiopathic or infectious pericarditis, and uremia. Both penetrating and nonpenetrating trauma are also wellrecognized causes of cardiac t a m p o n a d e . 1'~ Iatrogenic causes of traumatic tamponade are assuming increasing importance based on reports documenting associations with central venous catheters, cardiac catheterization, and following c a r d i a c s u r g e r y 2 .~ T h i s r e p o r t is t h e f i r s t d o c u mentation of cardiac tamponade caused by wire suture routinely used in sternotomy closure. In view of the increasing number of cardiac surgical procedures, an estimated 30,000 annually for coronary bypass alone, this potential postoperat i v e c o m p l i c a t i o n is n o t a b l e . 5
Case report A 16-year-old boy was admitted to Barnes Hospital on Dec. 7, 1974, for evaluation of chest pain. He was previously hospitalized in August, 1973, for cosmetic repair of a pectus excavatum deformity. At the final admission, he presented with complaints of sudden onset of severe, sharp, midsternal pain with radiation to both shoulders and minimal dyspnea. He denied trauma'to the chest and denied taking any medication. Physical examination revealed a temperature of 38 ~ C., a blood pressure of 120/80 mm: Hg with no paradoxical pulse, and a pulse of 85 per minute. Jugular venous pulses were not elevated. The lungs were clear to auscultation and percussion. A pectus deformity and a longitudinal scar were noted over the sternum. Cardiovascular examination revealed an increased pulmonic second sound and a two-component pericardial friction rub. The chest roentgenogram (Fig. 1) revealed evidence of the prior median sternotomy with two wire sutures in place. Though not initially appreciated, the lower wire suture was From the Cardiovascular Division, Washington University School of Medicine, St. Louis, Mo. Received for publication Dec. 15, 1975. Reprint requests: Alan N. Weiss, M.D., Cardiovascular Division, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, Mo:63110.
630
open with the tip pointing posteriorly. The cardiac silhouette was enlarged, and there was minimal pulmonary redistribution. The electrocardiogram (ECG) revealed an incomplete right bundle branch block t h a t was present on the previous hospitalization; additionally, marked ST elevation not evident on prior ECG was noted in the lateral leads. The hemoglobin was 14.4 Gm. per 100 ml. and the white blood count was 8,700 per square centimeter with normal differential count. Arterial blood gases, SMA-12, sedimentation rate, and urinalysis were normal. During the first hospital day, the patient noted diminution of the chest pain, and the two-component rub disappeared. Approximately 24 hours after admission, the chest pain recurred suddenly with an accompanying severe epigastric pain. Physical examination at this time revealed an acutely ill male patient who had a blood pressure of 86/70 mm. Hg with a 16 mm. Hg paradox, a pulse of 130 per minute, and a respiratory rate of 26 per minute. There was jugular venous distention, but Kussmaul's sign was not observed. The lungs were clear to auscultation. Heart sounds were distant, and the two-component pericardial rub was no longer audible. Examination of the abdomen revealed only tenderness to palpation and a slightly enlarged liver. The femoral pulses were minimally palpable during inspiration. A central venous catheter was inserted, and a pressure of 22 cm. HzO was recorded. Intravenous fluids and isoproterenol were administered, and the blood pressure increased to 100/70 mm. Hg. A repeat chest roentgenogram and ECG were unchanged. An emergency pericardiocentesis was performed, and 30 ml. of bloody fluid with a hematocrit of 45 per cent was withdrawn. The bloody fluid did not clot at 15 minutes. An echocardiogram (Fig. 2, A ) revealed definite evidence of pericardial effusion. The patient was taken immediately to the operating room, and an emergency thoracotomy was done under general anesthesia. The pericardium was opened, and approximately 500 ml. of blood were removed. Inserting a hand into the pericardium, the surgeon detected a wire protruding into the heart. The site of penetration was tamponaded with a finger, and the wire removed. When exposed, the right ventricle revealed multiple abrasions but no further bleeding sites. The patient tolerated the procedure well and had an uncomplicated postoperative course. Six months following discharge, he was in good health.
Discussion Clinical presentation and evaluation. The c]assical clinical description
of cardiac tamponade
by
November, 1976, Vol. 92, No. 5, pp. 630-633
Spontaneous tamponade due to sternotomy wire suture
Fig. 1. Posteroanterior (A) and lateral (B) roentgenogram of chest taken on admission, demonstrating opened lower stern0tomy wire pointing posteriorly. Beck features: a falling arterial pressure, a rising venous pressure, a n d a small, quiet heart. T h i s description e v o l v e d p r i m a r i l y f r o m a surgeon's exposure to acute, rapidly progressing cardiac t a m p o n a d e t h a t resulted f r o m t r a u m a t i c stab or g u n s h o t wounds. W h e n cardiac t a m p o n a d e evolves m o r e slowly, the clinical signs m a y be subtle. W i t h the elucidation of the p a t h o p h y s i o logic events u n d e r l y i n g cardiac t a m p o n a d e , the physician can now m o r e effectively discriminate the signs of cardiac t a m p o n a d e f r o m constrictive pericarditis or restrictive c a r d i o m y o p a t h y . 7' s T h e p a t i e n t presented here, nevertheless, h a d classic signs of a c u t e cardiac t a m p o n a d e . T h e e v a l u a t i o n of t h e p a t i e n t with suspected pericardial effusion should be accomplished by the selective use of a n u m b e r of available procedures. R o e n t g e n o g r a p h i c e v a l u a t i o n m a y show increased h e a r t size, usually w i t h o u t p u l m o n a r y v a s c u l a r prominence. In addition, d i s p l a c e m e n t of the epicardial fat line within the cardiac silhouette can be p a t h o g n o m o n i c for pericardial effusion." I n this patient, these findings were not a p p a r e n t , b u t the detection of the opened, posteriorly pointing wire s u t u r e t h a t was noted on the routine chest r o e n t g e n o g r a m w a s of critical i m p o r t a n c e . While a n g i o g r a p h y a n d i n t r a v e n o u s
American Heart Journal
Table I. Causes of a c u t e h e m o p e r i c a r d i u m A. Nontraumatic
I
I
B. Traumatic
I
1. Acute myocardial infarction 2. Rupture of aortic aneurysm 3. Neoplasm 4. Blood dyscrasias 5. Acute rheumatic fever 6. Idiopathic pericarditis 7. Uremia 8. Infectious pericarditis 9. Collagen vascular disease 10. Irradiation 11. Anticoagulation
1. Cardiac or pulmonary surgery 2. Cardiac catheterization 3. Intravenous catheters 4. Foreign body penetration 5. Blunt chest injury
c a r b o n dioxide injection m a y be of use, these procedures are t i m e - c o n s u m i n g a n d p o t e n t i a l l y d a n g e r o u s in the e m e r g e n t situation. TM Echocard i o g r a p h y was first r e p o r t e d to be of use in the diagnosis of pericardial effusion in 1965. ~1 I t i s now well established in clinical use and, indeed, is the m o s t expeditious m e t h o d of diagnosis. 1~ A m o r e recent s t u d y c o m p a r i n g pericardial fluid r e m o v e d at surgery with echocardiographic evidence of effusion h a s d o c u m e n t e d n o t only the
631
Mimbs and Weiss
2r ;
Fig. 2. Ech0cardiograms. (A) Preoperatively, revealing a large echo-free space posterior to the left ventricle consistent with a pericardia! effusion, and a small left ventrieular dimension. (B) Postoperatively, revealing the absence of pericardial effusion.
specificity b u t also the sensitivity of this m e t h od.,:~ Analysis of pericardial fluid. W h e n grossly bloody fluid is a s p i r a t e d during a t t e m p t e d pericardiocentesis, the source m a y be pericardial or intracardiac. T h e t e c h n i q u e of c o n t i n u o u s E C G m o n i t o r i n g with the paracentesis needle as an exploring electrode is one a t t e m p t to obviate p e n e t r a t i o n of the heart. ~~ I t is known, however, t h a t E C G S T - s e g m e n t changes m a y n o t appear, and, consequently, m y o c a r d i a l laceration m a y occur even with strict a d h e r e n c e t o this technique. 1~ Of p a r t i c u l a r i m p o r t a n c e , then, is proper analysis of the bloody a s p i r a t e to differentiate
632
pericardial f r o m i n t r a m y o c a r d i a l origin. T h e routinely advised tests are: ( 1 ) s i m u l t a n e o u s aspir a t e and venous h e m a t o c r i t s a n d (2) inspection of fluid for clot f o r m a t i o n , as pericardial fluid tends to be defibrinated and does n o t readily clot. ~.... Additionally, we r e c o m m e n d obtaining simultaneous PO~ m e a s u r e m e n t s f r o m the aspirate a n d venous blood. I t is of interest t h a t the h e m a t o c r i t of the pericardial aspirate o f this p a t i e n t was equal to t h a t of the venous sample, indicating the a c u t e n e s s of t b e t a m p o n a d e due to the right v e n t r i c u l a r lacerations. O t h e r m e a s u r e m e n t s for e v a l u a t i o n of the bloody aspirate include injection of sodium d e h y d r o c h o l a t e or calcium gluco-
November, 1976, Vol. 92, No. 5
Spontaneous tamponade due to sternotomy wire suture
nate, t h o u g h we advise against the e i t h e r o f t h e s e p r o c e d u r e s . 17 1~ E a r after indocyanine green injection proposed, b u t this requires special
r o u t i n e use o f densitometry h a s also b e e n e q u i p m e n t . 1''
Etiology of pericardial tamponade. The etiology o f a c u t e t a m p o n a d e is m o s t o f t e n i n f e c t i o u s , n e o p l a s t i c , or u r e m i c disease.:" ~~ O t h e r m e d i c a l c a u s e s i n c l u d e c o l l a g e n v a s c u l a r disease, a c u t e r h e u m a t i c fever, m y o c a r d i a l i n f a r c t i o n , a n d a n t i c o a g u l a t i o n . ~1. ~ H o w e v e r , w i t h e a r l i e r d i a g n o s i s and i m p r o v e d t h e r a p e u t i c approaches to uremia, n e o p l a s m , and a c u t e r h e u m a t i c fever, cardiac t a m p o n a d e a s s o c i a t e d w i t h t h e s e c a u s e s is n o w s e e n less f r e q u e n t l y . T r a u m a t i c c a u s e s of c a r d i a c t a m p o n a d e h a v e b e e n r e c o g n i z e d for s o m e t i m e , a n d t h e r e a r e r e c e n t r e v i e w s of e x p e r i e n c e w i t h p e n e t r a t i n g wounds of the heart. ~ ~ R e c e n t reports documenting acute cardiac tamponade s e c o n d a r y to c e n t r a l v e n o u s c a t h e t e r s , c a r d i a c catheterizaiton, and cardiac surgery emphasize t h e i n c r e a s i n g i m p o r t a n c e of i a t r o g e n i c c a u s e s o f t r a u m a t i c t a m p o n a d e . 1 :~ ~' ~0 T a b l e I s u m m a r i z e s the etiologies t h a t are m o s t c o m m o n l y associated
3. 4. 5. 6. 7. 8. 9. 10.
11.
12.
with acute tamponade and hemopericardium. -'~~ In addition to the etiologies noted in Table I, this report represents the first notation of cardiac tamponade due to penetration by a sternotomy wire suture.
13.
Summary
15.
The firstcase of spontaneous cardiac tamponade caused by wire suture for sternotomy closure is presented. The proper analysis of bloody pericardial fluid,including simultaneous aspirate and venous hematocrit, oxygen content, and coagulation studies, is emphasized. In addition, the causes of acute hemopericardium are reviewed. Spontaneous cardiac tamponade as a potential late complication of cardiac surgery should be considered in the postoperative patient w h o presents with pericarditis or a sudden change in cardiac status.
14.
16. 17. 18. 19. 20. 21. 22.
REFERENCES 1. Jones, E. W., and Helmsworth, J.: Penetrating wounds of the heart: thirty years' experience, Arch. Surg. 96:671, 1968. 2. Shoemaker, W., Carey, J. S., Yar, S. T., Mohr, P. A., Amato, J. J., Printen, K. J., Corley, R. D., Manson, D. O.,
American H e a r t J o u r n a l
23. 24.
Yousset, J., and Shoemaker, N. J.: Hemodynamic alterations in acute cardiac tamponade after penetrating injuries of the heart, Surgery 67:754, 1970. Stein, L, Shubin, H., and Weil, M. M.: Recognition and management of pericardial tamponade, J. A. M. A. 225:503, 1973. Dane, T. E. B, and King, E. E.: Fatal cardiac tamponade and other mechanical complications of central venous catheters, Br. J Surg~ 62:6, 1975. Mundth, E. D, and Austen, G. W.: Surgical measures for coronary heart disease, N. Engl. J. Med 293:124, 1975. Beck, C. S.: Two cardiac compression triads, J. A. M. A. 104:714, 1935. Shabetai, R., Fowler, I'4. O., and Guntheroth, W. G.: The hemodynamics of cardiac tamponade and constrictive pericarditis, Am. J. Cardiol. 26:480, 1970. Butch, G. E., and Phillips, J. H.: Methods in the diagnostic differentiation of myocardial dilatation from pericardial effusion. AM. HEART J. 64:266, 1962. Baron, M. G.: Pericardial effusion, Circulation 44:294, 1971. Moraski, R. E, Sandler, I. A., O'Hern, J. A., and Bonskaros, G.: Evaluation of right atriography for the detection of pericardial effusion, Am. J. Med. Sei. 256:360, 1968. Clark, R. L., Mildram, J. W., and Yawn, D. H.: Fatal aortic perforation and cardiac tamponade due to a Kirschner wire migrating from the right sternoclavicular joint, South. Med. J. 67:316, 1974. Feigenbaum, H.: Echocardiographic diagnosis of pericardial effusion, Am. J. Cardiol. 26:475, 1970. Horowitz, M. S., Schultz, C. S, Stinson, E. B., Harrison, D. C., and Popp, R. L.: Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion, Circulation 50:239, 1974. Bishop, L. H., Jr., Estes, E. M., Jr., and McIntoshl H. D.: The ECG as a safeguard in pericardiocentesis, J. A. M. A. 162:264, 1956. Sobol, J. M., Thomas, H. M., Jr., and Evans, R. W.: Myocardial laceration not demonstrated during pericardiocentesis, IN. Engl. J. Med. 292:1222, 1975. Shabetai, R., Fowler, N. O., and Fenton, J. C.: Restrictive cardiac disease, pericarditis and the myocardiopathies, AM. HEART J. 69:271, 1965. Wood, F. C.: Observations on pericardial disease, Med. Clin. North Am. 37:1639, 1953. Mills, C. W.: Simple clinical aid in diagnosis of hemorrhagic pericardiac effusion, J. A. M. A. 150:1208, 1952. Stone, J. R., and Martin, R. H.: Bloody pel~icardial fluid or intracardiac blood? Ann. Intern. Med. 71:592, 1972. Lajos, T. Z, Black, H. E., Cooper, R. G., and Wanka, J.: Pericardial decompression, Ann. Thorac. Surg. 19:47, 1975. Fowler, N. O.: Pericardial disease, in Hurst, J. W., editor: The heart, ed. 3, New York, 1974, McGraw-Hill Book Company, Inc. Friedberg, C. K.: Acute pericarditis, in Friedberg, C. K., editor: Diseases of the heart, ed 3, Philadelphia, 1966, W. B. Saunders Company. Sugg, W. L., Rea, W. J., Ecker, R. R., Webb, W. R:, Rose, E. F., and Shaw, R. R: Penetrating wounds of the heart, J. Thorac. Cardiovasc. Surg. 56:531, 1968. Cortes, F. M.: The pericardium and its disorders, Springfield, Ill., 1971, Charles C Thomas, Publisher.
633
st. Louis, Mo.
Spontaneous pericardial tamponade is m o s t frequently due to neoplastic invasion, idiopathic or infectious pericarditis, and uremia. Both penetrating and nonpenetrating trauma are also wellrecognized causes of cardiac t a m p o n a d e . 1'~ Iatrogenic causes of traumatic tamponade are assuming increasing importance based on reports documenting associations with central venous catheters, cardiac catheterization, and following c a r d i a c s u r g e r y 2 .~ T h i s r e p o r t is t h e f i r s t d o c u mentation of cardiac tamponade caused by wire suture routinely used in sternotomy closure. In view of the increasing number of cardiac surgical procedures, an estimated 30,000 annually for coronary bypass alone, this potential postoperat i v e c o m p l i c a t i o n is n o t a b l e . 5
Case report A 16-year-old boy was admitted to Barnes Hospital on Dec. 7, 1974, for evaluation of chest pain. He was previously hospitalized in August, 1973, for cosmetic repair of a pectus excavatum deformity. At the final admission, he presented with complaints of sudden onset of severe, sharp, midsternal pain with radiation to both shoulders and minimal dyspnea. He denied trauma'to the chest and denied taking any medication. Physical examination revealed a temperature of 38 ~ C., a blood pressure of 120/80 mm: Hg with no paradoxical pulse, and a pulse of 85 per minute. Jugular venous pulses were not elevated. The lungs were clear to auscultation and percussion. A pectus deformity and a longitudinal scar were noted over the sternum. Cardiovascular examination revealed an increased pulmonic second sound and a two-component pericardial friction rub. The chest roentgenogram (Fig. 1) revealed evidence of the prior median sternotomy with two wire sutures in place. Though not initially appreciated, the lower wire suture was From the Cardiovascular Division, Washington University School of Medicine, St. Louis, Mo. Received for publication Dec. 15, 1975. Reprint requests: Alan N. Weiss, M.D., Cardiovascular Division, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, Mo:63110.
630
open with the tip pointing posteriorly. The cardiac silhouette was enlarged, and there was minimal pulmonary redistribution. The electrocardiogram (ECG) revealed an incomplete right bundle branch block t h a t was present on the previous hospitalization; additionally, marked ST elevation not evident on prior ECG was noted in the lateral leads. The hemoglobin was 14.4 Gm. per 100 ml. and the white blood count was 8,700 per square centimeter with normal differential count. Arterial blood gases, SMA-12, sedimentation rate, and urinalysis were normal. During the first hospital day, the patient noted diminution of the chest pain, and the two-component rub disappeared. Approximately 24 hours after admission, the chest pain recurred suddenly with an accompanying severe epigastric pain. Physical examination at this time revealed an acutely ill male patient who had a blood pressure of 86/70 mm. Hg with a 16 mm. Hg paradox, a pulse of 130 per minute, and a respiratory rate of 26 per minute. There was jugular venous distention, but Kussmaul's sign was not observed. The lungs were clear to auscultation. Heart sounds were distant, and the two-component pericardial rub was no longer audible. Examination of the abdomen revealed only tenderness to palpation and a slightly enlarged liver. The femoral pulses were minimally palpable during inspiration. A central venous catheter was inserted, and a pressure of 22 cm. HzO was recorded. Intravenous fluids and isoproterenol were administered, and the blood pressure increased to 100/70 mm. Hg. A repeat chest roentgenogram and ECG were unchanged. An emergency pericardiocentesis was performed, and 30 ml. of bloody fluid with a hematocrit of 45 per cent was withdrawn. The bloody fluid did not clot at 15 minutes. An echocardiogram (Fig. 2, A ) revealed definite evidence of pericardial effusion. The patient was taken immediately to the operating room, and an emergency thoracotomy was done under general anesthesia. The pericardium was opened, and approximately 500 ml. of blood were removed. Inserting a hand into the pericardium, the surgeon detected a wire protruding into the heart. The site of penetration was tamponaded with a finger, and the wire removed. When exposed, the right ventricle revealed multiple abrasions but no further bleeding sites. The patient tolerated the procedure well and had an uncomplicated postoperative course. Six months following discharge, he was in good health.
Discussion Clinical presentation and evaluation. The c]assical clinical description
of cardiac tamponade
by
November, 1976, Vol. 92, No. 5, pp. 630-633
Spontaneous tamponade due to sternotomy wire suture
Fig. 1. Posteroanterior (A) and lateral (B) roentgenogram of chest taken on admission, demonstrating opened lower stern0tomy wire pointing posteriorly. Beck features: a falling arterial pressure, a rising venous pressure, a n d a small, quiet heart. T h i s description e v o l v e d p r i m a r i l y f r o m a surgeon's exposure to acute, rapidly progressing cardiac t a m p o n a d e t h a t resulted f r o m t r a u m a t i c stab or g u n s h o t wounds. W h e n cardiac t a m p o n a d e evolves m o r e slowly, the clinical signs m a y be subtle. W i t h the elucidation of the p a t h o p h y s i o logic events u n d e r l y i n g cardiac t a m p o n a d e , the physician can now m o r e effectively discriminate the signs of cardiac t a m p o n a d e f r o m constrictive pericarditis or restrictive c a r d i o m y o p a t h y . 7' s T h e p a t i e n t presented here, nevertheless, h a d classic signs of a c u t e cardiac t a m p o n a d e . T h e e v a l u a t i o n of t h e p a t i e n t with suspected pericardial effusion should be accomplished by the selective use of a n u m b e r of available procedures. R o e n t g e n o g r a p h i c e v a l u a t i o n m a y show increased h e a r t size, usually w i t h o u t p u l m o n a r y v a s c u l a r prominence. In addition, d i s p l a c e m e n t of the epicardial fat line within the cardiac silhouette can be p a t h o g n o m o n i c for pericardial effusion." I n this patient, these findings were not a p p a r e n t , b u t the detection of the opened, posteriorly pointing wire s u t u r e t h a t was noted on the routine chest r o e n t g e n o g r a m w a s of critical i m p o r t a n c e . While a n g i o g r a p h y a n d i n t r a v e n o u s
American Heart Journal
Table I. Causes of a c u t e h e m o p e r i c a r d i u m A. Nontraumatic
I
I
B. Traumatic
I
1. Acute myocardial infarction 2. Rupture of aortic aneurysm 3. Neoplasm 4. Blood dyscrasias 5. Acute rheumatic fever 6. Idiopathic pericarditis 7. Uremia 8. Infectious pericarditis 9. Collagen vascular disease 10. Irradiation 11. Anticoagulation
1. Cardiac or pulmonary surgery 2. Cardiac catheterization 3. Intravenous catheters 4. Foreign body penetration 5. Blunt chest injury
c a r b o n dioxide injection m a y be of use, these procedures are t i m e - c o n s u m i n g a n d p o t e n t i a l l y d a n g e r o u s in the e m e r g e n t situation. TM Echocard i o g r a p h y was first r e p o r t e d to be of use in the diagnosis of pericardial effusion in 1965. ~1 I t i s now well established in clinical use and, indeed, is the m o s t expeditious m e t h o d of diagnosis. 1~ A m o r e recent s t u d y c o m p a r i n g pericardial fluid r e m o v e d at surgery with echocardiographic evidence of effusion h a s d o c u m e n t e d n o t only the
631
Mimbs and Weiss
2r ;
Fig. 2. Ech0cardiograms. (A) Preoperatively, revealing a large echo-free space posterior to the left ventricle consistent with a pericardia! effusion, and a small left ventrieular dimension. (B) Postoperatively, revealing the absence of pericardial effusion.
specificity b u t also the sensitivity of this m e t h od.,:~ Analysis of pericardial fluid. W h e n grossly bloody fluid is a s p i r a t e d during a t t e m p t e d pericardiocentesis, the source m a y be pericardial or intracardiac. T h e t e c h n i q u e of c o n t i n u o u s E C G m o n i t o r i n g with the paracentesis needle as an exploring electrode is one a t t e m p t to obviate p e n e t r a t i o n of the heart. ~~ I t is known, however, t h a t E C G S T - s e g m e n t changes m a y n o t appear, and, consequently, m y o c a r d i a l laceration m a y occur even with strict a d h e r e n c e t o this technique. 1~ Of p a r t i c u l a r i m p o r t a n c e , then, is proper analysis of the bloody a s p i r a t e to differentiate
632
pericardial f r o m i n t r a m y o c a r d i a l origin. T h e routinely advised tests are: ( 1 ) s i m u l t a n e o u s aspir a t e and venous h e m a t o c r i t s a n d (2) inspection of fluid for clot f o r m a t i o n , as pericardial fluid tends to be defibrinated and does n o t readily clot. ~.... Additionally, we r e c o m m e n d obtaining simultaneous PO~ m e a s u r e m e n t s f r o m the aspirate a n d venous blood. I t is of interest t h a t the h e m a t o c r i t of the pericardial aspirate o f this p a t i e n t was equal to t h a t of the venous sample, indicating the a c u t e n e s s of t b e t a m p o n a d e due to the right v e n t r i c u l a r lacerations. O t h e r m e a s u r e m e n t s for e v a l u a t i o n of the bloody aspirate include injection of sodium d e h y d r o c h o l a t e or calcium gluco-
November, 1976, Vol. 92, No. 5
Spontaneous tamponade due to sternotomy wire suture
nate, t h o u g h we advise against the e i t h e r o f t h e s e p r o c e d u r e s . 17 1~ E a r after indocyanine green injection proposed, b u t this requires special
r o u t i n e use o f densitometry h a s also b e e n e q u i p m e n t . 1''
Etiology of pericardial tamponade. The etiology o f a c u t e t a m p o n a d e is m o s t o f t e n i n f e c t i o u s , n e o p l a s t i c , or u r e m i c disease.:" ~~ O t h e r m e d i c a l c a u s e s i n c l u d e c o l l a g e n v a s c u l a r disease, a c u t e r h e u m a t i c fever, m y o c a r d i a l i n f a r c t i o n , a n d a n t i c o a g u l a t i o n . ~1. ~ H o w e v e r , w i t h e a r l i e r d i a g n o s i s and i m p r o v e d t h e r a p e u t i c approaches to uremia, n e o p l a s m , and a c u t e r h e u m a t i c fever, cardiac t a m p o n a d e a s s o c i a t e d w i t h t h e s e c a u s e s is n o w s e e n less f r e q u e n t l y . T r a u m a t i c c a u s e s of c a r d i a c t a m p o n a d e h a v e b e e n r e c o g n i z e d for s o m e t i m e , a n d t h e r e a r e r e c e n t r e v i e w s of e x p e r i e n c e w i t h p e n e t r a t i n g wounds of the heart. ~ ~ R e c e n t reports documenting acute cardiac tamponade s e c o n d a r y to c e n t r a l v e n o u s c a t h e t e r s , c a r d i a c catheterizaiton, and cardiac surgery emphasize t h e i n c r e a s i n g i m p o r t a n c e of i a t r o g e n i c c a u s e s o f t r a u m a t i c t a m p o n a d e . 1 :~ ~' ~0 T a b l e I s u m m a r i z e s the etiologies t h a t are m o s t c o m m o n l y associated
3. 4. 5. 6. 7. 8. 9. 10.
11.
12.
with acute tamponade and hemopericardium. -'~~ In addition to the etiologies noted in Table I, this report represents the first notation of cardiac tamponade due to penetration by a sternotomy wire suture.
13.
Summary
15.
The firstcase of spontaneous cardiac tamponade caused by wire suture for sternotomy closure is presented. The proper analysis of bloody pericardial fluid,including simultaneous aspirate and venous hematocrit, oxygen content, and coagulation studies, is emphasized. In addition, the causes of acute hemopericardium are reviewed. Spontaneous cardiac tamponade as a potential late complication of cardiac surgery should be considered in the postoperative patient w h o presents with pericarditis or a sudden change in cardiac status.
14.
16. 17. 18. 19. 20. 21. 22.
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