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Myocardial infarction complicated by myocardial rupture and Bacteroides sepsis
Volume 89 Number 6
Brief communications
June, 1985
mobilization of the innominate vein to reach the left atrial appendage directly despite freeing up the internal jugular vein. A segment of saphenous vein was removed from the left thigh, divided longitudinally, wrapped around a No. 32 Fr. chest tube, and sutured with a 7-0 Prolene suture. This produced a tubular graft with an internal diameter of 14 mm (Fig. 2). The innominate vein was 10 mm in diameter. The appropriate length of spiral vein graft was calculated as previously described.' The patient was given heparin systemically. The innominate vein was opened longitudinally and an end-to-side anastomosis was performed. The spiral vein graft to the left atrial appendage anastomosis was performed in an end-to-end fashion with a partial occlusion clamp on the appendage. This anastomosis produced a large opening into the systemic venous atrium. The clamps were released and the external jugular venous pressure dropped from 34 to 17 mm Hg. Her postoperative course was uneventful. She was systemically improved and her parents noted that her face was much thinner and less blue. A first-pass nucleotide cardiac angiogram (technetium 99m) showed a widely patent graft and no venous stasis (Fig. 3). At her last outpatient evaluation, 6 months after the operation, the patient was totally asymptomatic and there were no physical signs of superior vena caval obstruction.
Discussion. Late baffle complications following the Mustard repair for transposition of the great arteries have been well documented. Either systemic or pulmonary venous obstruction has been reported in approximately 25% of cases repaired with either pericardial or Dacron baffles. Cobanoglu and associates' recently reported excellent results with a double patch reconstruction of the superior vena cava and the superior portion of the baffle to alleviate the superior vena caval syndrome in this clinical situation. Although there have been no deaths in their last 10 patients, this procedure does require cardiopulmonary bypass and an additional atrial incision. This incision and the patch must be placed near the sinus node. In view of the late arrhythmias reported following the Mustard operation, we believe that it is advantageous to be able to avoid an additional atrial incision. Use of the spiral vein graft in adults with superior vena caval syndrome has been very satisfactory.' Longterm results have shown patency up to 6 years postoperatively in patients operated on for benign disease. The use of this technique in children has not yet been reported to our knowledge, and the extended prognosis of the vein graft is uncertain. However, clinical and experimental experience with all other types of materials in the venous system have had poor long-term results.' Although we do not have long-term follow-up data as yet, we believe that this treatment is an excellent alternative when direct anastomosis is not possible. Use of the spiral vein graft avoids cardiopulmonary bypass and should result in a lower morbidity and mortality. An advantage over direct anastomosis is that
945
the vein graft also preserves the innominate and internal jugular continuity bilaterally. The result may be better decompression of the cerebral circulation and contralateral upper extremity. Cardiopulmonary bypass can still be performed when the child is older, if necessary. We are uncertain as to the smallest saphenous vein usable for this procedure, but we had no difficulty with the vein in this ll-year-old child. REFERENCES Coulson JD, Pitlick PT, Miller DC, French JW, Marshall WH, Fryer AD, Shumway NE: Severe superior vena cava syndrome and hydrocephalus after the Mustard procedure. Findings and a new surgical approach. Circulation 70:Suppl 1:47-53, 1984 2 Doty DB: Bypass of superior vena cava. J THORAC CARDIO. VASC SURG 83:326-337, 1982 3 Cobanoglu A, Abbruzzese PA, Freimanis I, Garcia CE, Grunkemeier G, Starr A: Pericardial baffle complications following the Mustard operation. Age-related incidence and ease of management. J THORAC CARDIOVASC SURG 87:371378, 1984 4 Hiratzka LF, Doty DB, Wright CB: Newer tissue and synthetic grafts in canine femoral veins. J Surg Res 31:324-331, 1981
Myocardial infarction complicated by myocardial rupture and Bacteroides sepsis Stephen A. Mills, M.D., C.M., Frederick Kahl, M.D., Michael Kutcher, M.D., and Abdel-Mohsen Nomeir, M.D., Winston-Salem. N. C. From the Section on Cardiothoracic Surgery, Department of Surgery, and the Section on Cardiology (Department of Medicine), Wake Forest University Medical Center, Bowman Gray School of Medicine, Winston-Salem, N. C.
A patient in whom a myocardial rupture complicated recent myocardial infarction was found to have cardiac and systemic Bacteroides sepsis; he had just completed a course of steroids. Surgical repair of the cardiac rupture, mediastinal irrigation with povidone-iodine, and broad-spectrum antibiotics resulted in the patient's recovery.
Cardiac rupture is a major cause of death following acute myocardial infarction. Whereas rupture of the free wall of the left ventricle usually results in acute hemopericardium and cardiac arrest despite continuing electrical activity, subacute rupture occasionally may Address for correspondence and reprints: Stephen A. Mills, M.D., Section on Cardiothoracic Surgery, Bowman Gray School of Medicine, 300 S. Hawthorne Rd., Winston-Salem, N. C. 27103.
The Journal of
946
Brief communications
Thoracic and Cardiovascular Surgery
Fig. 1. An apical two-chamber two-dimensional echocardiogram. DH, Dissecting myocardial hematoma. IVS, Interventricular septum. LA, Left atrium. LV, Left ventricle. MV, Mitral valve. The arrows point to the inner layer of the intramyocardial dissection.
Fig. 2. The cardiac rupture followed a tortuous path out to the pericardial space. An intra myocardial dissection was present and extended 5 to 8 em from the site of external rupture.
result in a syndrome resembling cardiogenic shock. When the latter clinical picture is present, there may be time for both diagnosis and surgical repair.!" This report documents the case of a patient in whom cardiac rupture following myocardial infarction was complicated by Bacteroides sepsis. Successful surgical repair was carried out. Case report. A 48-year-old man was hospitalized elsewhere with an uncomplicated, anterior myocardial infarction. He was discharged home 10 days later on a regimen of acetylsalicylic acid and propranolol. Two weeks after discharge, left anterior
chest pain developed, which was worse in the supine position and during inspiration. At readmission, a two-component cardiac apical rub could be heard over the left fifth intercostal space. The twelve-lead electrocardiogram showed an old diaphragmatic and anterior myocardial infarction with persistent ST and T-wave changes in the anterior leads consistent with aneurysm or pericarditis. He was treated with acetylsalicylic acid and later prednisone, the latter 40 mg four times a day. One week after readmission he was transferred to our institution. On the evening of admission he complained of chest pain radiating to the left shoulder and increasing with respiration. Nitroglycerin was given without improvement. His temperature rose from normal to 102° F; blood pressure was 90/65 mm Hg, pulse rate 84 beats/min, and respirations 32 breaths/ min. The electrocardiogram demonstrated no changes. Morphine was given with relief of pain. An echocardiogram demonstrated a large anterior apical infarct, a large apical thrombus, and a small pericardiaI effusion. Cardiac enzymes remained within normal limits. Two days later blood cultures grew gram-negative rods, and a regimen of cephapirin and tobramycin was started. Four days after admission, he had an episode of shaking chills and a temperature of 101 0 F. On the fifth hospital day, the chest pain recurred and repeat echocardiography showed enlargement of the pericardial effusion and a dissecting myocardial hematoma in addition to the previous findings (Fig. 1). Systemic blood pressure was 80/60 mm Hg. Cardiac catheterization showed equalization of right-sided pressures with a diastolic plateau. A left ventriculogram showed a large area of akinesia in the anterolateral septal apex with smoothing of the left ventricular lateral wall. No distinct pericardial communication was noted. The ejection fraction was 19%. The left anterior descending coronary artery was totally occluded; the other coronary arteries had minor irregularities. He was immediately taken to the operating room for a median sternotomy. A large amount of fresh and clotted blood
Volume 89
Brief communications
Number 6 June, 1985
was present within the pericardium. Cardiopulmonary bypass was instituted with moderate systemic hypothermia (30° C esophageal). A 6 cm tear was found in the apex of a large left ventricular infarct. Opening of the infarct showed an extensive myocardial dissection within the septum and including 5 to 8 em of the free wallsof the left and right ventricles (Fig. 2). The apex of the infarct was filled with clot. It was apparent that the rupture had occurred along a tortuous path within the left ventricular myocardium. A portion of the outer layer of the left ventricular infarct was debrided, and the infarct was repaired with Teflon strips and nonabsorbable monofilament suture. Cardiopulmonary bypass was discontinued while epinephrine was given intravenously. A Gram stain of the pericardiaI hematoma demonstrated leukocytosis (2+) with no organisms being seen. A blood culture obtained preoperatively grew Bacteroides fragilis. Antibiotic treatment included cephapirin, tobramycin, and clindamycin. Mediastinal irrigation was started with a 1% solutionof povidone-iodine at a rate of 75 rnl/hr and continued for 12 days. Ten days after operation, pericardial cultures and bloodcultures obtained at operation grew Bacteroides fragilis, subspecies thetaiotaomicron. A workup for the source of the Bacteroides infection showed extremely poor dental hygiene and a periodontal abscess, which were treated by extraction of all teeth and drainage of the abscess. The patient remained afebrile thereafter. A repeat echocardiogram 6 weeks after operation showed no changes from preoperative findings, other than diminished size of the pericardial effusion. He was discharged home I week later. At follow-up 3 months after the operation, he had no signs of infection or congestive heart failure.
Comment. Three cardiac infectious processes can complicate myocardial infarction: purulent pericarditis, mural endocarditis,' and myocardial abscess.' All are rare. In our patient, a periodontal abscess and poor dental hygiene probably were the source of cardiac sepsis. The recurrent chest pain was probably a result of extension of the intramyocardial dissection. A 6 day course of prednisone may well have contributed to delayed healing and rupture of the original myocardial infarction':" and development of sepsis. The ruptured tissue encountered at operation was not believed to be strong enough to allow primary closure without Teflon buttressing, although the use of pericardial strips as reported by Love and colleagues" following cardiac rupture at the site of left ventricular venting might have been effective. In cases of cardiac infection following repair of left ventricular aneurysm, debridement of Teflon combined
947
with an omental pedicle? or pectoral muscle flap'? has been used successfully. Although intrapericardial infection was not strongly suspected at the time of operation, subsequent cultures demonstrated Bacteroides infection, and a 12 day course of mediastinal irrigation with a 1% povidone-iodine solution in combination with a 6 week course of intravenous broad-spectrum antibiotics was begun. The result was apparent resolution of infection, and the patient is currently on a long-term regimen of penicillin and metronidazole.
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REFERENCES O'Rourke MF: Subacute heart rupture following myocardial infarction. Clinical features of a correctable condition. Lancet 2:124-126, 1973 Bashour T, Kabbani SS, Ellertson DG, Crew J, Hanna ES: Surgical salvage of heart rupture. Report of two cases and review of the literature. Ann Thorac Surg 36:209-213, 1983 Feneley MP, Chang VP, O'Rourke MF: Myocardial rupture after acute myocardial infarction. Ten year review. Br Heart J 49:550-556, 1983 Nunez L, de la Llana R, Sendon JL, Coma I, Aguado MG, Larrea JL: Diagnosis and treatment of subacute free wall ventricular rupture after infarction. Ann Thorac Surg 35:525-529, 1983 McCallum DG, Grow J Sr: Mural thrombus endocarditis complicating an acute myocardial infarction. Report of a case. Arch Intern Med 141:527-528, 1981 Roberts R, DeMello V, Sobel BE: Deleterious effects of methylprednisolonein patients with myocardial infarction. Circulation 53:Suppl 1:204-206, 1976 Bulkley BH, Roberts WC: Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm. Am J Med 56:244-250, 1974 Love JW, Jahnke EJ, McFadden RB, Fisher GU, Barbabella J, Anderson S, Vogel JHK: Left ventricular pseudoaneurysm secondary to infection after coronary bypass surgery. Chest 79:100-102, 1981 Looser KG, Allmendinger PD, Takata H, Ellison LH, Low HBC: Infection of cardiac suture line after ventricular aneurysmectomy. Report of two cases. J THORAC CARDIOVASC SURG 72:280-281, 1976 Schaff HV, Arnold PG, Reeder GS: Late mediastinal infection and pseudoaneurysm following left ventricular aneurysmectomy. Repair utilizing a pectoralis major muscle flap. J THORAC CARDIOVASC SURG 84:912-916, 1982
Brief communications
June, 1985
mobilization of the innominate vein to reach the left atrial appendage directly despite freeing up the internal jugular vein. A segment of saphenous vein was removed from the left thigh, divided longitudinally, wrapped around a No. 32 Fr. chest tube, and sutured with a 7-0 Prolene suture. This produced a tubular graft with an internal diameter of 14 mm (Fig. 2). The innominate vein was 10 mm in diameter. The appropriate length of spiral vein graft was calculated as previously described.' The patient was given heparin systemically. The innominate vein was opened longitudinally and an end-to-side anastomosis was performed. The spiral vein graft to the left atrial appendage anastomosis was performed in an end-to-end fashion with a partial occlusion clamp on the appendage. This anastomosis produced a large opening into the systemic venous atrium. The clamps were released and the external jugular venous pressure dropped from 34 to 17 mm Hg. Her postoperative course was uneventful. She was systemically improved and her parents noted that her face was much thinner and less blue. A first-pass nucleotide cardiac angiogram (technetium 99m) showed a widely patent graft and no venous stasis (Fig. 3). At her last outpatient evaluation, 6 months after the operation, the patient was totally asymptomatic and there were no physical signs of superior vena caval obstruction.
Discussion. Late baffle complications following the Mustard repair for transposition of the great arteries have been well documented. Either systemic or pulmonary venous obstruction has been reported in approximately 25% of cases repaired with either pericardial or Dacron baffles. Cobanoglu and associates' recently reported excellent results with a double patch reconstruction of the superior vena cava and the superior portion of the baffle to alleviate the superior vena caval syndrome in this clinical situation. Although there have been no deaths in their last 10 patients, this procedure does require cardiopulmonary bypass and an additional atrial incision. This incision and the patch must be placed near the sinus node. In view of the late arrhythmias reported following the Mustard operation, we believe that it is advantageous to be able to avoid an additional atrial incision. Use of the spiral vein graft in adults with superior vena caval syndrome has been very satisfactory.' Longterm results have shown patency up to 6 years postoperatively in patients operated on for benign disease. The use of this technique in children has not yet been reported to our knowledge, and the extended prognosis of the vein graft is uncertain. However, clinical and experimental experience with all other types of materials in the venous system have had poor long-term results.' Although we do not have long-term follow-up data as yet, we believe that this treatment is an excellent alternative when direct anastomosis is not possible. Use of the spiral vein graft avoids cardiopulmonary bypass and should result in a lower morbidity and mortality. An advantage over direct anastomosis is that
945
the vein graft also preserves the innominate and internal jugular continuity bilaterally. The result may be better decompression of the cerebral circulation and contralateral upper extremity. Cardiopulmonary bypass can still be performed when the child is older, if necessary. We are uncertain as to the smallest saphenous vein usable for this procedure, but we had no difficulty with the vein in this ll-year-old child. REFERENCES Coulson JD, Pitlick PT, Miller DC, French JW, Marshall WH, Fryer AD, Shumway NE: Severe superior vena cava syndrome and hydrocephalus after the Mustard procedure. Findings and a new surgical approach. Circulation 70:Suppl 1:47-53, 1984 2 Doty DB: Bypass of superior vena cava. J THORAC CARDIO. VASC SURG 83:326-337, 1982 3 Cobanoglu A, Abbruzzese PA, Freimanis I, Garcia CE, Grunkemeier G, Starr A: Pericardial baffle complications following the Mustard operation. Age-related incidence and ease of management. J THORAC CARDIOVASC SURG 87:371378, 1984 4 Hiratzka LF, Doty DB, Wright CB: Newer tissue and synthetic grafts in canine femoral veins. J Surg Res 31:324-331, 1981
Myocardial infarction complicated by myocardial rupture and Bacteroides sepsis Stephen A. Mills, M.D., C.M., Frederick Kahl, M.D., Michael Kutcher, M.D., and Abdel-Mohsen Nomeir, M.D., Winston-Salem. N. C. From the Section on Cardiothoracic Surgery, Department of Surgery, and the Section on Cardiology (Department of Medicine), Wake Forest University Medical Center, Bowman Gray School of Medicine, Winston-Salem, N. C.
A patient in whom a myocardial rupture complicated recent myocardial infarction was found to have cardiac and systemic Bacteroides sepsis; he had just completed a course of steroids. Surgical repair of the cardiac rupture, mediastinal irrigation with povidone-iodine, and broad-spectrum antibiotics resulted in the patient's recovery.
Cardiac rupture is a major cause of death following acute myocardial infarction. Whereas rupture of the free wall of the left ventricle usually results in acute hemopericardium and cardiac arrest despite continuing electrical activity, subacute rupture occasionally may Address for correspondence and reprints: Stephen A. Mills, M.D., Section on Cardiothoracic Surgery, Bowman Gray School of Medicine, 300 S. Hawthorne Rd., Winston-Salem, N. C. 27103.
The Journal of
946
Brief communications
Thoracic and Cardiovascular Surgery
Fig. 1. An apical two-chamber two-dimensional echocardiogram. DH, Dissecting myocardial hematoma. IVS, Interventricular septum. LA, Left atrium. LV, Left ventricle. MV, Mitral valve. The arrows point to the inner layer of the intramyocardial dissection.
Fig. 2. The cardiac rupture followed a tortuous path out to the pericardial space. An intra myocardial dissection was present and extended 5 to 8 em from the site of external rupture.
result in a syndrome resembling cardiogenic shock. When the latter clinical picture is present, there may be time for both diagnosis and surgical repair.!" This report documents the case of a patient in whom cardiac rupture following myocardial infarction was complicated by Bacteroides sepsis. Successful surgical repair was carried out. Case report. A 48-year-old man was hospitalized elsewhere with an uncomplicated, anterior myocardial infarction. He was discharged home 10 days later on a regimen of acetylsalicylic acid and propranolol. Two weeks after discharge, left anterior
chest pain developed, which was worse in the supine position and during inspiration. At readmission, a two-component cardiac apical rub could be heard over the left fifth intercostal space. The twelve-lead electrocardiogram showed an old diaphragmatic and anterior myocardial infarction with persistent ST and T-wave changes in the anterior leads consistent with aneurysm or pericarditis. He was treated with acetylsalicylic acid and later prednisone, the latter 40 mg four times a day. One week after readmission he was transferred to our institution. On the evening of admission he complained of chest pain radiating to the left shoulder and increasing with respiration. Nitroglycerin was given without improvement. His temperature rose from normal to 102° F; blood pressure was 90/65 mm Hg, pulse rate 84 beats/min, and respirations 32 breaths/ min. The electrocardiogram demonstrated no changes. Morphine was given with relief of pain. An echocardiogram demonstrated a large anterior apical infarct, a large apical thrombus, and a small pericardiaI effusion. Cardiac enzymes remained within normal limits. Two days later blood cultures grew gram-negative rods, and a regimen of cephapirin and tobramycin was started. Four days after admission, he had an episode of shaking chills and a temperature of 101 0 F. On the fifth hospital day, the chest pain recurred and repeat echocardiography showed enlargement of the pericardial effusion and a dissecting myocardial hematoma in addition to the previous findings (Fig. 1). Systemic blood pressure was 80/60 mm Hg. Cardiac catheterization showed equalization of right-sided pressures with a diastolic plateau. A left ventriculogram showed a large area of akinesia in the anterolateral septal apex with smoothing of the left ventricular lateral wall. No distinct pericardial communication was noted. The ejection fraction was 19%. The left anterior descending coronary artery was totally occluded; the other coronary arteries had minor irregularities. He was immediately taken to the operating room for a median sternotomy. A large amount of fresh and clotted blood
Volume 89
Brief communications
Number 6 June, 1985
was present within the pericardium. Cardiopulmonary bypass was instituted with moderate systemic hypothermia (30° C esophageal). A 6 cm tear was found in the apex of a large left ventricular infarct. Opening of the infarct showed an extensive myocardial dissection within the septum and including 5 to 8 em of the free wallsof the left and right ventricles (Fig. 2). The apex of the infarct was filled with clot. It was apparent that the rupture had occurred along a tortuous path within the left ventricular myocardium. A portion of the outer layer of the left ventricular infarct was debrided, and the infarct was repaired with Teflon strips and nonabsorbable monofilament suture. Cardiopulmonary bypass was discontinued while epinephrine was given intravenously. A Gram stain of the pericardiaI hematoma demonstrated leukocytosis (2+) with no organisms being seen. A blood culture obtained preoperatively grew Bacteroides fragilis. Antibiotic treatment included cephapirin, tobramycin, and clindamycin. Mediastinal irrigation was started with a 1% solutionof povidone-iodine at a rate of 75 rnl/hr and continued for 12 days. Ten days after operation, pericardial cultures and bloodcultures obtained at operation grew Bacteroides fragilis, subspecies thetaiotaomicron. A workup for the source of the Bacteroides infection showed extremely poor dental hygiene and a periodontal abscess, which were treated by extraction of all teeth and drainage of the abscess. The patient remained afebrile thereafter. A repeat echocardiogram 6 weeks after operation showed no changes from preoperative findings, other than diminished size of the pericardial effusion. He was discharged home I week later. At follow-up 3 months after the operation, he had no signs of infection or congestive heart failure.
Comment. Three cardiac infectious processes can complicate myocardial infarction: purulent pericarditis, mural endocarditis,' and myocardial abscess.' All are rare. In our patient, a periodontal abscess and poor dental hygiene probably were the source of cardiac sepsis. The recurrent chest pain was probably a result of extension of the intramyocardial dissection. A 6 day course of prednisone may well have contributed to delayed healing and rupture of the original myocardial infarction':" and development of sepsis. The ruptured tissue encountered at operation was not believed to be strong enough to allow primary closure without Teflon buttressing, although the use of pericardial strips as reported by Love and colleagues" following cardiac rupture at the site of left ventricular venting might have been effective. In cases of cardiac infection following repair of left ventricular aneurysm, debridement of Teflon combined
947
with an omental pedicle? or pectoral muscle flap'? has been used successfully. Although intrapericardial infection was not strongly suspected at the time of operation, subsequent cultures demonstrated Bacteroides infection, and a 12 day course of mediastinal irrigation with a 1% povidone-iodine solution in combination with a 6 week course of intravenous broad-spectrum antibiotics was begun. The result was apparent resolution of infection, and the patient is currently on a long-term regimen of penicillin and metronidazole.
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REFERENCES O'Rourke MF: Subacute heart rupture following myocardial infarction. Clinical features of a correctable condition. Lancet 2:124-126, 1973 Bashour T, Kabbani SS, Ellertson DG, Crew J, Hanna ES: Surgical salvage of heart rupture. Report of two cases and review of the literature. Ann Thorac Surg 36:209-213, 1983 Feneley MP, Chang VP, O'Rourke MF: Myocardial rupture after acute myocardial infarction. Ten year review. Br Heart J 49:550-556, 1983 Nunez L, de la Llana R, Sendon JL, Coma I, Aguado MG, Larrea JL: Diagnosis and treatment of subacute free wall ventricular rupture after infarction. Ann Thorac Surg 35:525-529, 1983 McCallum DG, Grow J Sr: Mural thrombus endocarditis complicating an acute myocardial infarction. Report of a case. Arch Intern Med 141:527-528, 1981 Roberts R, DeMello V, Sobel BE: Deleterious effects of methylprednisolonein patients with myocardial infarction. Circulation 53:Suppl 1:204-206, 1976 Bulkley BH, Roberts WC: Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm. Am J Med 56:244-250, 1974 Love JW, Jahnke EJ, McFadden RB, Fisher GU, Barbabella J, Anderson S, Vogel JHK: Left ventricular pseudoaneurysm secondary to infection after coronary bypass surgery. Chest 79:100-102, 1981 Looser KG, Allmendinger PD, Takata H, Ellison LH, Low HBC: Infection of cardiac suture line after ventricular aneurysmectomy. Report of two cases. J THORAC CARDIOVASC SURG 72:280-281, 1976 Schaff HV, Arnold PG, Reeder GS: Late mediastinal infection and pseudoaneurysm following left ventricular aneurysmectomy. Repair utilizing a pectoralis major muscle flap. J THORAC CARDIOVASC SURG 84:912-916, 1982