- Email: [email protected]
Inadvertent administration of streptokinase to patients with pericarditis
CASE REPORTS
Inadvertent Administration of Streptokinase to Patients with Pericarditis
W. SPENCER TILLEY, M.D.” W. EUGENE HARSTON, M.D. Nashville,
Tennessee
From the Department of Cardiology, Vanderbilt University Medical Center and Veterans Administration Medical Center, Nashville, Tennessee. Manuscript submitted March 12, 1985, and accepted May 8, 1985. *Current address and address for reprint requests: Greensboro Cardiology Associates, 1011 Professional Village, Greensboro, North Carolina 27401.
Two patients with acute pericarditii who received intravenous streptokinase for presumed acute myocardial infarction are described. Although the administration of streptokinase did not cause an immediate increase in pericardial effusion, delayed nonhemorrhagic pericardial tamponade developed in both. Since pericarditis and other disease entities may mimic the pain and early electrocardiographic manifestations of acute myocardial infarction, precautions should be taken if thrombolytic therapy is given when there are no angktgraphic data to confirm the myocardial infarction. Pericarditis should be included in the differential diagnosis of patients with chest pain and ST segment elevation for the sake of diagnostic accuracy to avoid inappropriate therapy that may have some inherent risk. Thrombolytic therapy to open an occluded coronary artery during acute myocardial infarction has gained wide acceptance in the United States during the past few years [I]. Following the introduction of thrombolytic therapy in 1960, prolonged infusions of intravenous streptokinase were given within 12 to 24 hours of the infarction [2]. More recently, intracoronary streptokinase has been used, requiring selective catheterization of the coronary arteries and thereby limiting the use of the therapy to centers with cardiac catheterization facilities. The requirement to perform cardiac catheterization also causes some delay in the institution of therapy [3]. Now, high-dose, briefly administered intravenous streptokinase has gained increasing acceptance because it can be given earlier in the course of infarction, theoretically increasing the potential for myocardial salvage, and can be used by facilities without the capability of performing cardiac catheterization [4]. However, when acute myocardial infarction due to an occluded coronary artery is not confirmed by coronary arteriography, the diagnosis is based solely on the clinical presentation and the initial electrocardiographic findings, since diagnostic changes in the electrocardiographic results and serum enzyme values occur later. Occasionally, other diseases that present with chest pain and ST segment elevation may mimic myocardial infarction and lead to inappropriate therapy with thrombolytic agents. We report our experience with two patients who were treated with streptokinase for presumed myocardial infarction but were later found to have pericarditis. CASE REPORTS Patient 1. A 40-year-old black male farm worker presented to his local emergency room following six hours of substernal chest pain. He was treated with nitroglycerin sublingually without relief of his pain and then was given meperidine. An electrocardiogram (Figure 1) showing generalized ST segment elevation was interpreted as an acute myocardial infarction. He
September 1986 The American Journal of Medicine Volume 81
541
INADVERTENT
ADMINISTRATION
OF STREPTOKINASE-TILLEY
and
HARSTON
Figure 1. Electrocardiogram of Patient 1 showing generalized ST segment e/e vation in all leads except aVR. Serial electrocardiograms failed to evolve Q waves or changes typical of myocardial infarction.
was treated with 800,000 units of streptokinase intravenously, and a glucose potassium insulin infusion was begun. Transient hypotension and ventricular ectopy developed and he was transferred to St. Thomas Hospital in Nashville, Tennessee for further evaluation. On arrival, systemic blood pressure was 90160 mm Hg without paradox. Temperature was 101.2OF orally. Cardiac examination showed distant heart sounds with clear lung fields. Upon further questioning, the patient complained of substernal pleuritic chest pain but was able to lie flat comfortably. He also gave a history of malaise, fevers, chills, and intermittent chest pain for one week. The electrocardiogram at that point was interpreted as being consistent with acute pericarditis because- of the diffuse ST elevation that was present. The initial white blood cell count was 17,200/mm3 with a “left shift.” Coagulation studies were consistent with a fibrinolytic state with fibrin split products greater than 1:40, fibrinogen level less than 50 mg/dl, partial thromboplastin time 62.91253 seconds, and prothrombin time of 18.9/10.3 seconds. Portable chest radiography showed haziness of the left diaphragm with a slight increase in the cardiac silhouette. The patient was taken to the cardiac catheterization laboratory and underwent left heart catheterization and coronary arteriography, results of both of which were normal. Echocardiography was performed the next morning, showing a small anterior and posterior echo-free space consistent with pericardial effusion. When results of coagulation studies returned to normal, he began to receive indomethacin. Blood, urine, and sputum culture specimens were obtained and he was not treated with antibiotics. Serial creatine phosphokinase measurements returned within normal limits. On the third hospital day, increasing jugular venous distention was noted and a 20 mm pulsus paradoxus was present. A Swan-Ganz catheter was placed showing a right atrial pressure of 20 mm Hg, pulmonary artery pressure 45122 mm Hg, and pulmonary capillary wedge pressure 22 mm Hg. The similar pressures in the right atrium and pulmonary capillary wedge position were
542
September
1986
The American
Journal
of Medicine
indicative of cardiac tamponade. Repeated echocardiography showed a larger anterior and posterior echo-free space, suggesting that the pericardial effusion had increased. He underwent subxiphoid pericardiocentesis with removal of 600 ml of cloudy tan fluid. The white blood cell count was 214,000/mm3 with predominantly polymorphonuclear cells; red blood cell count was 28,000/mm3; and protein level was 5.4 g/liter. Following pericardiocentesis, the right atrial pressure fell from 20 to 8 mm Hg with disappearance of the pulsus paradoxus. Gram stain of the fluid showed gram-negative diplococci, and culture specimens eventually grew Neisseria meningitidis. He was initially treated with an aminoglycoside and cephalosporin, and when culture results were obtained, therapy was changed to high-dose penicillin, which he received for two weeks. Because of reaccumulation of the fluid, a subxiphoid pericardial window was placed for irrigation and drainage. He subsequently recovered without incident, and follow-up echocardiography has shown no re-accumulation of fluid. Patient 2. A 58-year-old black male truck driver presented to the Nashville Veterans Administration Medical Center in August 1984 following 45 minutes of chest pain. Other medical problems included insulin-dependent diabetes mellitus of two years’ duration and a history of poorly differentiated squamous cell carcinoma of the lung diagnosed by biopsy in March 1982. Surgery was recommended but he refused and underwent radiation therapy, receiving 5,700 rads to his mediastinum and left lung. For two years he had done well and had no evidence of tumor recurrence and no specific symptoms. On the day of admission, severe substernal chest pain abruptly developed while he was resting at home. He complained of mild dyspnea on exertion but had no pleuritic or positional component to his pain. He presented to the emergency room where an electrocardiogram (Figure 2) showing ST elevation in leads I, II, Ill, aVF, and V4 through Vs was interpreted as being consistent with an inferolateral myocardial infarction. He received sublingual nitroglycerin with moderate relief of his pain.
Volume
81
INADVERTENT
II
ADMINISTRATION
OF STREPTOKINASE-TILLEY
0’8.
yz Figure 2. Electrocardiogram of Patient 2 showing generalized ST segment e/e vation in all leads except aVL and aVR. Also noted is an abnormal P wave axis suggestive of an ectopic atrial pacemaker. Serial tracings showed resolution of the S-T elevation without the develop ment of Q waves.
and HARSTON
?;l::ii_,,; I
LM-k
/I,
0°F
fi:.;\&kQJ-: L
Physical examination showed bi-basilar rales, normal venous pressure, and normal cardiac sounds without a third heart sound or pericardial rub. Chest radiography showed hilar scarring, slight cardiomegaly, and increased markings at the left base. After transfer to the coronary care unit, he began to receive nitrates and diltiazem, and he was given 1.5 million units of streptokinase intravenously over one hour. Several hours later, administration of heparin was begun. He continued to complain of chest pain, and because of mild hypotension and bi-basilar rales, a SwanGanz catheter was placed showing right atrial pressure of 10 mm Hg, right ventricular pressure 30110 mm Hg, pulmonary artery pressure 30/10 mm Hg, and pulmonary capillary wedge pressure IO mm Hg. He was treated with intravenous fluids, and the next morning a loud pericardial friction rub was heard. Serial creatine phosphokinase enzyme levels were normal, and serial electrocardiograms did not show QRS changes indicative of myocardial infarction. An echocardiogram at that time showed a small anterior and posterior pericardial effusion. Heparin, diltiazem, and nitrates were discontinued and the patient began to receive indomethacin with dramatic relief of his pain. Over the next several days, he complained of intermittent chest pain until the fourth hospital day when he had increasing chest pain, fever, and mild hypotension. A 15 mm puisus paradoxus was noted along with jugular venous distention and tachycardia. Echocardiography showed a large anterior and posterior pericardial effusion. Right heart catheterization was performed and atrial and pulmonary wedge pressures were consistent with cardiac tamponade. Subxiphoid pericardiocentesis was performed and 500 ml of straw-colored fluid was removed. Mean right atrial pressure fell from 16 to 12 mm Hg and the pulsus paradoxus disappeared. Right atrial pressure curves after pericardiocentesis showed a rapid Y descent and continued elevation of mean right atrial pressure, which were believed to be due to an effusive constrictive pericardial process. Air contrast radiography showed a thickened pericardium. Analysis of the pericardial fluid showed a white blood cell count of 10,800/mm3 with predominantly mononuclear cells, red blood cell count of 33/mm3, total protein level 5.1 g/liter, and lactic dehydrogenase level of 1,560 IU/dl. Results of bacterial and tuberculin cultures were negative, and cyto-
September
logic examination demonstrated no malignancy. The patient subsequently was treated with indomethacin with no further rsaccumulation of the fluid. The diagnosis of post-radiation pericarditis was made, and on follow-up visits to the clinic, he has continued to do well. COMMENTS The two patients presented had electrocardiographic findings that were typical of pericarditis. In both cases, serial cardiac enzyme levels and electrocardiographic results failed to demonstrate myocardial necrosis. The inadver-
tent administration of intravenous streptokinase with the development of a fibrinolytic state did not result in hemopericardium or worsening of the patients’ condition. Pericardial tamponade developed slowly, and the fluid obtained at pericardiocentesis two to four days later was nonhemorrhagic, suggesting that the systemic thrombolytic state did not contribute to tamponade or convert the pericarditis to a hemorrhagic one. On the basis of this observation, it is postulated that the propensity of patients with pericarditis to bleed while receiving anticoagulation is a function of the underlying pericardial process rather than the state of anticoagulation in itself. if the underlying pericardial process had caused a hemorrhagic effusion, it is conceivable that fibrinolysis would have caused a rapid increase in the pericardial fluid. Taylor et al [5] demonstrated the efficacy and feasibility of the use of intravenous streptokinase in the treatment of myocardial infarction in hospitals without cardiac catheterization facilities. The arterial patency rate with intravenous streptokinase was similar to that achieved with intracoronary streptokinase, and had the advantage of earlier administration. The ease of administration and earlier onset of the initiation of therapy have made the intravenous route theoretically attractive as a means to broaden the application of fibrinolytic therapy. Consequently, many hospitals without catheterization facilities are now using intravenous
streptokinase
in the treatment
of patients with acute myocardial infarction,
1988
The
American
Journal
of Medicine
Volume
81
543
INADVERTENT
ADMINISTRATION
OF STREPTOKINASE-TILLEY
and HARSTON
The use of intravenous fibrinolytic therapy poses special considerations in the management of patients with acute myocardial infarction. Acute pericarditis can masquerade as myocardial infarction with a clinical presentation of substernal chest pain and ST segment elevation. In pericarditis, the ST segment elevation is usually generalized but on occasion may be localized, and resemble other cardiac problems [6]. If the diagnosis is not readily apparent after a careful history and physical examination, the distinction between pericarditis and myocardial infarction can usually be made after serial analysis of the cardiac enzyme level and the electrocardiographic findings. However, these data are not available to the physician at the time when a decision must be made regarding the initiation of fibrinolytic therapy. It is not surprising that some patients with pericarditis will mistakenly be given thrombolytic therapy. Other acute medical problems can mimic myocardial infarction. Satler et al [7] have described three patients with aottic dissection whose clinical story and electrocardiographic results were suggestive of myocardial infarction. These patients were considered for the intracoronary thrombolytic therapy; however, cardiac catheterization revealed the true cause of their medical condition with no evidence of coronary occlusion. The administration of intravenous thrombolytic therapy to these patients could have theoretically worsened the clinical course and made surgical interventions difficult. Metastatic involvement of the heart has been reported to cause an electrocardio-
graphic picture identical to acute myocardial infarction [8]. Acute central nervous system processes such as subdural hematoma, subarachnoid hemorrhage, or tumor have also been reported to mimic acute myocardial infarction [9]. Patients with repolarization abnormalities such as Wolff-Parkinson-White syndrome or early repolarization who present with noncardiac chest pain may have a misdiagnosis of myocardial infarction [IO]. Since the clinical presentation of pericarditis, aortic dissection, and other noncardiac entities can mimic an acute myocardial infarction, special precautions should be taken when administering thrombolytic therapy when corroborating arteriographic evidence is not available. When diagnostic QRS changes are not present, the ST elevation should be characteristic of ischemic injury and be clearly localized to leads indicating the anatomic distribution of one coronary artery. The presence of PR segment depression and the absence of reciprocal ST segment changes may be useful in distinguishing pericarditis from myocardial infarction [ 1 I]. If there is any doubt about the electrocardiographic changes, echocardiography performed promptly would be helpful in confirming the appropriate regional wall motion abnormality and in excluding pericardial effusion. ACKNOWLEDGMENT We thank Gottlieb C. Friesinger, M.D., and Raphael Smith, M.D., for their comments and review, and Dot Black for assistance in preparation of the manuscript.
REFERENCES 1.
2.
3.
4.
5.
644
Laffel GL, Braunwald E: Thrombolytic treatment: a new strategy for the treatment of acute myocardial infarction. N Engl J Med 1984; 311: 710-717,770-776. European Cooperative Study Group for Streptokinase Treatment in Acute Myocardial Infarction: Streptokinase in acute myocardial infarction. N Engl J Med 1979; 301: 797-802. Rentrop KP, Blanke H, Korsch KR, Kreuzer H: Initial experience with transluminal recanalization of the recently oceluded infarction-related coronary artery in acute myocardial infarction: comparison with conventionally treated patients. Clin Cardiol 1979; 2: 92-105. Schroder R, Giancarlo BV, v. Leitner ER, et al: Intravenous short-term effects of streptokinase in acute myocardial infarction. Circulation 1983; 67: 536-548. Taylor GJ, Mikell FL, Moses HW, et al: Intravenous versus intracoronary streptokinase therapy in acute myocardial infarction in community hospitals. Am J Cardiol 1984; 54: 256-260.
September
1966
The
American
Journal
of Medicine
6.
Bruce MA, Spodick DH: Atypical electrocardiogram in acute pericarditis: characteristics and prevalence. J Electrocard 1980; 13: 61-66.6. Satler LF, Levine S, Kent KM, et al: Aortic dissection masquerading as acute myocardialinfarction: implicationfor thrombolytic therapy without cardiac catheterization. Am J Cardiol 1984; 54: 1134-1135. Hartman RB, Clark PI, Schulman P: Pronounced and prolonged ST segment elevation: a pathognomonic sign of tumor invasion of the heart. Arch Intern Med 1982; 142: 1917-1919. Yamour BJ, Sudhara MR, Rice JF, Flowers NC: Electrocardiographic changes in cerebrovascular hemorrhage. Am Heart J 1980; 99: 294-298. Goldberger AL: Recognition of pseudoinfarct patterns. Mod Concept Cardiovasc Dis 1980; 49: 13-17. Spodick DH: Diagnostic electrocardiographic sequences in acute pericarditis: significance of PR segment and PR vector changes. Circulation 1973; 48: 573-580.
7.
8.
9.
10. 11.
Volume
61
Inadvertent Administration of Streptokinase to Patients with Pericarditis
W. SPENCER TILLEY, M.D.” W. EUGENE HARSTON, M.D. Nashville,
Tennessee
From the Department of Cardiology, Vanderbilt University Medical Center and Veterans Administration Medical Center, Nashville, Tennessee. Manuscript submitted March 12, 1985, and accepted May 8, 1985. *Current address and address for reprint requests: Greensboro Cardiology Associates, 1011 Professional Village, Greensboro, North Carolina 27401.
Two patients with acute pericarditii who received intravenous streptokinase for presumed acute myocardial infarction are described. Although the administration of streptokinase did not cause an immediate increase in pericardial effusion, delayed nonhemorrhagic pericardial tamponade developed in both. Since pericarditis and other disease entities may mimic the pain and early electrocardiographic manifestations of acute myocardial infarction, precautions should be taken if thrombolytic therapy is given when there are no angktgraphic data to confirm the myocardial infarction. Pericarditis should be included in the differential diagnosis of patients with chest pain and ST segment elevation for the sake of diagnostic accuracy to avoid inappropriate therapy that may have some inherent risk. Thrombolytic therapy to open an occluded coronary artery during acute myocardial infarction has gained wide acceptance in the United States during the past few years [I]. Following the introduction of thrombolytic therapy in 1960, prolonged infusions of intravenous streptokinase were given within 12 to 24 hours of the infarction [2]. More recently, intracoronary streptokinase has been used, requiring selective catheterization of the coronary arteries and thereby limiting the use of the therapy to centers with cardiac catheterization facilities. The requirement to perform cardiac catheterization also causes some delay in the institution of therapy [3]. Now, high-dose, briefly administered intravenous streptokinase has gained increasing acceptance because it can be given earlier in the course of infarction, theoretically increasing the potential for myocardial salvage, and can be used by facilities without the capability of performing cardiac catheterization [4]. However, when acute myocardial infarction due to an occluded coronary artery is not confirmed by coronary arteriography, the diagnosis is based solely on the clinical presentation and the initial electrocardiographic findings, since diagnostic changes in the electrocardiographic results and serum enzyme values occur later. Occasionally, other diseases that present with chest pain and ST segment elevation may mimic myocardial infarction and lead to inappropriate therapy with thrombolytic agents. We report our experience with two patients who were treated with streptokinase for presumed myocardial infarction but were later found to have pericarditis. CASE REPORTS Patient 1. A 40-year-old black male farm worker presented to his local emergency room following six hours of substernal chest pain. He was treated with nitroglycerin sublingually without relief of his pain and then was given meperidine. An electrocardiogram (Figure 1) showing generalized ST segment elevation was interpreted as an acute myocardial infarction. He
September 1986 The American Journal of Medicine Volume 81
541
INADVERTENT
ADMINISTRATION
OF STREPTOKINASE-TILLEY
and
HARSTON
Figure 1. Electrocardiogram of Patient 1 showing generalized ST segment e/e vation in all leads except aVR. Serial electrocardiograms failed to evolve Q waves or changes typical of myocardial infarction.
was treated with 800,000 units of streptokinase intravenously, and a glucose potassium insulin infusion was begun. Transient hypotension and ventricular ectopy developed and he was transferred to St. Thomas Hospital in Nashville, Tennessee for further evaluation. On arrival, systemic blood pressure was 90160 mm Hg without paradox. Temperature was 101.2OF orally. Cardiac examination showed distant heart sounds with clear lung fields. Upon further questioning, the patient complained of substernal pleuritic chest pain but was able to lie flat comfortably. He also gave a history of malaise, fevers, chills, and intermittent chest pain for one week. The electrocardiogram at that point was interpreted as being consistent with acute pericarditis because- of the diffuse ST elevation that was present. The initial white blood cell count was 17,200/mm3 with a “left shift.” Coagulation studies were consistent with a fibrinolytic state with fibrin split products greater than 1:40, fibrinogen level less than 50 mg/dl, partial thromboplastin time 62.91253 seconds, and prothrombin time of 18.9/10.3 seconds. Portable chest radiography showed haziness of the left diaphragm with a slight increase in the cardiac silhouette. The patient was taken to the cardiac catheterization laboratory and underwent left heart catheterization and coronary arteriography, results of both of which were normal. Echocardiography was performed the next morning, showing a small anterior and posterior echo-free space consistent with pericardial effusion. When results of coagulation studies returned to normal, he began to receive indomethacin. Blood, urine, and sputum culture specimens were obtained and he was not treated with antibiotics. Serial creatine phosphokinase measurements returned within normal limits. On the third hospital day, increasing jugular venous distention was noted and a 20 mm pulsus paradoxus was present. A Swan-Ganz catheter was placed showing a right atrial pressure of 20 mm Hg, pulmonary artery pressure 45122 mm Hg, and pulmonary capillary wedge pressure 22 mm Hg. The similar pressures in the right atrium and pulmonary capillary wedge position were
542
September
1986
The American
Journal
of Medicine
indicative of cardiac tamponade. Repeated echocardiography showed a larger anterior and posterior echo-free space, suggesting that the pericardial effusion had increased. He underwent subxiphoid pericardiocentesis with removal of 600 ml of cloudy tan fluid. The white blood cell count was 214,000/mm3 with predominantly polymorphonuclear cells; red blood cell count was 28,000/mm3; and protein level was 5.4 g/liter. Following pericardiocentesis, the right atrial pressure fell from 20 to 8 mm Hg with disappearance of the pulsus paradoxus. Gram stain of the fluid showed gram-negative diplococci, and culture specimens eventually grew Neisseria meningitidis. He was initially treated with an aminoglycoside and cephalosporin, and when culture results were obtained, therapy was changed to high-dose penicillin, which he received for two weeks. Because of reaccumulation of the fluid, a subxiphoid pericardial window was placed for irrigation and drainage. He subsequently recovered without incident, and follow-up echocardiography has shown no re-accumulation of fluid. Patient 2. A 58-year-old black male truck driver presented to the Nashville Veterans Administration Medical Center in August 1984 following 45 minutes of chest pain. Other medical problems included insulin-dependent diabetes mellitus of two years’ duration and a history of poorly differentiated squamous cell carcinoma of the lung diagnosed by biopsy in March 1982. Surgery was recommended but he refused and underwent radiation therapy, receiving 5,700 rads to his mediastinum and left lung. For two years he had done well and had no evidence of tumor recurrence and no specific symptoms. On the day of admission, severe substernal chest pain abruptly developed while he was resting at home. He complained of mild dyspnea on exertion but had no pleuritic or positional component to his pain. He presented to the emergency room where an electrocardiogram (Figure 2) showing ST elevation in leads I, II, Ill, aVF, and V4 through Vs was interpreted as being consistent with an inferolateral myocardial infarction. He received sublingual nitroglycerin with moderate relief of his pain.
Volume
81
INADVERTENT
II
ADMINISTRATION
OF STREPTOKINASE-TILLEY
0’8.
yz Figure 2. Electrocardiogram of Patient 2 showing generalized ST segment e/e vation in all leads except aVL and aVR. Also noted is an abnormal P wave axis suggestive of an ectopic atrial pacemaker. Serial tracings showed resolution of the S-T elevation without the develop ment of Q waves.
and HARSTON
?;l::ii_,,; I
LM-k
/I,
0°F
fi:.;\&kQJ-: L
Physical examination showed bi-basilar rales, normal venous pressure, and normal cardiac sounds without a third heart sound or pericardial rub. Chest radiography showed hilar scarring, slight cardiomegaly, and increased markings at the left base. After transfer to the coronary care unit, he began to receive nitrates and diltiazem, and he was given 1.5 million units of streptokinase intravenously over one hour. Several hours later, administration of heparin was begun. He continued to complain of chest pain, and because of mild hypotension and bi-basilar rales, a SwanGanz catheter was placed showing right atrial pressure of 10 mm Hg, right ventricular pressure 30110 mm Hg, pulmonary artery pressure 30/10 mm Hg, and pulmonary capillary wedge pressure IO mm Hg. He was treated with intravenous fluids, and the next morning a loud pericardial friction rub was heard. Serial creatine phosphokinase enzyme levels were normal, and serial electrocardiograms did not show QRS changes indicative of myocardial infarction. An echocardiogram at that time showed a small anterior and posterior pericardial effusion. Heparin, diltiazem, and nitrates were discontinued and the patient began to receive indomethacin with dramatic relief of his pain. Over the next several days, he complained of intermittent chest pain until the fourth hospital day when he had increasing chest pain, fever, and mild hypotension. A 15 mm puisus paradoxus was noted along with jugular venous distention and tachycardia. Echocardiography showed a large anterior and posterior pericardial effusion. Right heart catheterization was performed and atrial and pulmonary wedge pressures were consistent with cardiac tamponade. Subxiphoid pericardiocentesis was performed and 500 ml of straw-colored fluid was removed. Mean right atrial pressure fell from 16 to 12 mm Hg and the pulsus paradoxus disappeared. Right atrial pressure curves after pericardiocentesis showed a rapid Y descent and continued elevation of mean right atrial pressure, which were believed to be due to an effusive constrictive pericardial process. Air contrast radiography showed a thickened pericardium. Analysis of the pericardial fluid showed a white blood cell count of 10,800/mm3 with predominantly mononuclear cells, red blood cell count of 33/mm3, total protein level 5.1 g/liter, and lactic dehydrogenase level of 1,560 IU/dl. Results of bacterial and tuberculin cultures were negative, and cyto-
September
logic examination demonstrated no malignancy. The patient subsequently was treated with indomethacin with no further rsaccumulation of the fluid. The diagnosis of post-radiation pericarditis was made, and on follow-up visits to the clinic, he has continued to do well. COMMENTS The two patients presented had electrocardiographic findings that were typical of pericarditis. In both cases, serial cardiac enzyme levels and electrocardiographic results failed to demonstrate myocardial necrosis. The inadver-
tent administration of intravenous streptokinase with the development of a fibrinolytic state did not result in hemopericardium or worsening of the patients’ condition. Pericardial tamponade developed slowly, and the fluid obtained at pericardiocentesis two to four days later was nonhemorrhagic, suggesting that the systemic thrombolytic state did not contribute to tamponade or convert the pericarditis to a hemorrhagic one. On the basis of this observation, it is postulated that the propensity of patients with pericarditis to bleed while receiving anticoagulation is a function of the underlying pericardial process rather than the state of anticoagulation in itself. if the underlying pericardial process had caused a hemorrhagic effusion, it is conceivable that fibrinolysis would have caused a rapid increase in the pericardial fluid. Taylor et al [5] demonstrated the efficacy and feasibility of the use of intravenous streptokinase in the treatment of myocardial infarction in hospitals without cardiac catheterization facilities. The arterial patency rate with intravenous streptokinase was similar to that achieved with intracoronary streptokinase, and had the advantage of earlier administration. The ease of administration and earlier onset of the initiation of therapy have made the intravenous route theoretically attractive as a means to broaden the application of fibrinolytic therapy. Consequently, many hospitals without catheterization facilities are now using intravenous
streptokinase
in the treatment
of patients with acute myocardial infarction,
1988
The
American
Journal
of Medicine
Volume
81
543
INADVERTENT
ADMINISTRATION
OF STREPTOKINASE-TILLEY
and HARSTON
The use of intravenous fibrinolytic therapy poses special considerations in the management of patients with acute myocardial infarction. Acute pericarditis can masquerade as myocardial infarction with a clinical presentation of substernal chest pain and ST segment elevation. In pericarditis, the ST segment elevation is usually generalized but on occasion may be localized, and resemble other cardiac problems [6]. If the diagnosis is not readily apparent after a careful history and physical examination, the distinction between pericarditis and myocardial infarction can usually be made after serial analysis of the cardiac enzyme level and the electrocardiographic findings. However, these data are not available to the physician at the time when a decision must be made regarding the initiation of fibrinolytic therapy. It is not surprising that some patients with pericarditis will mistakenly be given thrombolytic therapy. Other acute medical problems can mimic myocardial infarction. Satler et al [7] have described three patients with aottic dissection whose clinical story and electrocardiographic results were suggestive of myocardial infarction. These patients were considered for the intracoronary thrombolytic therapy; however, cardiac catheterization revealed the true cause of their medical condition with no evidence of coronary occlusion. The administration of intravenous thrombolytic therapy to these patients could have theoretically worsened the clinical course and made surgical interventions difficult. Metastatic involvement of the heart has been reported to cause an electrocardio-
graphic picture identical to acute myocardial infarction [8]. Acute central nervous system processes such as subdural hematoma, subarachnoid hemorrhage, or tumor have also been reported to mimic acute myocardial infarction [9]. Patients with repolarization abnormalities such as Wolff-Parkinson-White syndrome or early repolarization who present with noncardiac chest pain may have a misdiagnosis of myocardial infarction [IO]. Since the clinical presentation of pericarditis, aortic dissection, and other noncardiac entities can mimic an acute myocardial infarction, special precautions should be taken when administering thrombolytic therapy when corroborating arteriographic evidence is not available. When diagnostic QRS changes are not present, the ST elevation should be characteristic of ischemic injury and be clearly localized to leads indicating the anatomic distribution of one coronary artery. The presence of PR segment depression and the absence of reciprocal ST segment changes may be useful in distinguishing pericarditis from myocardial infarction [ 1 I]. If there is any doubt about the electrocardiographic changes, echocardiography performed promptly would be helpful in confirming the appropriate regional wall motion abnormality and in excluding pericardial effusion. ACKNOWLEDGMENT We thank Gottlieb C. Friesinger, M.D., and Raphael Smith, M.D., for their comments and review, and Dot Black for assistance in preparation of the manuscript.
REFERENCES 1.
2.
3.
4.
5.
644
Laffel GL, Braunwald E: Thrombolytic treatment: a new strategy for the treatment of acute myocardial infarction. N Engl J Med 1984; 311: 710-717,770-776. European Cooperative Study Group for Streptokinase Treatment in Acute Myocardial Infarction: Streptokinase in acute myocardial infarction. N Engl J Med 1979; 301: 797-802. Rentrop KP, Blanke H, Korsch KR, Kreuzer H: Initial experience with transluminal recanalization of the recently oceluded infarction-related coronary artery in acute myocardial infarction: comparison with conventionally treated patients. Clin Cardiol 1979; 2: 92-105. Schroder R, Giancarlo BV, v. Leitner ER, et al: Intravenous short-term effects of streptokinase in acute myocardial infarction. Circulation 1983; 67: 536-548. Taylor GJ, Mikell FL, Moses HW, et al: Intravenous versus intracoronary streptokinase therapy in acute myocardial infarction in community hospitals. Am J Cardiol 1984; 54: 256-260.
September
1966
The
American
Journal
of Medicine
6.
Bruce MA, Spodick DH: Atypical electrocardiogram in acute pericarditis: characteristics and prevalence. J Electrocard 1980; 13: 61-66.6. Satler LF, Levine S, Kent KM, et al: Aortic dissection masquerading as acute myocardialinfarction: implicationfor thrombolytic therapy without cardiac catheterization. Am J Cardiol 1984; 54: 1134-1135. Hartman RB, Clark PI, Schulman P: Pronounced and prolonged ST segment elevation: a pathognomonic sign of tumor invasion of the heart. Arch Intern Med 1982; 142: 1917-1919. Yamour BJ, Sudhara MR, Rice JF, Flowers NC: Electrocardiographic changes in cerebrovascular hemorrhage. Am Heart J 1980; 99: 294-298. Goldberger AL: Recognition of pseudoinfarct patterns. Mod Concept Cardiovasc Dis 1980; 49: 13-17. Spodick DH: Diagnostic electrocardiographic sequences in acute pericarditis: significance of PR segment and PR vector changes. Circulation 1973; 48: 573-580.
7.
8.
9.
10. 11.
Volume
61