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Postoperative constrictive pericarditis
LETTERS TO THE EDITOR
effusion had previously been noted, because it is inaccurate. In their description of the electrocardiographic changes Levison and Semple stated: “By this time Q waves had developed in the chest leads Vl-V4 of the electrocardiogram, suggesting coronary occlusion as another possible cause of enzyme rise.” Nowhere in the discussion is the possibility of the effusion being responsible for the Q waves mentioned; the electrocardiographic changes occurred after a traumatic pericardiocentesis and, even though coronary occlusion is implied, there is no description of the coronary arteries in the anatomopathologic report. The context of the letter submitted to you is clearly different from that of the article. If in retrospect Semple believed that the electrocardiographic changes were probably due to major positional changes incurred by the pericardiocentesis, he failed to discuss it in his article. Jaime Benrey, MD, FACC Mark Schnee, MB, FACC Texas Heart Institute Houston, Texas Carlos M. de Castro, MD, FACC Division of Cardiology, The Clayton Foundation for Research Laboratory St. Luke’s Episcopal Hospital Houston, Texas
in any decent hospital is to record and note the details of all procedures. This is surely the standard in teaching hospitals and the report of Kilpatrick and Chapman is from a teaching hospital. In any case, even these authors agree to pericardial puncture when “time is of the essence.” Moreover, large effusions are relatively easy to tap and should provide no difficulties for those willing to apply the exquisite care and patience necessary to avoid mishap.5 David H. Spodick, MD, DSc, FACC University of Massachusetts Medical School Division of Cardiology St. Vincent Hospital Worcester, Massachusetts References 1. Becker RY, Achuff SC. Wel JY. Management of pericardial effusion [letters], Am J Cardlol 1960:45:188-9. 2. Bpodick DH. Acute pericarditis. New York, London: Grune & Stratton: 1959. 3. Bpodkk DH. Electric alternation of the heart. Its relation to the kinetics and physiokgy of the heart during cardiac tamponad& Am J Cardiol 1962;10:155-65. 4. Spodkk DH. Acute cardiac tamponade: pathophysiology, diagnosis and management. Pmg Cardiovasc Ois 1967;10:64-96. 5. BfwJkk DH. PeriCardial tamponade. In: Chung E, ed. Cardiac Emergency Care. Philadelphia: Lea 8 Febiger, 1975235-45. 6. Kllpafrkk ZM, Chapman CB. On paricardiocentesis. Am J Cardiol 1965:16:722-6.
POSTOPERATlVE
DRAINAGE OF PERICARDIAL
EFFUSION
The exchange of letters over “medical” vs. surgical drainage of pericardial effusion by Becker, Achuff and Wei’ sheds considerable light on the approach to management of a first class emergency-cardiac tamponade. I have been doing pericardial catheterization drainage for over 20 yearss-4 and, although in two cases a ventricle was entered, I have been fortunate to have had no mishaps (although an occasional “dry tap”). This may be due to luck or to the prevalence of very large effusions, which are easier to drain. I also prefer to aim for the left rather than the right shoulder and to proceed in a very slow, worm-gear motion as outlined elsewhere.5 I think all points made by both “opponent.s”r are valid and that, despite my own good luck, a limited subxiphoid surgical approach is probably optimal. When one does not have sufficient time and the situation is deteriorating rapidly, a needle pericardiocentesis must be done. I would only plead that the catheterization technique be used always, because once you are “in,” a relatively soft catheter rather than a hard needle is pointed at the heart. On the other hand, I must disagree strongly with Becker’s citation of the report by Kilpatrick and Chapman6 as providing competent evidence. This was, indeed, an interesting, largely historical account. That part of it from their personal experience involved only 12 cases, in which the only death occurred in a patient with malignant invasion of the pericardium immediately after instillation of nitrogen mustard into the pericardial space-certainly not a complication of the tap itself. The authors make the incomprehensible statement: “Probably most attempts at pericardiocentesis have gone unrecorded unless they provide diagnostic information of dramatic input. Unsuccessful attempts, and not infrequently complications, may also fail to find their way into hospital records.“6 Plainly, this will not do. It is conjecture and not supported by a scintilla of evidence. Routine practice
712
October 1990
The American Journal of CARDIOLOGY
CONSTRICTIVE
PERICARDITIS
In their report of three cases of constrictive pericarditis after myocardial revascularization Marsa and colleagues1 present well formulated conclusions regarding the role of povidoneiodine solution (Betadine@). In light of the appearance of these cases after the routine use of Betadine, it was reasonable to assign it a role in producing constriction. Previous work supports the role of the iodine moiety of Betadine. At least 28 agents or procedures have been employed to cause experimental pericardial scarring.2 These data include the early work of Beck and Moore3 and Musser and Herrmann, who used iodine tincture to produce pericardial adhesions. David H. Spodick, MD, DSc, FACC University of Massachusetts Medical School Division of Cardiology St. Vincent Hospital Worcester, Massachusetts References 1. Becker RM, Achuff SC, Wel JY. Management of pwicardial effusion [letters]. Am J Cardiil 1980;45: 188-9. 2. Bpodlck DH. Chronic and Constrictive Pericarditis. New York: Grune 6 Stratton. 196460. 3. Back CS, Moore RL. Arch Surg 1925;11:550. 4. Mwaer JH, Hwrmrmn OR. JAMA 1926;67:459.
REPLY
We appreciate Spodick’s considerate and informative observations. Also we wish to draw attention to Cohen and Greenberg’s report’ of postoperative constrictive pericarditis, published after submission of our manuscript. Two additional cases of surgically confirmed postoperative constrictive pericarditis have been seen by our group: Case 1: Nine months after an uncomplicated pulmonary commissurotomy performed in Saudi Arabia by members of our surgical team, an 18 year old Saudi Arabian youth presented with right heart failure (mean right atrial pressure 20 mm Hg)
Volume 46
effusion had previously been noted, because it is inaccurate. In their description of the electrocardiographic changes Levison and Semple stated: “By this time Q waves had developed in the chest leads Vl-V4 of the electrocardiogram, suggesting coronary occlusion as another possible cause of enzyme rise.” Nowhere in the discussion is the possibility of the effusion being responsible for the Q waves mentioned; the electrocardiographic changes occurred after a traumatic pericardiocentesis and, even though coronary occlusion is implied, there is no description of the coronary arteries in the anatomopathologic report. The context of the letter submitted to you is clearly different from that of the article. If in retrospect Semple believed that the electrocardiographic changes were probably due to major positional changes incurred by the pericardiocentesis, he failed to discuss it in his article. Jaime Benrey, MD, FACC Mark Schnee, MB, FACC Texas Heart Institute Houston, Texas Carlos M. de Castro, MD, FACC Division of Cardiology, The Clayton Foundation for Research Laboratory St. Luke’s Episcopal Hospital Houston, Texas
in any decent hospital is to record and note the details of all procedures. This is surely the standard in teaching hospitals and the report of Kilpatrick and Chapman is from a teaching hospital. In any case, even these authors agree to pericardial puncture when “time is of the essence.” Moreover, large effusions are relatively easy to tap and should provide no difficulties for those willing to apply the exquisite care and patience necessary to avoid mishap.5 David H. Spodick, MD, DSc, FACC University of Massachusetts Medical School Division of Cardiology St. Vincent Hospital Worcester, Massachusetts References 1. Becker RY, Achuff SC. Wel JY. Management of pericardial effusion [letters], Am J Cardlol 1960:45:188-9. 2. Bpodick DH. Acute pericarditis. New York, London: Grune & Stratton: 1959. 3. Bpodkk DH. Electric alternation of the heart. Its relation to the kinetics and physiokgy of the heart during cardiac tamponad& Am J Cardiol 1962;10:155-65. 4. Spodkk DH. Acute cardiac tamponade: pathophysiology, diagnosis and management. Pmg Cardiovasc Ois 1967;10:64-96. 5. BfwJkk DH. PeriCardial tamponade. In: Chung E, ed. Cardiac Emergency Care. Philadelphia: Lea 8 Febiger, 1975235-45. 6. Kllpafrkk ZM, Chapman CB. On paricardiocentesis. Am J Cardiol 1965:16:722-6.
POSTOPERATlVE
DRAINAGE OF PERICARDIAL
EFFUSION
The exchange of letters over “medical” vs. surgical drainage of pericardial effusion by Becker, Achuff and Wei’ sheds considerable light on the approach to management of a first class emergency-cardiac tamponade. I have been doing pericardial catheterization drainage for over 20 yearss-4 and, although in two cases a ventricle was entered, I have been fortunate to have had no mishaps (although an occasional “dry tap”). This may be due to luck or to the prevalence of very large effusions, which are easier to drain. I also prefer to aim for the left rather than the right shoulder and to proceed in a very slow, worm-gear motion as outlined elsewhere.5 I think all points made by both “opponent.s”r are valid and that, despite my own good luck, a limited subxiphoid surgical approach is probably optimal. When one does not have sufficient time and the situation is deteriorating rapidly, a needle pericardiocentesis must be done. I would only plead that the catheterization technique be used always, because once you are “in,” a relatively soft catheter rather than a hard needle is pointed at the heart. On the other hand, I must disagree strongly with Becker’s citation of the report by Kilpatrick and Chapman6 as providing competent evidence. This was, indeed, an interesting, largely historical account. That part of it from their personal experience involved only 12 cases, in which the only death occurred in a patient with malignant invasion of the pericardium immediately after instillation of nitrogen mustard into the pericardial space-certainly not a complication of the tap itself. The authors make the incomprehensible statement: “Probably most attempts at pericardiocentesis have gone unrecorded unless they provide diagnostic information of dramatic input. Unsuccessful attempts, and not infrequently complications, may also fail to find their way into hospital records.“6 Plainly, this will not do. It is conjecture and not supported by a scintilla of evidence. Routine practice
712
October 1990
The American Journal of CARDIOLOGY
CONSTRICTIVE
PERICARDITIS
In their report of three cases of constrictive pericarditis after myocardial revascularization Marsa and colleagues1 present well formulated conclusions regarding the role of povidoneiodine solution (Betadine@). In light of the appearance of these cases after the routine use of Betadine, it was reasonable to assign it a role in producing constriction. Previous work supports the role of the iodine moiety of Betadine. At least 28 agents or procedures have been employed to cause experimental pericardial scarring.2 These data include the early work of Beck and Moore3 and Musser and Herrmann, who used iodine tincture to produce pericardial adhesions. David H. Spodick, MD, DSc, FACC University of Massachusetts Medical School Division of Cardiology St. Vincent Hospital Worcester, Massachusetts References 1. Becker RM, Achuff SC, Wel JY. Management of pwicardial effusion [letters]. Am J Cardiil 1980;45: 188-9. 2. Bpodlck DH. Chronic and Constrictive Pericarditis. New York: Grune 6 Stratton. 196460. 3. Back CS, Moore RL. Arch Surg 1925;11:550. 4. Mwaer JH, Hwrmrmn OR. JAMA 1926;67:459.
REPLY
We appreciate Spodick’s considerate and informative observations. Also we wish to draw attention to Cohen and Greenberg’s report’ of postoperative constrictive pericarditis, published after submission of our manuscript. Two additional cases of surgically confirmed postoperative constrictive pericarditis have been seen by our group: Case 1: Nine months after an uncomplicated pulmonary commissurotomy performed in Saudi Arabia by members of our surgical team, an 18 year old Saudi Arabian youth presented with right heart failure (mean right atrial pressure 20 mm Hg)
Volume 46