Constrictive Pericarditis After Myocardial Revascularization Report of Three Cases
ROBERT MARSA, MD SUKH MEHTA, MD, FACC WILLIAM WILLIS, MD, FACC LEONARD BAILEY, MD Loma Linda, California
Although postoperative constrictive pericarditis is rare, the diagnosis should be conskfered when unexplained right-&fed heart failure deveb after cardiac surgery. Within a 6 week interval, evidence of constrictive pericarditis developed in three patients who had recently undergone myocardial revascularization. One patient presented with biventricular failure, pericardial effusion and suspected tamponade. Severe constrictive pericarditis was demonstrated at subsequent operation. An apparent postpericardiotomy syndrome preceded evidence of right heart failure in the other two patients. Etiologic considerations include the possibility that pericardial irrigation with povidone-iodine (Betadine) solution may have contributed to subsequent fibrosis.
Although constrictive pericarditis is frequently idiopathic, a wide variety of causes, including cardiac surgery, have been described.1-7 An estimated 300,000 to 400,000 coronary arterial bypass operations were performed from 1967 to 1977 and the number performed annually is now thought to approach 100,000.8 Yet to our knowledge, only seven cases of overt constrictive pericarditis occurring after heart surgery have been reported in English language studies.4-7 Experience at our institution supports the rarity of this finding; in nearly 2,000 cardiac surgical procedures performed in the past 8 years, constrictive pericarditis was not recognized as a postoperative complication. Recently, however, we encountered three patients (Table I) who had evidence of pericardial constriction after myocardial revascularization. Possible causes of postoperative constrictive pericarditis include hemopericardium, mediastinal Plasmanate@ infusion, postpericardiotomy syndrome and previous mediastinal irradiation. Review of our three cases led us to entertain the possibility of an additional, previously unrecognized cause. Case Reports
From the Departments of Medicine and Surgery, Loma Linda University School of Medicine, Loma Linda, California. Manuscript received January 10, 1979, accepted February 1, 1979. Address for reprints: Robert Marsa, MD. Division of Cardiology, Deparmwnt of Medicine, Lorna Linda University Medical Center, Loma Linda, California 92350.
Case 1: This 54 year old white man, an insurance inspector, had known bronchial asthma and coronary artery disease. Coronary arteriography and left ventriculography on August 17, 1977 revealed extensive coronary artery disease with occlusion of the dominant right coronary artery and severe stenosis of the left anterior descending and the obtuse marginal arteries. The left ventricular inferior wall was severely hypokinetic and the lateral wall moderately hypokinetic. Left ventricular diastolic pressures were normal (Table II). Two weeks after coronary arteriography myocardial revascularization was performed with placement of a sequential saphenous vein graft to the left anterior descending and superior obtuse marginal arteries. Myocardial preservation was accomplished by bathing in iced saline solution. The pericardium was irrigated with povidone-iodine (Betadine@) solution, diluted approximately 1:20 in isotonic saline solution, and was left open before closure of the sternotomy incision. Transient S-T segment elevation was observed in the electrocardiogram on the 1st postoperative day. The patient’s initial postoperative course was otherwise
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TABLE I Clinical Summary of Three Cases
Age (yr) & sex Vessels diseased on coronary angiography Course after myocardial revascularization
Electrocardiography* Chest X-ray film* Echocardiography’ Angiography’
Case 3
Case 2
Case 1 54M 3 vessels
50M 3 vessels
61M 2 vessels
Rehospitalized 5 weeks postoperatively with suspected tamponade. Pericardial effusion cleared with corticosteroids. Severe constrictive pericarditis confirmed surgically Low voltage, T wave inversion
Post pericardiotomy syndrome early in course. Rehospitalized 5 weeks postoperatively with right heart failure and pericardial knock
Mediastinal widening 1 day postoperatively. Subsequent postpericardiotomy syndrome. Rehospitalized 4 weeks postoperatively with evidence of right heart failure.
Widespread T wave inversion Normal Suspected pericardial thickening All arafts oatent
Widespread T wave inversion Left pleural effusion Asymmetric septal hypertrophy
Cardiomegaly, congestive failure Disappearance of pericardial effusion All grafts patent
All arafts oatent
* Findings near time of postoperative cardias catheterization.
uncomplicated, and he was discharged 8 days after operation on a regimen of dipyridamole and aspirin. Five weeks after operation, he was rehospitalized because of severe shortness of breath with chest X-ray and clinical findings of biventricular failure. A pericardial friction rub, marked jugular venous distension and a 20 mm Hg paradoxic pulse suggested cardiac tamponade. An echocardiogram demonstrated a moderately large posterior pericardial effusion. Although the patient was afebrile and had a normal erythrocyte sedimentation rate (Zeta sedimentation ratio),9 a postpericardiotomy syndrome with tamponade was suspected, and he was treated with digoxin, furosemide and prednisone (60 mg/day tapered over several days to 10 mg daily). At the time of discharge 7 weeks after operation, the paradoxic pulse had decreased to 10 mm Hg and there had been mild reduction of jugular venous distension. However, 5 days later the patient was again hospitalized because of persistent dyspnea and weakness. Marked jugular venous distension was again observed and a 10 mm Hg paradoxic pulse was noted. No pericardial knock or friction rub was detected. The liver was palpable 6 cm below the right costal margin, and mild ankle edema was present. The echocardiogram indicated disappearance of the previously demonstrated pericardial effusion. The electrocardiogram shotier+! diminished QRS voltage, by comparison wiq the early postoperative tracings, and generalized T wave inversion. The chest X-ray film revealed moderate cardiomegaly, blunting of both costophrenic angles as well as pulmonary vascular congestion (Fig. 1).
Cardiac catheterization on October 31 (2 months after operation) revealed severely elevated and virtually equal left ventricular diastolic, pulmonary arterial wedge, pulmonary arterial diastolic, right ventricular diastolic and right atria1 pressures. A typical “square root” contour was present in the ventricular pressure tracings (Fig. 2), and the aortic pressure tracing had a 20 mm Hg paradoxic pulse. The sequential saphenous vein graft was widely patent. Mild progression of disease was noted in the left coronary system, but did not account for deterioration of left ventricular function with moderate generalized hypokinesia in addition to the previously observed inferior and lateral wall hypokinesia. No pericardial calcification was seen. At operation performed later the same day, several hours were required for decortication of a very adherent and densely fibrous thickened pericardium and epicardial peel. Subsequent histopathologic examination of the pericardium disclosed extensive fibrosis, chronic inflammatory changes and scattered areas with foreign body-type giant cells. The early postoperative course was complicated by congestive heart failure and pulmonary edema. On follow-up 10 months after pericardiectomy, the patient continued to require furosemide for control of heart failure but had a normal jugular venous pressure and no paradoxic pulse. Case 2: This 50 year old white man, a hydraulics technician, had an acute anteroseptal myocardial infarction in May 1977. Coronary arteriography and left ventricular angiography were performed on August 23,1977 and revealed hypokinesia of the
TABLE II Comparison of Preoperative (Pre) and Postoperative (Post) Catheterization Data
LVEF Pressures (mm Hg) Right atrium Right ventricle Pulmonary artery Pulmonary arterial wedge Left ventricle Aorta
0.42
Post
Pre 0.51
0.27 28 40124’ 35122 28
130112 135178
150114 160198
110/26’+ 110/82+
Plateauing of mid and late diastolic pressures. + 20 mm Hg paradoxic pulse. l
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Case 3
Case 2
Case 1 Pre
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Pre
Post
0.48
0.53
0.41
29&’ 30114 15
25:4 25/12 7
26::3’ 26113 13
130117’ 132192
150114 150195
108115’ 115183
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anterolateral and apical left ventricle, occlusion of the left anterior descending coronary artery and multiple stenoses of the circumflex and right coronary systems. Left ventricular diastolic pressures were normal. On September 2,1977 a saphenous vein graft was placed to the right coronary artery and a sequential graft to the left anterior descending and inferior obtuse marginal arteries. Myocardial preservation was accomplished by bathing in iced saline solution. The pericardium was irrigated with povidone-iodine solution in saline solution of approximately 1:20 concentration and was left open. The patient’s initial postoperative course was uncomplicated. However, on the 3rd postoperative day he experienced anorexia and nausea and had a temperature of 38°C. Results of serum liver function tests became abnormal:Total bilirubin was 2.9 mg/lOO ml, direct bilirubin 1 mg/lOO ml, glutamic pyruvate transaminase 327 units (normal 0 to 40 units), alkaline phosphatase 103 units (normal 30 to 100 units) and hepatitis-associated antigen negative. Serial electrocardiograms were not appreciably changed from a preoperative tracing. The patient’s appetite gradually improved, and an intermittent low grade fever cleared in several days. The initial postoperative chest X-ray films showed no abnormality, but the film obtained 10 days postoperatively revealed a significant increase in cardiac size and a small left pleural effusion.
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FIGURE 1. pulmonary
ET AL.
Case 1. Chest roentgenogram showing cardiomegaly vascular congestion 4 days before pericardiectomy.
and
FKXJRE 2. Case 1. Pressure tracings. Top, simultaneous right (RV) and left (LV) ventricular pressure tracings typical of constrictive pericarditis. Bottom, aortic (AO) pressure tracing revealing a prominent paradoxic pulse.
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Despite persistence of moderately abnormal serum liver enzymes, the patient was discharged 12 days postoperatively on a regimen of dipyridamole and aspirin. A subsequent oral cholecystogram demonstrated cholelithiasis. Five weeks postoperatively the patient was hospitalized in another hospital with a several day history of frank pretibial, scrotal and presacral edema. The examining physician reported elevation of the jugular venous pressure and a third heart sound. No paradoxic pulse was detected. The chest X-ray film revealed bilateral pleural effusion without pulmonary vascular congestion. Serum liver enzyme determinations and total bilirubin were normal. The patient was treated with furosemide, digoxin and prednisone and had an 8 kg weight loss in 12 days. Two months after operation, he returned to this medical center for further evaluation. Despite continued use of furosemide, 80 mg each morning, the jugular venous pressure was elevated to the angle of the jaw with the patient at 30”. There was no paradoxic pulse or peripheral edema, although a prominent third heart sound or pericardial knock was present. An echocardiogram suggested pericardial thickening but did not reveal effusion. The heart size shown in the chest X-ray film had returned to normal from that in the film obtained 10 days postoperatively. Serum enzymes and albumin were normal, although total bilirubin was mildly elevated (1.7 mg/lOO ml). Cardiac catheterization revealed findings typical of constrictive pericarditis with abnormally elevated and nearly equal diastolic pressures in all cardiac chambers. Prominent X and Y descents were seen in the right atria1 pressure recording, and the ventricular pressure tracings showed a typical “dip and plateau” diastolic pressure contour (Fig. 3), with mid and late ventricular diastolic pressures averaging about 15 mm Hg (right ventricular systolic pressure 29 mm Hg). Straightening of the right heart border was demonstrated with right atria1 angiography. The left ventriculogram was not appreciably changed from the preoperative study. Coronary arteriography revealed well functioning saphenous vein grafts. Although the right coronary arterial stenoses were unchanged, there was a striking reduction of right coronary mobility as viewed in the right anterior oblique projection with apparent fixation of anterior right ventricular branches. Although this patient is thought to have moderately severe constrictive pericarditis, he is now being treated medically. Case 3: This 61 year old white man, a mechanic, had a 1 year history of gradually worsening angina and was hospitalized
for coronary arteriography. Cardiovascular examination was normal except for the presence of a grade 216 blowing, nonholosystolic apical murmur that did not change significantly with the Valsalva maneuver or with inspiration. The chest X-ray film revealed borderline cardiomegaly and the electrocardiogram showed minor nonspecific S-T segment depression. An echocardiogram demonstrated asymmetric septal hypertrophy. Cardiac catheterization and coronary arteriography, performed on October 4, 1977, revealed two vessel coronary artery disease with multiple stenoses of the left anterior descending coronary artery and critical stenosis distally in the small but technically dominant right coronary artery. Right heart pressures and left ventricular contractions were normal, although the left ventricular end-diastolic pressure was mildly elevated. No gradient could be demonstrated across the left ventricular outflow tract even with provocative maneuvers. On October 12, 1977 the patient underwent myocardial revascularization with placement of saphenous vein grafts to the distal right coronary artery and sequentially to the mid and distal left anterior descending coronary artery. Myocardial preservation was accomplished by aortic root infusion of an iced dextrose solution followed by topical cooling with iced saline solution. The pericardium was irrigated with povidone-iodine in saline solution of approximately 1:20 strength and was left open. A chest X-ray film obtained 1 day postoperatively revealed mediastinal widening and cardiomegaly. The early postoperative course was complicated by pulmonary congestion, left basal atelectasis, a left pleural effusion and an intermittent low grade fever. A matching ventilationperfusion defect of the left lung base was revealed in a lung scan. The electrocardiogram 3 days after operation was consistent with pericarditis and showed widespread S-T segment elevation not seen in the tracing 1 day after operation. On the day of discharge 1 week postoperatively, the lung fields were clear to auscultation and the patient was afebrile. Four weeks after operation the patient reported the recent onset of exertionally induced nausea, chest tightness and abdominal distress associated with a low grade fever. He denied pleuritic pain or recurrence of angina1 chest pain. On physical examination he was observed to have a heart rate of 70 beats/min, a blood pressure of 1lo/80 mm Hg and 6 to 7 mm Hg inspiratory decrease in systolic blood pressure. The venous pressure was moderately increased with prominent A and V waves extending to the angle of the mandible with the patient at 30”. Dullness was noted at the left lower lung base and was
40
I” E 3o E s a 20 2 g 10
-I
01 1 SEC F
+-
180
FIGURE 3. Case 2. Pressure tracings. Superimposed right (RV) and left (LV) ventricular pressure tracings exhibiting the classic “square root” configuration of constrictive pericarditis.
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associated with bronchial breath sounds. Cardiac examination was unchanged from the preoperative evaluation. The liver was palpable, but it had a normal span and there was no peripheral edema. A chest roentgenogram revealed mild cardiac enlargement, reduced from that shown in the early postoperative films, and increased size of the left pleural effusion with apparently normal pulmonary vasculature. An electrocardiogram showed generalized nonspecific T wave inversion. The echocardiogram did not indicate pericardial effusion, but again revealed asymmetric septal hypertrophy. The patient was treated with digoxin and furosemide, 40 mg daily, and after a 3 kg weight loss underwent repeat cardiac catheterization. Pressure data on cardiac catheterization were consistent with moderate constrictive pericarditis with nearly equal diastolic pressures in all cardiac chambers (Fig. 4). The mean right atria1 pressure was 11 mm Hg compared with the preoperative valve of 2 mm Hg. There was an 8 to 10 mm Hg
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respiratory variation in the aortic systolic pressure. Right atria1 angiography revealed straightening of the right heart border and left ventricular angiography demonstrated a mild, global decrease in left ventricular contractions with an ejection fraction of 0.41 compared with the preoperative value of 0.53. The parent coronary arteries were not appreciably changed from the preoperative study and the saphenous vein bypass grafts were widely patent. This patient is not considered to have severe constrictive pericarditis and is being treated medically.
Discussion Causes of postoperative pericardial adhesions, fibrosis and constriction: Although pericardial adhesions are readily produced by surgical and chemical trauma, fibrosis leading to recognized constriction is
0 RA preoperative
FIGURE 4. Case 3. Pressure tracings. lop, comparison of the pre- and postoperative right atrial (RA) pressure tracings reveals development of equal A and V waves with prominent X and Y descents in the postoperative tracing. Bottom, postoperative left ventricular diastolic and right atrial pressures are virtually identical.
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infrequent and is usually unpredictable.2Jo Approximately 50 years ago constrictive pericarditis was produced experimentally in dogs by pericardial instillation of Dakin’s solution (sodium hypochlorite solution, a topical antiseptic). l”,ll Dakin’s solution had been described as a treatment for purulent pericarditis, but was subsequently shown to produce a hemorrhagic pericarditis in normal animals. Animals surviving intrapericardial instillation of this solution frequently manifested constrictive pericarditis in 1 or 2 months. In a more recent experiment, intrapericardial injection of lipid extract of blood resulted in adhesions and fibrosis.12 However, only one of six dogs had definite constriction. Atraumatic injection of autologous blood into the pericardial space is generally not followed by appreciable fibrosis, whereas hemopericardium in association with pericardial injury leads to variable fibrosis.13J4 This synergistic effect has been observed after direct mechanical injury and (using a rabbit model) after 5 to 7 minutes’ drying of the pericardial serosal surface with a “gentle” stream of compressed air. Of particular interest, in the later experiment, serosal drying without addition of blood did not produce adhesions or fibrosis.14 Normal serosal tissue has well demonstrated fibrinolytic activity. Drying of a serosal surface results in loss of mesothelial cells lining the surface and total loss of fibrinolytic activity. It has been suggested that clotted blood may adhere to the denuded, nonfibrinolytic surface and may subsequently predispose to a granulation tissue response and fibrosis.r4 Also, chemical agents capable of producing fibrosis (10 percent formalin, phenol and nitrogen mustard) and trauma have been shown to reduce fibrinolytic activity of pericardium, pleura and peritoneum.15 An inference is that this loss of fibrinolytic activity contributes to fibrosis. It seems probable that the development of posttraumatic and postoperative constrictive pericarditis is related to the interaction of more than one etiologic factor or process. The extensiveness of serosal injury,13J4 the degree and persistence of bleeding,14 adequacy of fibrinolytic and absorptive mechanisms,14J5 and the occurrence of a postpericardiotomy syndromei may be important variables. In addition, undefined host factors may contribute to the unpredictable manner in which constrictive pericarditis develops both experimentally and clinically. In the setting of several interacting etiologic factors, the contribution of any one factor may be obscured, especially if the etiologic relation is fairly weak. Diagnosis of postoperative pericardial constriction: Undoubtedly, postoperative pericardial constriction occasionally goes unrecognized. The diag-
nosis should be considered in the presence of unexpected postoperative right heart failure-even in the presence of cardiomegaly and left heart failure. Constrictive pericarditis is occasionally rapid in onset1 and, unlike tamponade, is frequently not associated with pulsus paradoxus.17Js Coexistent tamponade may confuse the clinical picture.le Milder forms of pericardial constriction may be apparent only with provocative
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maneuvers such as volume overload, although such mild constrictive pericarditis is of debated clinical significance.20,21 Previously reported cases: Detailed information is available in relation to only four of the previously reported cases of constrictive pericarditis occurring after cardiac surgery. 44 Three of the patients had pericardial constriction after coronary bypass surgery and successful reoperation.4*6 One patient died of unsuspected constrictive pericarditis after aortic and mitral valve replacement.5 Two patients had evidence of postoperative mediastinal hemorrhage4T6; one had inadvertent mediastinal Plasmanate infusion4 and a fourth had previous mediastinal irradiation, not believed to be of etiologic significance.” Three patients, including the latter patient, were receiving warfarin on hospital discharge after operation.4 Evidence of pericarditis in the postoperative period is described in only two of the cases,4 but may have been unrecognized in the other cases. Clinical features of our three cases: Only one of our three patients had surgical confirmation of constrictive pericarditis. Right ventricular infarction, restrictive myocardial disease and cardiac tamponade may result in constrictive hemodynamics.22 However, these patients did not have antecedent restrictive myocardial disease and had no clinical or coronary arteriographic evidence of postoperative right ventricular infarction. Pericardial effusions were excluded echocardiographically. Our three patients had evidence of postoperative constrictive pericarditis within a 6 week period. This is of interest, especially since constrictive pericarditis following cardiac surgery had not been previously recognized at our institution. While possibly coincidental, the temporal proximity of these cases leads to the questions of a common etiology. Each of the patients had hypothermic myocardial preservation, received one or more saphenous vein bypass grafts, had the pericardium left open, and experienced an uncomplicated intraoperative course. The early postoperative course was relatively benign although chest X-ray films in the third and least severely affected of these patients showed postoperative mediastinal widening suggestive of mediastinal accumulation of blood. Subsequently, all three patients had manifestations consistent with a post-pericardiotomy syndrome. Each of the patients was placed on dipyridamole and aspirin at time of discharge from the hospital. Although the postoperative use of dipyridamole and aspirin had been fairly routine at our institution during the past several years, the possibility exists that these drugs may have contributed to subclinical oozing of blood into the pericardium with subsequent pericardial fibrosis. Role of pericardial irrigation with povidoneiodine (Betadine) solution: The pericardium in all
three patients had been irrigated at the time of surgery with povidone-iodine solution in saline solution of approximately 1:20 strength. This practice had been initiated a few months earlier and was carried out on approximately 100 patients to provide improved anti-
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sepsis. Irrigation of infected mediastinal wounds with povidone-iodine solution has been reported,23 and the use of povidone-iodine for antisepsis in abdominal surgery has been recently reviewed.24 Povidone-iodine solution is apparently successful in the treatment of mediastinal infections and is effective for prevention of peritonitis and abdominal wound infection. Unlike antibiotics, povidone-iodine has not been associated with the development of bacterial resistance. Most antiseptics are capable of injuring normal tissues. Experimentally, however, povidone-iodine has been shown to have very little tissue toxicity.25,26 Still, one would reasonably wonder about the effects of intrapericardial instillation of this chemical. Accordingly, a somewhat limited and preliminary investigation at this institution was undertaken using an animal model. Under general anesthesia six goats had the pericardium exposed and one-fourth strength povidone-iodine was injected into the pericardial space with a fine gauge needle. Inadvertent intramyocardial injection in one of the animals was associated with ventricular arrhythmias. All animals survived. Central venous pressure was measured
AFTER
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ET AL.
weekly during the following 6 weeks and remained normal. At 6 weeks the goats underwent a second thoracotomy. Appreciable pericardial fibrosis had developed in only the animal which had had traumatic, intramyocardial injection of povidone-iodine. These data suggest that intrapericardial instillation of povidone-iodine is well tolerated in instances where myocardial and pericardial injury have not occurred. However, the experimental model differs from the clinical model in which pericardial and epicardial trauma with associated bleeding occur invariably. It is possible that povidone-iodine in conjunction with pericardial trauma and bleeding may predispose to the development of constrictive pericarditis. The three cases of apparent postoperative constrictive pericarditis described in this report lead us to question the advisability of routine intrapericardial irrigation of this substance despite considerable data supporting its benignity. A randomized, prospective study to further ascertain possible clinical effects of such pericardial irrigation is probably necessary before final conclusions can be made.
References
5. 6.
7.
6. 9. 10.
11.
12. 13.
14.
Spodick OH: The pericardium: structure, function and disease spectrum. Cardiovasc Clin 7:1-10, 1976 Wise DE, Conti CR: Constrictive pericarditis. Cardiovasc Clin 7: 197-209, 1976 Hkschmann JV: Pericardial constriction. Am Heart J 96: 1 lo- 122, 1978 Kendall ME, Rhodes OR, Wolte W: Cardiac constriction following aorta-to-coronary bypass surgery. J Thorac Cardiovasc Surg 64:142-153, 1972 Simon JS, Pluth JR: Constrictive pericarditis. Ann Thorac Surg 21: 440-441. 1976 Brown DF, Dkfer 1: Pericardial constriction as a late complication of coronary bypass surgery. J Thorac Cardiovasc Surg 74:61-64, 1977 Kllman JW, Busk CA, Wooley ff, StangJM, lepty J, Baba N: The changing spectrum of pericardiectomy for chonic pericarditis: occult constrictive pericarditis. J Thorac Cardiovasc Surg 74: 668-673, 1977 Molntosh HD, Garcia JA: The first decade of aortocoronary bypass grafting, 1967-1977: a review. Circulation 57:405-431, 1978 Bull BS, Brallsford JD: The Zeta sedimentation ratio. Blood 40: 550-559.1972 Beck CS, Griswold RA: Pericardiectomy in the treatment of the Pick syndrome: experimental and clinical observations. Arch Surg 21:1064-1113, 1930 Beck CS: The effect of surgical solution of chlorinated soda (Dakin’s solution) in the pericardial cavity. Arch Surg 18:1659-1671, 1929 Ehrenhaft JL, Taber RE: Hemopericardium and constrictive pericarditis. J Thorac Surg 24:355-368, 1952 Sbokos CG, Karayannacos PE, Kontaxis A, Kambylafkas J, SkaWceasGD: Traumatic hemopericardium and chronic constrictive pericarditis. Ann Thorac Surg 23:225-229, 1977 Clfff WJ, Groberty J, Ryan GB: Postoperative pericardial adhesions.
15. 16. 17. 18.
19. 20.
21 22.
23.
24. 25.
26.
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The role of mild serosal injury and spilled blood. J Thorac Cardiovast Surg 65:744-750, 1973 Porter JM, Ball AP, Silver D: Mesothelial fibrinolysis. J Thorac Cardiovasc Surg 62:725-730, 1971 Goldstein S, Yu PN: Constrictive pericarditis after blunt chest trauma. Am Heart J 69:544-550, 1969 Wood P: Chronic constrictive pericarditis. Am J Cardiol7:48-61, 1961 Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 26:460-469, 1970 Hancock EW: Subacute effusive-constrictive pericarditis. Circulation 43:i83-192. 1971 Bush CA, Stang JY, Wooley CF, Kllman JW: Occult constrictive pericardial disease: diagnosis by rapid volume expansion and correction by pericardiectomy. Circulation 56:924-930, 1977 Fowler NO: Occult constrictive pericardial disease (letter). Circulation 58:189, 1978 Jensen D, Goolsby J, Oliva P: Hemodynamic pattern resembling pericardial constriction after acute inferior myocardial infarction with right ventricular infarction. Am J Cardiol 42:858-861, 1978 Thurer R, Bognolo D. Vargas A, lsch JH, Kaiser GA: The management of mediastinal infection following cardiac surgery. An experience utilizing continuous irrigation with povidone-iodine. J Thorac Cardiovasc Surg 68:962-968, 1974 Gillmore OJA: A reappraisal of the use of antiseptics in surgical practice. Ann R Coll Surg Engl 59:93-103, 1977 Branemark PI, Ekholm R, Albrektsson 8, Lindetrom J, Lundborg G, Lundskog J: Tissue injw caused by wound disinfectants. J Bone Jt Surg 49-A:48-62. 1967 Faddh D, Daniel D, Bayer J: Tissue toxicity of antiseptic solutions. A study of rabbit articular and periarticular tissues. J Trauma 17: 895-897, 1977
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ROBERT MARSA, MD SUKH MEHTA, MD, FACC WILLIAM WILLIS, MD, FACC LEONARD BAILEY, MD Loma Linda, California
Although postoperative constrictive pericarditis is rare, the diagnosis should be conskfered when unexplained right-&fed heart failure deveb after cardiac surgery. Within a 6 week interval, evidence of constrictive pericarditis developed in three patients who had recently undergone myocardial revascularization. One patient presented with biventricular failure, pericardial effusion and suspected tamponade. Severe constrictive pericarditis was demonstrated at subsequent operation. An apparent postpericardiotomy syndrome preceded evidence of right heart failure in the other two patients. Etiologic considerations include the possibility that pericardial irrigation with povidone-iodine (Betadine) solution may have contributed to subsequent fibrosis.
Although constrictive pericarditis is frequently idiopathic, a wide variety of causes, including cardiac surgery, have been described.1-7 An estimated 300,000 to 400,000 coronary arterial bypass operations were performed from 1967 to 1977 and the number performed annually is now thought to approach 100,000.8 Yet to our knowledge, only seven cases of overt constrictive pericarditis occurring after heart surgery have been reported in English language studies.4-7 Experience at our institution supports the rarity of this finding; in nearly 2,000 cardiac surgical procedures performed in the past 8 years, constrictive pericarditis was not recognized as a postoperative complication. Recently, however, we encountered three patients (Table I) who had evidence of pericardial constriction after myocardial revascularization. Possible causes of postoperative constrictive pericarditis include hemopericardium, mediastinal Plasmanate@ infusion, postpericardiotomy syndrome and previous mediastinal irradiation. Review of our three cases led us to entertain the possibility of an additional, previously unrecognized cause. Case Reports
From the Departments of Medicine and Surgery, Loma Linda University School of Medicine, Loma Linda, California. Manuscript received January 10, 1979, accepted February 1, 1979. Address for reprints: Robert Marsa, MD. Division of Cardiology, Deparmwnt of Medicine, Lorna Linda University Medical Center, Loma Linda, California 92350.
Case 1: This 54 year old white man, an insurance inspector, had known bronchial asthma and coronary artery disease. Coronary arteriography and left ventriculography on August 17, 1977 revealed extensive coronary artery disease with occlusion of the dominant right coronary artery and severe stenosis of the left anterior descending and the obtuse marginal arteries. The left ventricular inferior wall was severely hypokinetic and the lateral wall moderately hypokinetic. Left ventricular diastolic pressures were normal (Table II). Two weeks after coronary arteriography myocardial revascularization was performed with placement of a sequential saphenous vein graft to the left anterior descending and superior obtuse marginal arteries. Myocardial preservation was accomplished by bathing in iced saline solution. The pericardium was irrigated with povidone-iodine (Betadine@) solution, diluted approximately 1:20 in isotonic saline solution, and was left open before closure of the sternotomy incision. Transient S-T segment elevation was observed in the electrocardiogram on the 1st postoperative day. The patient’s initial postoperative course was otherwise
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TABLE I Clinical Summary of Three Cases
Age (yr) & sex Vessels diseased on coronary angiography Course after myocardial revascularization
Electrocardiography* Chest X-ray film* Echocardiography’ Angiography’
Case 3
Case 2
Case 1 54M 3 vessels
50M 3 vessels
61M 2 vessels
Rehospitalized 5 weeks postoperatively with suspected tamponade. Pericardial effusion cleared with corticosteroids. Severe constrictive pericarditis confirmed surgically Low voltage, T wave inversion
Post pericardiotomy syndrome early in course. Rehospitalized 5 weeks postoperatively with right heart failure and pericardial knock
Mediastinal widening 1 day postoperatively. Subsequent postpericardiotomy syndrome. Rehospitalized 4 weeks postoperatively with evidence of right heart failure.
Widespread T wave inversion Normal Suspected pericardial thickening All arafts oatent
Widespread T wave inversion Left pleural effusion Asymmetric septal hypertrophy
Cardiomegaly, congestive failure Disappearance of pericardial effusion All grafts patent
All arafts oatent
* Findings near time of postoperative cardias catheterization.
uncomplicated, and he was discharged 8 days after operation on a regimen of dipyridamole and aspirin. Five weeks after operation, he was rehospitalized because of severe shortness of breath with chest X-ray and clinical findings of biventricular failure. A pericardial friction rub, marked jugular venous distension and a 20 mm Hg paradoxic pulse suggested cardiac tamponade. An echocardiogram demonstrated a moderately large posterior pericardial effusion. Although the patient was afebrile and had a normal erythrocyte sedimentation rate (Zeta sedimentation ratio),9 a postpericardiotomy syndrome with tamponade was suspected, and he was treated with digoxin, furosemide and prednisone (60 mg/day tapered over several days to 10 mg daily). At the time of discharge 7 weeks after operation, the paradoxic pulse had decreased to 10 mm Hg and there had been mild reduction of jugular venous distension. However, 5 days later the patient was again hospitalized because of persistent dyspnea and weakness. Marked jugular venous distension was again observed and a 10 mm Hg paradoxic pulse was noted. No pericardial knock or friction rub was detected. The liver was palpable 6 cm below the right costal margin, and mild ankle edema was present. The echocardiogram indicated disappearance of the previously demonstrated pericardial effusion. The electrocardiogram shotier+! diminished QRS voltage, by comparison wiq the early postoperative tracings, and generalized T wave inversion. The chest X-ray film revealed moderate cardiomegaly, blunting of both costophrenic angles as well as pulmonary vascular congestion (Fig. 1).
Cardiac catheterization on October 31 (2 months after operation) revealed severely elevated and virtually equal left ventricular diastolic, pulmonary arterial wedge, pulmonary arterial diastolic, right ventricular diastolic and right atria1 pressures. A typical “square root” contour was present in the ventricular pressure tracings (Fig. 2), and the aortic pressure tracing had a 20 mm Hg paradoxic pulse. The sequential saphenous vein graft was widely patent. Mild progression of disease was noted in the left coronary system, but did not account for deterioration of left ventricular function with moderate generalized hypokinesia in addition to the previously observed inferior and lateral wall hypokinesia. No pericardial calcification was seen. At operation performed later the same day, several hours were required for decortication of a very adherent and densely fibrous thickened pericardium and epicardial peel. Subsequent histopathologic examination of the pericardium disclosed extensive fibrosis, chronic inflammatory changes and scattered areas with foreign body-type giant cells. The early postoperative course was complicated by congestive heart failure and pulmonary edema. On follow-up 10 months after pericardiectomy, the patient continued to require furosemide for control of heart failure but had a normal jugular venous pressure and no paradoxic pulse. Case 2: This 50 year old white man, a hydraulics technician, had an acute anteroseptal myocardial infarction in May 1977. Coronary arteriography and left ventricular angiography were performed on August 23,1977 and revealed hypokinesia of the
TABLE II Comparison of Preoperative (Pre) and Postoperative (Post) Catheterization Data
LVEF Pressures (mm Hg) Right atrium Right ventricle Pulmonary artery Pulmonary arterial wedge Left ventricle Aorta
0.42
Post
Pre 0.51
0.27 28 40124’ 35122 28
130112 135178
150114 160198
110/26’+ 110/82+
Plateauing of mid and late diastolic pressures. + 20 mm Hg paradoxic pulse. l
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Case 3
Case 2
Case 1 Pre
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Post
Pre
Post
0.48
0.53
0.41
29&’ 30114 15
25:4 25/12 7
26::3’ 26113 13
130117’ 132192
150114 150195
108115’ 115183
CONSTRICTIVE
anterolateral and apical left ventricle, occlusion of the left anterior descending coronary artery and multiple stenoses of the circumflex and right coronary systems. Left ventricular diastolic pressures were normal. On September 2,1977 a saphenous vein graft was placed to the right coronary artery and a sequential graft to the left anterior descending and inferior obtuse marginal arteries. Myocardial preservation was accomplished by bathing in iced saline solution. The pericardium was irrigated with povidone-iodine solution in saline solution of approximately 1:20 concentration and was left open. The patient’s initial postoperative course was uncomplicated. However, on the 3rd postoperative day he experienced anorexia and nausea and had a temperature of 38°C. Results of serum liver function tests became abnormal:Total bilirubin was 2.9 mg/lOO ml, direct bilirubin 1 mg/lOO ml, glutamic pyruvate transaminase 327 units (normal 0 to 40 units), alkaline phosphatase 103 units (normal 30 to 100 units) and hepatitis-associated antigen negative. Serial electrocardiograms were not appreciably changed from a preoperative tracing. The patient’s appetite gradually improved, and an intermittent low grade fever cleared in several days. The initial postoperative chest X-ray films showed no abnormality, but the film obtained 10 days postoperatively revealed a significant increase in cardiac size and a small left pleural effusion.
PERICARDITIS AFTER MYOCARDIAL REVASCULARIZATION-MARSA
FIGURE 1. pulmonary
ET AL.
Case 1. Chest roentgenogram showing cardiomegaly vascular congestion 4 days before pericardiectomy.
and
FKXJRE 2. Case 1. Pressure tracings. Top, simultaneous right (RV) and left (LV) ventricular pressure tracings typical of constrictive pericarditis. Bottom, aortic (AO) pressure tracing revealing a prominent paradoxic pulse.
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Despite persistence of moderately abnormal serum liver enzymes, the patient was discharged 12 days postoperatively on a regimen of dipyridamole and aspirin. A subsequent oral cholecystogram demonstrated cholelithiasis. Five weeks postoperatively the patient was hospitalized in another hospital with a several day history of frank pretibial, scrotal and presacral edema. The examining physician reported elevation of the jugular venous pressure and a third heart sound. No paradoxic pulse was detected. The chest X-ray film revealed bilateral pleural effusion without pulmonary vascular congestion. Serum liver enzyme determinations and total bilirubin were normal. The patient was treated with furosemide, digoxin and prednisone and had an 8 kg weight loss in 12 days. Two months after operation, he returned to this medical center for further evaluation. Despite continued use of furosemide, 80 mg each morning, the jugular venous pressure was elevated to the angle of the jaw with the patient at 30”. There was no paradoxic pulse or peripheral edema, although a prominent third heart sound or pericardial knock was present. An echocardiogram suggested pericardial thickening but did not reveal effusion. The heart size shown in the chest X-ray film had returned to normal from that in the film obtained 10 days postoperatively. Serum enzymes and albumin were normal, although total bilirubin was mildly elevated (1.7 mg/lOO ml). Cardiac catheterization revealed findings typical of constrictive pericarditis with abnormally elevated and nearly equal diastolic pressures in all cardiac chambers. Prominent X and Y descents were seen in the right atria1 pressure recording, and the ventricular pressure tracings showed a typical “dip and plateau” diastolic pressure contour (Fig. 3), with mid and late ventricular diastolic pressures averaging about 15 mm Hg (right ventricular systolic pressure 29 mm Hg). Straightening of the right heart border was demonstrated with right atria1 angiography. The left ventriculogram was not appreciably changed from the preoperative study. Coronary arteriography revealed well functioning saphenous vein grafts. Although the right coronary arterial stenoses were unchanged, there was a striking reduction of right coronary mobility as viewed in the right anterior oblique projection with apparent fixation of anterior right ventricular branches. Although this patient is thought to have moderately severe constrictive pericarditis, he is now being treated medically. Case 3: This 61 year old white man, a mechanic, had a 1 year history of gradually worsening angina and was hospitalized
for coronary arteriography. Cardiovascular examination was normal except for the presence of a grade 216 blowing, nonholosystolic apical murmur that did not change significantly with the Valsalva maneuver or with inspiration. The chest X-ray film revealed borderline cardiomegaly and the electrocardiogram showed minor nonspecific S-T segment depression. An echocardiogram demonstrated asymmetric septal hypertrophy. Cardiac catheterization and coronary arteriography, performed on October 4, 1977, revealed two vessel coronary artery disease with multiple stenoses of the left anterior descending coronary artery and critical stenosis distally in the small but technically dominant right coronary artery. Right heart pressures and left ventricular contractions were normal, although the left ventricular end-diastolic pressure was mildly elevated. No gradient could be demonstrated across the left ventricular outflow tract even with provocative maneuvers. On October 12, 1977 the patient underwent myocardial revascularization with placement of saphenous vein grafts to the distal right coronary artery and sequentially to the mid and distal left anterior descending coronary artery. Myocardial preservation was accomplished by aortic root infusion of an iced dextrose solution followed by topical cooling with iced saline solution. The pericardium was irrigated with povidone-iodine in saline solution of approximately 1:20 strength and was left open. A chest X-ray film obtained 1 day postoperatively revealed mediastinal widening and cardiomegaly. The early postoperative course was complicated by pulmonary congestion, left basal atelectasis, a left pleural effusion and an intermittent low grade fever. A matching ventilationperfusion defect of the left lung base was revealed in a lung scan. The electrocardiogram 3 days after operation was consistent with pericarditis and showed widespread S-T segment elevation not seen in the tracing 1 day after operation. On the day of discharge 1 week postoperatively, the lung fields were clear to auscultation and the patient was afebrile. Four weeks after operation the patient reported the recent onset of exertionally induced nausea, chest tightness and abdominal distress associated with a low grade fever. He denied pleuritic pain or recurrence of angina1 chest pain. On physical examination he was observed to have a heart rate of 70 beats/min, a blood pressure of 1lo/80 mm Hg and 6 to 7 mm Hg inspiratory decrease in systolic blood pressure. The venous pressure was moderately increased with prominent A and V waves extending to the angle of the mandible with the patient at 30”. Dullness was noted at the left lower lung base and was
40
I” E 3o E s a 20 2 g 10
-I
01 1 SEC F
+-
180
FIGURE 3. Case 2. Pressure tracings. Superimposed right (RV) and left (LV) ventricular pressure tracings exhibiting the classic “square root” configuration of constrictive pericarditis.
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associated with bronchial breath sounds. Cardiac examination was unchanged from the preoperative evaluation. The liver was palpable, but it had a normal span and there was no peripheral edema. A chest roentgenogram revealed mild cardiac enlargement, reduced from that shown in the early postoperative films, and increased size of the left pleural effusion with apparently normal pulmonary vasculature. An electrocardiogram showed generalized nonspecific T wave inversion. The echocardiogram did not indicate pericardial effusion, but again revealed asymmetric septal hypertrophy. The patient was treated with digoxin and furosemide, 40 mg daily, and after a 3 kg weight loss underwent repeat cardiac catheterization. Pressure data on cardiac catheterization were consistent with moderate constrictive pericarditis with nearly equal diastolic pressures in all cardiac chambers (Fig. 4). The mean right atria1 pressure was 11 mm Hg compared with the preoperative valve of 2 mm Hg. There was an 8 to 10 mm Hg
PERICARDITIS
AFTER MYOCARDIAL
REVASCULARIZATION-MARSA
ET AL.
respiratory variation in the aortic systolic pressure. Right atria1 angiography revealed straightening of the right heart border and left ventricular angiography demonstrated a mild, global decrease in left ventricular contractions with an ejection fraction of 0.41 compared with the preoperative value of 0.53. The parent coronary arteries were not appreciably changed from the preoperative study and the saphenous vein bypass grafts were widely patent. This patient is not considered to have severe constrictive pericarditis and is being treated medically.
Discussion Causes of postoperative pericardial adhesions, fibrosis and constriction: Although pericardial adhesions are readily produced by surgical and chemical trauma, fibrosis leading to recognized constriction is
0 RA preoperative
FIGURE 4. Case 3. Pressure tracings. lop, comparison of the pre- and postoperative right atrial (RA) pressure tracings reveals development of equal A and V waves with prominent X and Y descents in the postoperative tracing. Bottom, postoperative left ventricular diastolic and right atrial pressures are virtually identical.
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PERICARDITIS AFTER MYOCARDIAL REVASCULARIZATION-MARSA
infrequent and is usually unpredictable.2Jo Approximately 50 years ago constrictive pericarditis was produced experimentally in dogs by pericardial instillation of Dakin’s solution (sodium hypochlorite solution, a topical antiseptic). l”,ll Dakin’s solution had been described as a treatment for purulent pericarditis, but was subsequently shown to produce a hemorrhagic pericarditis in normal animals. Animals surviving intrapericardial instillation of this solution frequently manifested constrictive pericarditis in 1 or 2 months. In a more recent experiment, intrapericardial injection of lipid extract of blood resulted in adhesions and fibrosis.12 However, only one of six dogs had definite constriction. Atraumatic injection of autologous blood into the pericardial space is generally not followed by appreciable fibrosis, whereas hemopericardium in association with pericardial injury leads to variable fibrosis.13J4 This synergistic effect has been observed after direct mechanical injury and (using a rabbit model) after 5 to 7 minutes’ drying of the pericardial serosal surface with a “gentle” stream of compressed air. Of particular interest, in the later experiment, serosal drying without addition of blood did not produce adhesions or fibrosis.14 Normal serosal tissue has well demonstrated fibrinolytic activity. Drying of a serosal surface results in loss of mesothelial cells lining the surface and total loss of fibrinolytic activity. It has been suggested that clotted blood may adhere to the denuded, nonfibrinolytic surface and may subsequently predispose to a granulation tissue response and fibrosis.r4 Also, chemical agents capable of producing fibrosis (10 percent formalin, phenol and nitrogen mustard) and trauma have been shown to reduce fibrinolytic activity of pericardium, pleura and peritoneum.15 An inference is that this loss of fibrinolytic activity contributes to fibrosis. It seems probable that the development of posttraumatic and postoperative constrictive pericarditis is related to the interaction of more than one etiologic factor or process. The extensiveness of serosal injury,13J4 the degree and persistence of bleeding,14 adequacy of fibrinolytic and absorptive mechanisms,14J5 and the occurrence of a postpericardiotomy syndromei may be important variables. In addition, undefined host factors may contribute to the unpredictable manner in which constrictive pericarditis develops both experimentally and clinically. In the setting of several interacting etiologic factors, the contribution of any one factor may be obscured, especially if the etiologic relation is fairly weak. Diagnosis of postoperative pericardial constriction: Undoubtedly, postoperative pericardial constriction occasionally goes unrecognized. The diag-
nosis should be considered in the presence of unexpected postoperative right heart failure-even in the presence of cardiomegaly and left heart failure. Constrictive pericarditis is occasionally rapid in onset1 and, unlike tamponade, is frequently not associated with pulsus paradoxus.17Js Coexistent tamponade may confuse the clinical picture.le Milder forms of pericardial constriction may be apparent only with provocative
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maneuvers such as volume overload, although such mild constrictive pericarditis is of debated clinical significance.20,21 Previously reported cases: Detailed information is available in relation to only four of the previously reported cases of constrictive pericarditis occurring after cardiac surgery. 44 Three of the patients had pericardial constriction after coronary bypass surgery and successful reoperation.4*6 One patient died of unsuspected constrictive pericarditis after aortic and mitral valve replacement.5 Two patients had evidence of postoperative mediastinal hemorrhage4T6; one had inadvertent mediastinal Plasmanate infusion4 and a fourth had previous mediastinal irradiation, not believed to be of etiologic significance.” Three patients, including the latter patient, were receiving warfarin on hospital discharge after operation.4 Evidence of pericarditis in the postoperative period is described in only two of the cases,4 but may have been unrecognized in the other cases. Clinical features of our three cases: Only one of our three patients had surgical confirmation of constrictive pericarditis. Right ventricular infarction, restrictive myocardial disease and cardiac tamponade may result in constrictive hemodynamics.22 However, these patients did not have antecedent restrictive myocardial disease and had no clinical or coronary arteriographic evidence of postoperative right ventricular infarction. Pericardial effusions were excluded echocardiographically. Our three patients had evidence of postoperative constrictive pericarditis within a 6 week period. This is of interest, especially since constrictive pericarditis following cardiac surgery had not been previously recognized at our institution. While possibly coincidental, the temporal proximity of these cases leads to the questions of a common etiology. Each of the patients had hypothermic myocardial preservation, received one or more saphenous vein bypass grafts, had the pericardium left open, and experienced an uncomplicated intraoperative course. The early postoperative course was relatively benign although chest X-ray films in the third and least severely affected of these patients showed postoperative mediastinal widening suggestive of mediastinal accumulation of blood. Subsequently, all three patients had manifestations consistent with a post-pericardiotomy syndrome. Each of the patients was placed on dipyridamole and aspirin at time of discharge from the hospital. Although the postoperative use of dipyridamole and aspirin had been fairly routine at our institution during the past several years, the possibility exists that these drugs may have contributed to subclinical oozing of blood into the pericardium with subsequent pericardial fibrosis. Role of pericardial irrigation with povidoneiodine (Betadine) solution: The pericardium in all
three patients had been irrigated at the time of surgery with povidone-iodine solution in saline solution of approximately 1:20 strength. This practice had been initiated a few months earlier and was carried out on approximately 100 patients to provide improved anti-
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sepsis. Irrigation of infected mediastinal wounds with povidone-iodine solution has been reported,23 and the use of povidone-iodine for antisepsis in abdominal surgery has been recently reviewed.24 Povidone-iodine solution is apparently successful in the treatment of mediastinal infections and is effective for prevention of peritonitis and abdominal wound infection. Unlike antibiotics, povidone-iodine has not been associated with the development of bacterial resistance. Most antiseptics are capable of injuring normal tissues. Experimentally, however, povidone-iodine has been shown to have very little tissue toxicity.25,26 Still, one would reasonably wonder about the effects of intrapericardial instillation of this chemical. Accordingly, a somewhat limited and preliminary investigation at this institution was undertaken using an animal model. Under general anesthesia six goats had the pericardium exposed and one-fourth strength povidone-iodine was injected into the pericardial space with a fine gauge needle. Inadvertent intramyocardial injection in one of the animals was associated with ventricular arrhythmias. All animals survived. Central venous pressure was measured
AFTER
MYOCARDIAL
REVASCULARIZATION-MARSA
ET AL.
weekly during the following 6 weeks and remained normal. At 6 weeks the goats underwent a second thoracotomy. Appreciable pericardial fibrosis had developed in only the animal which had had traumatic, intramyocardial injection of povidone-iodine. These data suggest that intrapericardial instillation of povidone-iodine is well tolerated in instances where myocardial and pericardial injury have not occurred. However, the experimental model differs from the clinical model in which pericardial and epicardial trauma with associated bleeding occur invariably. It is possible that povidone-iodine in conjunction with pericardial trauma and bleeding may predispose to the development of constrictive pericarditis. The three cases of apparent postoperative constrictive pericarditis described in this report lead us to question the advisability of routine intrapericardial irrigation of this substance despite considerable data supporting its benignity. A randomized, prospective study to further ascertain possible clinical effects of such pericardial irrigation is probably necessary before final conclusions can be made.
References
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12. 13.
14.
Spodick OH: The pericardium: structure, function and disease spectrum. Cardiovasc Clin 7:1-10, 1976 Wise DE, Conti CR: Constrictive pericarditis. Cardiovasc Clin 7: 197-209, 1976 Hkschmann JV: Pericardial constriction. Am Heart J 96: 1 lo- 122, 1978 Kendall ME, Rhodes OR, Wolte W: Cardiac constriction following aorta-to-coronary bypass surgery. J Thorac Cardiovasc Surg 64:142-153, 1972 Simon JS, Pluth JR: Constrictive pericarditis. Ann Thorac Surg 21: 440-441. 1976 Brown DF, Dkfer 1: Pericardial constriction as a late complication of coronary bypass surgery. J Thorac Cardiovasc Surg 74:61-64, 1977 Kllman JW, Busk CA, Wooley ff, StangJM, lepty J, Baba N: The changing spectrum of pericardiectomy for chonic pericarditis: occult constrictive pericarditis. J Thorac Cardiovasc Surg 74: 668-673, 1977 Molntosh HD, Garcia JA: The first decade of aortocoronary bypass grafting, 1967-1977: a review. Circulation 57:405-431, 1978 Bull BS, Brallsford JD: The Zeta sedimentation ratio. Blood 40: 550-559.1972 Beck CS, Griswold RA: Pericardiectomy in the treatment of the Pick syndrome: experimental and clinical observations. Arch Surg 21:1064-1113, 1930 Beck CS: The effect of surgical solution of chlorinated soda (Dakin’s solution) in the pericardial cavity. Arch Surg 18:1659-1671, 1929 Ehrenhaft JL, Taber RE: Hemopericardium and constrictive pericarditis. J Thorac Surg 24:355-368, 1952 Sbokos CG, Karayannacos PE, Kontaxis A, Kambylafkas J, SkaWceasGD: Traumatic hemopericardium and chronic constrictive pericarditis. Ann Thorac Surg 23:225-229, 1977 Clfff WJ, Groberty J, Ryan GB: Postoperative pericardial adhesions.
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The role of mild serosal injury and spilled blood. J Thorac Cardiovast Surg 65:744-750, 1973 Porter JM, Ball AP, Silver D: Mesothelial fibrinolysis. J Thorac Cardiovasc Surg 62:725-730, 1971 Goldstein S, Yu PN: Constrictive pericarditis after blunt chest trauma. Am Heart J 69:544-550, 1969 Wood P: Chronic constrictive pericarditis. Am J Cardiol7:48-61, 1961 Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 26:460-469, 1970 Hancock EW: Subacute effusive-constrictive pericarditis. Circulation 43:i83-192. 1971 Bush CA, Stang JY, Wooley CF, Kllman JW: Occult constrictive pericardial disease: diagnosis by rapid volume expansion and correction by pericardiectomy. Circulation 56:924-930, 1977 Fowler NO: Occult constrictive pericardial disease (letter). Circulation 58:189, 1978 Jensen D, Goolsby J, Oliva P: Hemodynamic pattern resembling pericardial constriction after acute inferior myocardial infarction with right ventricular infarction. Am J Cardiol 42:858-861, 1978 Thurer R, Bognolo D. Vargas A, lsch JH, Kaiser GA: The management of mediastinal infection following cardiac surgery. An experience utilizing continuous irrigation with povidone-iodine. J Thorac Cardiovasc Surg 68:962-968, 1974 Gillmore OJA: A reappraisal of the use of antiseptics in surgical practice. Ann R Coll Surg Engl 59:93-103, 1977 Branemark PI, Ekholm R, Albrektsson 8, Lindetrom J, Lundborg G, Lundskog J: Tissue injw caused by wound disinfectants. J Bone Jt Surg 49-A:48-62. 1967 Faddh D, Daniel D, Bayer J: Tissue toxicity of antiseptic solutions. A study of rabbit articular and periarticular tissues. J Trauma 17: 895-897, 1977
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