[POSTAPOPLEXY SYNDROME. SUPPLEMENT: POSTMYOCARDIAL INFARCTION SYNDROME, POSTPERICARDIOTOMY SYNDROME].
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Postpericardiotomy syndrome often delays recovery from cardiac operation. Pericardial effusion is an important sequela of postpericardiotomy syndrome. To define the relationship between postpericardiotomy syndrome and pericardial effusion, we performed four to seven serial echocardiograms (echoes) between postoperative day 0 and postoperative day 10 in 40 children who had operation requiring pericardiotomy. We also performed daily physical examination on each patient for clinical evidence of postpericardiotomy syndrome. Echocardiographic signs of pericardial effusion developed in 21/40 patients (53%). The effusion was present by postoperative day 5 in 19/21 patients. Clinical signs of postpericardiotomy syndrome occurred in 18/40 patients (45%). Among the 18 patients with postpericardiotomy syndrome, 16 had echocardiographic evidence of pericardial effusion. Thus the sensitivity of the echocardiogram was 89%. The pericardial effusion always developed prior to and persisted through clinical symptoms. We conclude that (1) pericardial effusion is present in over 50% of the patients following cardiac surgery, (2) it develops early in the postoperative period, and (3) once present, the effusion is persistent and frequently followed by clinical evidence of postpericardiotomy syndrome.
Postpericardiotomy syndrome is an immune phenomenon that occurs from several days to months after surgical incision of the pericardium. Prominent clinical features include fever, pericarditis, and pleuritis. Of 161 patients with Wolff-Parkinson-White syndrome who underwent surgical treatment, 50 (31%) developed postpericardiotomy syndrome 4-12 days later. Of these 50 patients, 38 had sufficiently complete records for analysis. Significant radiographic abnormalities were present in 30 (79%) of these 38 patients, pericardial effusions in 19 (50%), pleural effusions in 26 (68%), and pulmonary infiltrates in four (10%). These radiographic signs almost always developed within 2 days of the onset of symptoms, either before or after, and were essentially absent in the 76 patients who did not clinically develop the syndrome. Postoperative radiographs can be extremely valuable in first suggesting or confirming the suspicion of postpericardiotomy syndrome.
Postpericardiotomy syndrome has been recognized as a frequent complication following coronary artery bypass graft (CABG) surgery. We observed five cases of postpericardiotomy syndrome resulting in exudative pleural effusions with white blood cell differential counts greater than 80% lymphocytes. Tuberculosis, lymphoma, and other neoplasma have been major diseases associated with lymphocytic exudative pleural effusions. We feel postpericardiotomy syndrome is another important etiology that should be considered in post-CABG patients with lymphocytic pleural effusion.
Postpericardiotomy syndrome, a frequent complication of open-heart surgery, is characterized by fever, chest pain, and pericardial and pleural effusions. These signs may develop 1 to 12 weeks after intracardiac surgery in approximately 30 percent of patients. Although the etiology of the syndrome is unknown, evidence points to a viral and/or autoimmune cause. Postpericardiotomy syndrome is diagnosed after excluding other conditions such as endocarditis and pneumonia. In many cases, the syndrome is self-limiting and occurs only once, but in other cases the symptoms have recurred as many as eight times. When the symptoms recur, management is more difficult because optimal pharmacologic treatment is not known. Antiinflammatory agents, such as salicylates and steroids, represent the drugs most commonly used. Although analgesics with codeine or oxycodone are important for the patients' symptomatic relief, early recognition of the syndrome is the key to limiting the discomfort and possible complications associated with this condition.
Postpericardiotomy syndrome (PPS) is a frequent complication after cardiac surgery. In a recent study, elevated anticardiolipin antibody (ACLA) titres were observed in patients with PPS. The value of anti-heart muscle antibodies (AHA) for the diagnosis of PPS remains controversial. Therefore, a prospective double-blind study was performed to test the sensitivity and specificity of ACLA and AHA for the diagnosis of PPS. ACLA titres (ELISA) and AHA, elevated by immunofluorescence, the clinical course and routine laboratory parameters were assessed in 57 patients before and after elective cardiac surgery. ACLA increased and AHA first appeared after surgery in patients both with and without PPS. The sensitivities of a > or = 1.5-fold increase in IgM-ACLA titres, of a > or = 2-fold increase in IgG-ACLA titres and of the occurrence of AHA > or = 2+ for the diagnosis of PPS were 60%, 20% and 20%. The respective specificities were 43%, 79% and 85%. Thus, after cardiac surgery, increased ACLA titres and the occurrence of AHA, as assessed by immunofluorescence, may only contribute to the diagnosis of PPS to a limited extent.
The postpericardiotomy syndrome occurs in 10% to 40% of patients who undergo open-heart surgery. Its frequency is reportedly decreased when pericardial drainage is used. To challenge this, 50 consecutive patients (1 was disqualified) were randomly assigned to two groups: one in which only the anterior mediastinum was drained (group 1) and the other in which the anterior mediastinum and posterior pericardium were drained (group 2). The surgical procedures performed were: coronary artery bypass grafting in 14 patients, valve surgery in 23 and repair of congenital defects in 12. The two groups were similar with respect to age and the volume of blood drained. Significant differences were found only for the duration of bypass and volume of blood given. At 7 to 10 days there were no differences in the frequency of fever, thoracic pain or presence of arthralgia. Findings were similar in both groups for leukocyte count, sedimentation rate, serum lactic dehydrogenase value and for the frequency of positive blood, urine and sputum cultures. Six patients (three in each group) had a postpericardiotomy syndrome that required steroid treatment and prolonged hospitalization for 10 more days. However, none had postpericardiotomy syndrome complicating coronary artery bypass surgery. None of the patients had cardiac tamponade. This study demonstrates that pericardial drainage has no effect on the frequency of postpericardiotomy syndrome and appears to be unnecessary after open-heart surgery.
The postpericardiotomy syndrome occurs in up to one-third of children undergoing cardiac surgery. Its treatment includes anti-inflammatory agents, diuresis, and drainage of effusions. Administration of steroids can have a dramatic effect, but is limited by adverse effects. Usually the syndrome lasts weeks only, and persistence beyond six months is exceptional. We describe a rare case of chronic postpericardiotomy syndrome, with recurrent pericardial effusions and steroid dependency, that was treated successfully with a low weekly dose of methotrexate.
The postpericardiotomy syndrome is a febrile illness with pericardial and pleural reaction that either persists or appears beyond the 1st postoperative week. We believe that it begins in the 1st week after intrapericardial cardiac surgery, and that clinical signs of illness correlate with appearance of AHA and with significant rise in titer to AVA. Our present working hypothesis is that myocardial damage with bleeding into the pericardial sac at the time of surgery combines with concurrently acquired or reactivated viral illness to set the stage for the syndrome. The immune response is triggered by viral invasion of traumatized myocardium and an immune response is mounted, not against autologous myocardium per se but against the neo-antigen, the virus-infected myocardium. The illness is self-limited. It sometimes recurs but it seems to leave no sequelae other than the bad memory of a painful postoperative complication that prolonged hospitalization and delayed the realization of the full benefits of that heart operation.
BACKGROUND: Postpericardiotomy syndrome (PPS) is a troublesome complication of cardiac surgery, occurring in 10-45% of cases. Accepted modalities of treatment include nonsteroidal anti-inflammatory drugs, corticosteroids, and pericardiectomy in severe cases. The optimal method for prevention of PPS has not been established. Recent trial data have shown that colchicine is efficient in the secondary prevention of recurrent episodes of pericarditis. The aim of the present study was to evaluate the possible benefit of colchicine for the primary prevention of PPS in patients after cardiac surgery. To the best of our knowledge, this is the first study addressing this issue. PATIENTS AND METHODS: A prospective, randomized, double-blind design was used. The initial study group included 163 patients who underwent cardiac surgery in two centers in Israel between October 1997 and September 1998. On the 3rd postoperative day, the patients were randomly assigned to receive colchicine (1.5 mg/day) or placebo for 1 month. All were evaluated monthly for the first 3 postoperative months for development of PPS. RESULTS: 52 of the 163 patients were excluded because of postoperative complications, noncompliance, or gastrointestinal side effects of treatment. Of the 111 patients who completed the study, 47 (42.3%) received colchicine and 64 (57.7%) placebo. There was no statistically significant difference between the groups in clinical or surgical characteristics. PPS was diagnosed in 19 patients (17.1%), 5/47 cases (10.6%) in the colchicine group and 14/64 (21.9%) in the placebo group. The difference showed a trend toward statistical significance (p < 0.135). CONCLUSIONS: Colchicine may be efficacious for the prevention of PPS in patients after cardiac surgery. Further evaluations in larger clinical trials are warranted.
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Although the postpericardiotomy syndrome is a common complication of cardiac operations, the most effective drug regimen for the treatment of this condition has not been established. The present study was designed to evaluate the effectiveness of nonsteroidal antiinflammatory drugs (NSAIDs) in the treatment of postpericardiotomy syndrome, in a double-blind, placebo-controlled randomized trial with a 10-day course of ibuprofen or indomethacin. Of 1019 adult patients undergoing cardiac operations during a 14-month period, a diagnosis of postpericardiotomy syndrome was made in 187, and 149 were enrolled in the study. Diagnosis was based on the presence of at least two of the following: fever, anterior chest pain, and friction rub. Drug efficacy was defined as the resolution of at least two of these criteria within 48 hours of drug initiation. Ibuprofen and indomethacin were 90.2% and 88.7% effective, respectively, and both were significantly more effective than placebo (62.5%, p = 0.003). The occurrence of side effects, including nausea, vomiting, renal failure, and fluid retention, was low in all groups (13.1% for ibuprofen, 16.1% for indomethacin, and 16.7% for placebo [p = not significant). Length of hospital stay, incidence of ischemic events, and accumulation of significant pericardial effusions were similar in all groups. The results of this study demonstrate that both ibuprofen and indomethacin provide safe and effective symptomatic treatment for postpericardiotomy syndrome.
Postpericardiotomy syndrome (PPS) is a complication of any cardiac surgery or procedure involving entry into the pericardium. The syndrome presents as a delayed pleural or pericardial reaction, characterized by fever, chest pain, and a friction rub. Although symptoms often identify PPS, diagnosis may be aided by the use of radiography, echocardiography, electrocardiography, and laboratory analysis. PPS can cause considerable discomfort and anxiety. Furthermore, patients are at risk of pericardial effusion and cardiac tamponade. For these reasons and because the complication often extends hospitalization, health care professionals must familiarize themselves with the syndrome, recognize signs and symptoms early, and plan interventions accordingly.
We followed 34 consecutive patients with the postpericardiotomy syndrome for a median of 7 years. In each patient, the syndrome was documented by the occurrence of: (1) a pericardial type of pain or pericardial rub (or both); and (2) fever or an elevated erythrocyte sedimentation rate. The postpericardiotomy syndrome occurred at a median postoperative time of 4 weeks (range, 2 to 52 weeks). The duration of the syndrome was highly variable (range, 2 to 100 days; median, 22 days) and depended primarily on treatment; the median duration of symptoms in 21 patients treated with salicylates alone was only 4 days. Of the 9 patients receiving anticoagulants alone and in whom this treatment was continued, none had clinical evidence of hemopericardium. On follow-up, 7 patients (21%) had an initial recurrence at an interval of 1 to 3 months; 5 of these patients had further recurrences at an interval of 3 to 30 months. This long-term study indicates that the postperiocardiotomy syndrome is a benign but often recurrent clinical entity, presumably related to viral and/or immunologic factors.
BACKGROUND: Postpericardiotomy syndrome has been considered a disorder induced by viral infection. This conclusion is based on serologic criterions, but these may be unreliable following either cardiopulmonary bypass or transfusion therapy. Previous studies have not verified the proposed etiology either by isolation of viruses, or by detection of their genome. We sought, therefore, to clarify the role, if any, of viruses in this syndrome. METHODS AND RESULTS: We studied prospectively 149 children aged from 6 months to 16 years who were undergoing open heart surgery. Blood samples were collected from all prior to operation, and again 7 to 10 days post-operatively, and 47 were sampled at the time of development of symptoms of pericardial involvement. Serums were analyzed for the presence of IgM and IgG antibodies to cytomegalovirus, herpes simplex virus, and Epstein-Barr virus. The polymerase chain reaction was used for amplification when assessing the genome of the enteroviruses. Cultures for viruses were established on samples of stool, urine, and throat swabs collected 7 days post-operatively, and at the time of postpericardial symptoms. Pericardial fluid obtained from 5 patients with the syndrome was cultured for viruses, and tested for enterovirus genome. On the basis of clinical and echocardiographic findings, 34 children were determined to have definite evidence of the syndrome, 13 were considered to have possible evidence, and the results from these patients were compared to those from patients with no pericardial symptoms, the latter being matched for age and transfusion status. We isolated viruses from one or more sites in five patients with definite evidence (16%), from one (9%) of those with possible evidence, and from seven (19%) of the controls. All serums and pericardial samples were negative for enterovirus genome. IgM antibodies were found in only 5 patients, three with symptoms of pericardial involvement and two without. Rates of seroconversion to IgG for the viruses were lower in the patients with symptoms of pericardial involvement compared to controls, but were strongly influenced by transfusion status. CONCLUSION: Our study has provided no evidence to support a viral etiology for the postpericardiotomy syndrome.
Cardiac tamponade is a rare complication of the postpericardiotomy syndrome in the absence of anticoagulation therapy. Three cases are presented where cardiac tamponade developed as a result of the postpericardiotomy syndrome with normal coagulation parameters. The pericardial effusions were serous in two and serosanguinous in the third case. Pericardial fluid studies were consistent with an exudate. The effusion resolved following a single pericardial tap and short-term corticosteroid therapy in one case. Repeated pericardiocentesis and drainage via an indwelling catheter were required in the other two cases.
The postpericardiotomy syndrome occurs frequently after cardiac surgery, and shows a strong tendency to recur. It is characterized by febrile illness with an elevated erythrocyte sedimentation rate, leucocytosis, and symptoms of pulmonary and pleuro-pericardial inflammation. Pleural effusion is a common manifestation of this syndrome, and is usually left-sided. We describe a patient who shows a periodic left-sided pleural effusion with an interval of 5 to 6 weeks 18 months after cardiac surgery. This is the first description of a 'cyclic' pleural effusion due to the postpericardiotomy syndrome. On the basis of this case report and the literature, we discuss the pathogenesis, therapy and clinical outcome of this syndrome.
After nearly any form of cardiac surgery, an acute febrile illness characterized by leukocytosis, pericarditis with pericardial effusion, and pleural effusion may occur. In some instances, this postpericardiotomy syndrome may suggest the presence of mediastinal infection. Treatment of postpericardiotomy syndrome is conservative, and symptoms typically resolve with nonsteroidal antiinflammatory medication. We report a case of postpericardiotomy syndrome that mimicked recurrent mediastinal infection and developed after muscle flap closure of an infected sternal wound. Pericardial, pleural, and periflap fluid accumulated postmuscle flap closure and was sterile on culture. A diagnosis of postpericardiotomy syndrome was made, and the patient improved while receiving oral indomethacin. She has remained free of infection as of the 2-year follow-up.